Shakuyaku-kanzo-to induces pseudoaldosteronism characterized by hypokalemia, rhabdomyolysis, metabolic alkalosis with respiratory compensation, and increased urinary cortisol levels.

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Kinoshita, Hiroyuki; Okabayashi, Misako; Kaneko, Masakazu; Yasuda, Mutsuko; Abe, Keisuke; Machida, Akira; Ohkubo, Takuya; Kamata, Tomoyuki; Yakushiji, Fumiatsu

2009-04-01

Licorice, the primary ingredient of the Japanese herbal medicine shakuyaku-kanzo-to, can cause pseudoaldosteronism. Thus, shakuyaku-kanzo-to can cause this condition. A 79-year-old woman was brought to the emergency room. She had been experiencing general fatigue, numbness in the hands, and weakness in the lower limbs and could not stand up without assistance. She presented with hypokalemia (potassium level, 1.7 mEq/L), increased urinary excretion of potassium (fractional excretion of K, 21.2%), abnormalities on an electrocardiogram (flat T waves in II, III, AVF, and V1-6), rhabdomyolysis (creatine kinase level, 28,376 U/L), myopathy, metabolic alkalosis with respiratory compensation (O(2) flow rate, 2 L/min; pH, 7.473; pco(2), 61.0 mm Hg; po(2), 78.0 mm Hg; HCO(3), 44.1 mmol/L), hypertension (174/93 mm Hg), hyperglycemia (blood glucose level, 200-300 mg/dL), frequent urination, suppressed plasma renin activity (0.1 ng/mL/hour), decreased aldosterone levels (2.6 ng/dL), and increased urinary cortisol levels (600.6 microg/day; reference range, 26.0-187.0 microg/day). In this case, the observed reduction in the urinary cortisol levels, from 600.6 to 37.8 microg/day, led to a definitive diagnosis of pseudoaldosteronism instead of the apparent mineralocorticoid excess syndrome. Discontinuing shakuyaku-kanzo-to treatment and administering spironolactone and potassium proved effective in improving the patient's condition. Medical practitioners prescribing shakuyaku-kanzo-to should take into account the association between licorice, which is its main ingredient, and pseudoaldosteronism.

Baking soda induced severe metabolic alkalosis in a haemodialysis patient.

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Solak, Yalcin; Turkmen, Kultigin; Atalay, Huseyin; Turk, Suleyman

2009-08-01

Metabolic alkalosis is a rare occurence in hemodialysis population compared to metabolic acidosis unless some precipitating factors such as nasogastric suction, vomiting and alkali ingestion or infusion are present. When metabolic alkalosis develops, it may cause serious clinical consequences among them are sleep apnea, resistent hypertension, dysrhythmia and seizures. Here, we present a 54-year-old female hemodialysis patient who developed a severe metabolic alkalosis due to baking soda ingestion to relieve dyspepsia. She had sleep apnea, volume overload and uncontrolled hypertension due to metabolic alkalosis. Metabolic alkalosis was corrected and the patient's clinical condition was relieved with negative-bicarbonate hemodialysis.

[Alkalosis].

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Kościelska, Malgorzata; Mieczkowski, Mariusz

2013-01-01

An elevation of arterial blood pH called alkalosis remains an underestimated condition in hospitalized patients. Serious alkalosis can be associated with high risk of death. The disorder can be caused by increased concentration of bicarbonate (metabolic alkalosis) or decreased concentration of carbon dioxide (respiratory alkalosis). In most cases of metabolic alkalosis it is generated by vomiting or diuretic use, whereas respiratory alkalosis is provoked by hyperventilation associated with respiratory or neurological disorder. Maintenance of metabolic alkalosis is possible only in patients with impaired renal base excretion which is most often produced by hypochloremia. In both respiratory and metabolic alkaloses treatment depends on the underlying factor. In hyperventilation syndrome is based on behavioral therapy. In most cases of metabolic alkalosis the administration of sodium and potassium chloride forms a substantial part of therapy.

Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.

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Myrianthefs, Pavlos M; Briva, Arturo; Lecuona, Emilia; Dumasius, Vidas; Rutschman, David H; Ridge, Karen M; Baltopoulos, George J; Sznajder, Jacob Iasha

2005-06-01

Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.

Alkalosis

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... different types of alkalosis. These are described below. Respiratory alkalosis is caused by a low carbon dioxide level ... test, such as basic metabolic panel to confirm alkalosis and show ... respiratory or metabolic alkalosis. Other tests may be needed ...

Extreme metabolic alkalosis in intensive care.

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Tripathy, Swagata

2009-10-01

Metabolic alkalosis is a commonly seen imbalance in the intensive care unit (ICU). Extreme metabolic alkalemia, however, is less common. A pH greater than 7.65 may carry a high risk of mortality (up to 80%). We discuss the entity of life threatening metabolic alkalemia by means of two illustrative cases - both with a pH greater than 7.65 on presentation. The cause, modalities of managing and complications of this condition is discussed from the point of view of both the traditional method of Henderson and Hasselbalch and the mathematical model based on physiochemical model described by Stewart. Special mention to the pitfalls in managing patients of metabolic alkalosis with concomitant renal compromise is made.

Respiratory compensation to a primary metabolic alkalosis in humans.

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Feldman, Mark; Alvarez, Naiara M; Trevino, Michael; Weinstein, Gary L

2012-11-01

There is limited and disparate information about the extent of the respiratory compensation (hypoventilation) that occurs in response to a primary metabolic alkalosis in humans. Our aim was to examine the influence of the plasma bicarbonate concentration, the plasma base excess, and the arterial pH on the arterial carbon dioxide tension in 52 adult patients with primary metabolic alkalosis, mostly due to diuretic use or vomiting. Linear regression analysis was used to correlate degrees of alkalosis with arterial carbon dioxide tensions. In this alkalotic cohort, whose arterial plasma bicarbonate averaged 31.6 mEq/l, plasma base excess averaged 7.8 mEq/l, and pH averaged 7.48, both plasma bicarbonate and base excess correlated closely with arterial carbon dioxide tensions (r = 0.97 and 0.96, respectively; p respiratory compensation (hypoventilation) to primary metabolic alkalosis than has been reported in prior smaller studies.

Inherited renal tubular defects with hypokalemia

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Muthukrishnan J

2009-01-01

Full Text Available Bartter′s and Gitelman′s syndrome are two ends of a spectrum of inherited renal tubular disorders that present with hypokalemic metabolic alkalosis of varying severity. Clinical features and associated calcium and magnesium ion abnormalities are used to diagnose these cases after excluding other commoner causes. We report on two cases, the first being a young boy, born of pregnancy complicated by polyhydramnios, who had classical dysmorphic features, polyuria, hypokalemia and hypercalciuria and was diagnosed as having Bartter′s syndrome. The second patient is a lady who had recurrent tetany as the only manifestation of Gitelman′s syndrome, which is an unusual presentation. Potassium replacement with supplementation of other deficient ions led to satisfactory clinical and biochemical response.

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease.

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Bear, R.; Goldstein, M.; Phillipson, E.; Ho, M.; Hammeke, M.; Feldman, R.; Handelsman, S.; Halperin, M.

1977-01-01

Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis. PMID:21028

Direct suppressive effect of acute metabolic and respiratory alkalosis on parathyroid hormone secretion in the dog.

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Lopez, Ignacio; Rodriguez, Mariano; Felsenfeld, Arnold J; Estepa, Jose Carlos; Aguilera-Tejero, Escolastico

2003-08-01

Acute alkalosis may directly affect PTH secretion. The effect of acute metabolic and respiratory alkalosis was studied in 20 dogs. PTH values were lower in the metabolic (5.6 +/- 0.8 pg/ml) and respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml). Acute alkalosis is an independent factor that decreases PTH values during normocalcemia and delays the PTH response to hypocalcemia. We recently showed that acute metabolic and respiratory acidosis stimulated PTH secretion. This study was designed to evaluate whether acute metabolic and respiratory alkalosis suppressed parathyroid hormone (PTH) secretion. Three groups of 10 dogs were studied: control, acute metabolic alkalosis, and acute respiratory alkalosis. Metabolic alkalosis was induced with an infusion of sodium bicarbonate and respiratory alkalosis by hyperventilation. Calcium chloride was infused to prevent alkalosis-induced hypocalcemia during the first 60 minutes. During the next 30 minutes, disodium EDTA was infused to induce hypocalcemia and to evaluate the PTH response to hypocalcemia. Because the infusion of sodium bicarbonate resulted in hypernatremia, the effect of hypernatremia was studied in an additional group that received hypertonic saline. After 60 minutes of a normocalcemic clamp, PTH values were less (p respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml); the respective blood pH values were 7.61 +/- 0.01, 7.59 +/- 0.02, and 7.39 +/- 0.02. The maximal PTH response to hypocalcemia was similar among the three groups. However, the maximal PTH response was observed after a decrease in ionized calcium of 0.20 mM in the control group but not until a decrease of 0.40 mM in the metabolic and respiratory alkalosis groups. In contrast to the metabolic alkalosis group, hypernatremia (157 +/- 2 mEq/liter) in the hypertonic saline group was associated with an increased PTH value (46 +/- 4 pg/ml). Finally, the half-life of intact PTH

Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis.

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Li, Kai; Xu, Yuan

2015-01-01

Metabolic alkalosis commonly results from excessive hydrochloric acid (HCl), potassium (K(+)) and water (H2O) loss from the stomach or through the urine. The plasma anion gap increases in non-hypoproteinemic metabolic alkalosis due to an increased negative charge equivalent on albumin and the free ionized calcium (Ca(++)) content of plasma decreases. The mean citrate load in all patients was 8740±7027 mg from 6937±6603 mL of transfused blood products. The citrate load was significantly higher in patients with alkalosis (9164±4870 vs. 7809±3967, P alkalosis + respiratory acidosis and electrolyte imbalance may develop, blood transfusions may result in certain complications.

Metabolic Alkalosis in Adults with Stable Cystic Fibrosis

OpenAIRE

Al-Ghimlas, Fahad; Faughnan, Marie E; Tullis, Elizabeth

2012-01-01

Background: The frequency of metabolic alkalosis among adults with stable severe CF-lung disease is unknown. Methods: Retrospective chart review. Results: Fourteen CF and 6 COPD (controls) patients were included. FEV1 was similar between the two groups. PaO2 was significantly higher in the COPD (mean ± 2 SD is 72.0 ± 6.8 mmHg,) than in the CF group (56.1 ± 4.1 mmHg). The frequency of metabolic alkalosis in CF patients (12/14, 86%) was significantly greater (p=0.04) than in the COPD group (2/6...

Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis

International Nuclear Information System (INIS)

Schroeck, H.K.; Kuschinsky, W.

1989-01-01

Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis

Clinical presentation of metabolic alkalosis in an adult patient with cystic fibrosis.

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Sweetser, Lisel J; Douglas, James A; Riha, Renata L; Bell, Scott C

2005-03-01

In subtropical and tropical climates, dehydration is common in cystic fibrosis patients with respiratory exacerbations. This may lead to a clinical presentation of metabolic alkalosis with associated hyponatraemia and hypochloraemia. An adult cystic fibrosis patient who presented with a severe respiratory exacerbation accompanied by metabolic alkalosis is presented and the effects of volume correction are reported.

Metabolic alkalosis in children: Study of patients admitted to pediatrics center

OpenAIRE

Sobhani A; Radmehr B; Raji AR

2001-01-01

Metabolic alkalosis is characterized by high HCO3- as it is seen in chronic respiratory acidosis, but PH differentiates the two disorders. There is no characteristic symptom or sign. Orthostatic hypotension may be encountered. Weakness and hyporeflexia occur if serum K+ is markerdly low. Tetany and neuromuscular irritability occur rarely. We report the results of retrospective data analysis of metabolic alkalosis in 15463 patients hospitalized Pediatric Medical Center in Tehran during years 1...

Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis.

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Holland, Anne E; Wilson, John W; Kotsimbos, Thomas C; Naughton, Matthew T

2003-08-01

and study objectives: Patients with end-stage cystic fibrosis (CF) develop respiratory failure and hypercapnia. In contrast to COPD patients, altered electrolyte transport and malnutrition in CF patients may predispose them to metabolic alkalosis and, therefore, may contribute to hypercapnia. The aim of this study was to determine the prevalence of metabolic alkalosis in adults with hypercapnic respiratory failure in the setting of acute exacerbations of CF compared with COPD. Levels of arterial blood gases, plasma electrolytes, and serum albumin from 14 consecutive hypercapnic CF patients who had been admitted to the hospital with a respiratory exacerbation were compared with 49 consecutive hypercapnic patients with exacerbations of COPD. Hypercapnia was defined as a PaCO(2) of > or = 45 mm Hg. Despite similar PaCO(2) values, patients in the CF group were significantly more alkalotic than were those in the COPD group (mean [+/- SD] pH, 7.43 +/- 0.03 vs 7.37 +/- 0.05, respectively; p respiratory acidosis and metabolic alkalosis was evident in 71% of CF patients and 22% of COPD patients (p alkalosis contributes to hypercapnic respiratory failure in adults with acute exacerbations of CF. This acid-base disturbance occurs in conjunction with reduced total body salt levels and hypoalbuminemia.

Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients.

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López, Carolina; Alcaraz, Andrés José; Toledo, Blanca; Cortejoso, Lucía; Gil-Ruiz, Maite Augusta

2016-12-01

Patients in PICUs frequently present hypochloremic metabolic alkalosis secondary to loop diuretic treatment, especially those undergoing cardiac surgery. This study evaluates the effectiveness of acetazolamide therapy for metabolic alkalosis in PICU patients. Retrospective, observational study. A tertiary care children's hospital PICU. Children receiving at least a 2-day course of enteral acetazolamide. None. Demographic variables, diuretic treatment and doses of acetazolamide, urine output, serum electrolytes, urea and creatinine, acid-base excess, pH, and use of mechanical ventilation during treatment were collected. Patients were studied according to their pathology (postoperative cardiac surgery, decompensated heart failure, or respiratory disease). A total of 78 episodes in 58 patients were identified: 48 were carried out in cardiac postoperative patients, 22 in decompensated heart failure, and eight in respiratory patients. All patients received loop diuretics. A decrease in pH and PCO2 in the first 72 hours, a decrease in serum HCO3 (mean, 4.65 ± 4.83; p alkalosis secondary to diuretic therapy. Cardiac postoperative patients present a significant increase in urine output after acetazolamide treatment.

Citrate metabolism and its complications in non-massive blood transfusions: association with decompensated metabolic alkalosis+respiratory acidosis and serum electrolyte levels.

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Bıçakçı, Zafer; Olcay, Lale

2014-06-01

Metabolic alkalosis, which is a non-massive blood transfusion complication, is not reported in the literature although metabolic alkalosis dependent on citrate metabolism is reported to be a massive blood transfusion complication. The aim of this study was to investigate the effect of elevated carbon dioxide production due to citrate metabolism and serum electrolyte imbalance in patients who received frequent non-massive blood transfusions. Fifteen inpatients who were diagnosed with different conditions and who received frequent blood transfusions (10-30 ml/kg/day) were prospectively evaluated. Patients who had initial metabolic alkalosis (bicarbonate>26 mmol/l), who needed at least one intensive blood transfusion in one-to-three days for a period of at least 15 days, and whose total transfusion amount did not fit the massive blood transfusion definition (alkalosis+respiratory acidosis developed as a result of citrate metabolism. There was a positive correlation between cumulative amount of citrate and the use of fresh frozen plasma, venous blood pH, ionized calcium, serum-blood gas sodium and mortality, whereas there was a negative correlation between cumulative amount of citrate and serum calcium levels, serum phosphorus levels and amount of urine chloride. In non-massive, but frequent blood transfusions, elevated carbon dioxide production due to citrate metabolism causes intracellular acidosis. As a result of intracellular acidosis compensation, decompensated metabolic alkalosis+respiratory acidosis and electrolyte imbalance may develop. This situation may contribute to the increase in mortality. In conclusion, it should be noted that non-massive, but frequent blood transfusions may result in certain complications. Copyright © 2014 Elsevier Ltd. All rights reserved.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

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Batlle, Daniel; Chin-Theodorou, Jamie; Tucker, Bryan M

2017-09-01

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed. Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

Acetazolamide improves oxygenation in patients with respiratory failure and metabolic alkalosis.

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Gulsvik, Ragnhild; Skjørten, Ingunn; Undhjem, Kenneth; Holø, Lars; Frostad, Anne; Saure, Eirunn Waatevik; Lejlic, Vasvija; Humerfelt, Sjur; Hansen, Gunnar; Bruun Wyller, Torgeir

2013-10-01

Coexistent respiratory failure and metabolic alkalosis is a common finding. Acidotic diuretics cause a fall in pH that may stimulate respiration. The purpose of the study was to evaluate the effectiveness of short-term treatment with acetazolamide for combined respiratory failure and metabolic alkalosis. A randomised, placebo-controlled and double-blind parallel group trial where oral acetazolamide 250 mg three times a day for 5 days were administered to patients hospitalised for respiratory failure because of a pulmonary disease (Pa O2 ≤ 8 kPa and/or Pa CO2 ≥ 7 kPa) who had concurrent metabolic alkalosis [base excess (BE) ≥ 8 mmol/L]. Pa O2 after 5 days was the primary effect variable. Secondary effect variables were Pa CO2 , BE and pH on day 5, and the total number of days in hospital. Of 70 patients enrolled (35 in each group), data from 54 were analysed per protocol, while last observation carried forward was used for the remaining 16. During the 5-day treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03-1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group. Acetazolamide may constitute a useful adjuvant treatment mainly to be considered in selected patients with respiratory failure combined with prominent metabolic alkalosis or where non-invasive ventilation is insufficient or infeasible. © 2013 John Wiley & Sons Ltd.

The effect of metabolic alkalosis on the ventilatory response in healthy subjects

NARCIS (Netherlands)

Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Petrus H.; van Hees, H.W.H.; Heunks, L.M.A.

Background Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma

Sleep apnoea during upper respiratory infection and metabolic alkalosis in infancy.

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Abreu e Silva, F A; MacFadyen, U M; Williams, A; Simpson, H

1986-01-01

Three to four hour polygraphic sleep studies were carried out in 10 infants, five with upper respiratory infection and five with metabolic alkalosis secondary to vomiting during and after recovery from illness. During upper respiratory infection, the main abnormality detected was brief (greater than 3 less than 6 seconds) or prolonged (greater than 6 seconds) attacks of obstructive apnoea. Other indices of apnoea were similar to recovery data. Gross body movements were also increased. In infants with metabolic alkalosis indices of central apnoea were significantly increased when compared with recovery or case control data. Prolonged (greater than 15 seconds) attacks of central apnoea and obstructive apnoea (greater than 6 seconds) were only observed during illness. Gross body movements and periodic breathing were also increased. These findings suggest that the functional consequences of apparently 'mild' illnesses in young infants may be greater than is generally suspected and perhaps relevant to mechanism(s) of death in sudden infant death syndrome. PMID:3789786

Acetazolamide for the management of chronic metabolic alkalosis in neonates and infants.

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Tam, Bonnie; Chhay, Annie; Yen, Lilly; Tesoriero, Linda; Ramanathan, Rangasamy; Seri, Istvan; Friedlich, Philippe S

2014-01-01

In this study, we evaluated the efficacy and safety of acetazolamide in the management of chronic metabolic alkalosis in neonates and infants with chronic respiratory insufficiency. A retrospective chart review of 90 patients treated with acetazolamide between 2006 and 2007 admitted to the neonatal intensive care unit was performed. Blood gases and electrolytes obtained at baseline and by 24 hours after acetazolamide administration were compared. Compared with baseline and after 24 hours of acetazolamide, mean measured serum bicarbonate (29.5±3.7 vs. 26.9±3.8 mEq/L, Prespiratory acidosis developed in 4 (3.1%) treatment courses. Acetazolamide may be effective in decreasing serum bicarbonate in carefully selected patients. Its use and safety as an adjunctive therapy for chronic metabolic alkalosis in neonates and infants with chronic respiratory insufficiency needs further study.

Respiratory alkalosis and metabolic acidosis in a child treated with sulthiame.

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Weissbach, Avichai; Tirosh, Irit; Scheuerman, Oded; Hoffer, Vered; Garty, Ben Zion

2010-10-01

To report on severe acid-base disturbance in a child with symptomatic epilepsy treated with sulthiame. A 9.5-year-old boy with chronic generalized tonic-clonic seizures was treated with carbamazepine and valproic acid. Because of poor seizure control, sulthiame was added to the treatment. Two months later, he presented at the emergency department with severe weakness, headache, dizziness, dyspnea, anorexia, and confusional state. Arterial blood gas analysis showed mixed respiratory alkalosis with high anion gap metabolic acidosis. Sulthiame-induced acid-base disturbance was suspected. The drug was withheld for the first 24 hours and then restarted at a reduced dosage. The arterial blood gases gradually normalized, the confusion disappeared, and the patient was discharged home.Three months later, 4 weeks after an increase in sulthiame dosage, the patient was once again admitted with the same clinical picture. Improvement was noted after the drug dosage was reduced. This is the first report of mixed respiratory alkalosis and metabolic acidosis in a child treated with sulthiame. Monitoring of the acid-base status should be considered in patients treated with sulthiame.

Baking soda pica: a case of hypokalemic metabolic alkalosis and rhabdomyolysis in pregnancy.

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Grotegut, Chad A; Dandolu, Vani; Katari, Sunita; Whiteman, Valerie E; Geifman-Holtzman, Ossie; Teitelman, Melissa

2006-02-01

We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

A Quick Reference on Respiratory Alkalosis.

Science.gov (United States)

Johnson, Rebecca A

2017-03-01

Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco 2 , increases in pH, and compensatory decreases in blood HCO 3 - levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO 3 - and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO 3 - ; the arterial pH can approach near-normal values. Copyright © 2016 Elsevier Inc. All rights reserved.

Effectiveness of acetazolamide for reversal of metabolic alkalosis in weaning COPD patients from mechanical ventilation.

Science.gov (United States)

Faisy, Christophe; Mokline, Amel; Sanchez, Olivier; Tadié, Jean-Marc; Fagon, Jean-Yves

2010-05-01

To evaluate the effects of a single daily dose of acetazolamide (ACET) on metabolic alkalosis and respiratory parameters in weaning chronic obstructive pulmonary disease (COPD) patients from invasive mechanical ventilation. Case-control study. An 18-bed intensive care unit (ICU) in a university hospital. Twenty-six intubated COPD patients with mixed metabolic alkalosis (serum bicarbonate >26 mmol/l and arterial pH >or=7.38) were compared with a historical control group (n = 26) matched for serum bicarbonate, arterial pH, age, and severity of illness at admission to ICU. ACET administration (500 mg intravenously) was monitored daily according to arterial blood gas analysis from readiness to wean until extubation. ACET was administered 4 (1-11) days throughout the weaning period. Patients with ACET treatment significantly decreased their serum bicarbonate (p = 0.01 versus baseline) and arterial blood pH (p respiratory parameters except PaO(2)/FiO(2) ratio (p = 0.03). ACET patients and their matched controls had similar duration of weaning. Extubation success rate was not significantly different between groups, and causes of reintubation were comparable. ACET used at the dosage of 500 mg per day reduces metabolic alkalosis but has no benefit in terms of improving PaCO(2) or respiratory parameters in weaning COPD patients from mechanical ventilation.

Changes in bone sodium and carbonate in metabolic acidosis and alkalosis in the dog

Science.gov (United States)

Burnell, James M.

1971-01-01

Metabolic acidosis and alkalosis were produced in adult dogs over 5- to 10-day periods. Midtibial cortical bone was analyzed for calcium, sodium, phosphorus, and carbonate. In acidosis bone CO3/Ca decreased 9.5% and bone Na/Ca decreased 6.3%. In alkalosis bone CO3/Ca increased 3.1% and bone Na/Ca increased 3.0%. Previous attempts to account for changes in net acid balance by summation of extra- and intracellular acid-base changes have uniformly resulted in about 40-60% of acid gained or lost being “unaccounted for.” If it is assumed that changes in tibial cortex reflect changes in the entire skeletal system, changes in bone CO3= are sufficiently large to account for the “unaccounted for” acid change without postulating changes in cellular metabolic acid production. PMID:5540172

Acidosis, but Not Alkalosis, Affects Anaerobic Metabolism and Performance in a 4-km Time Trial.

Science.gov (United States)

Correia-Oliveira, Carlos Rafaell; Lopes-Silva, João Paulo; Bertuzzi, Romulo; McConell, Glenn K; Bishop, David John; Lima-Silva, Adriano Eduardo; Kiss, Maria Augusta Peduti Dal'molin

2017-09-01

This study aimed to determine the effect of preexercise metabolic acidosis and alkalosis on power output (PO) and aerobic and anaerobic energy expenditure during a 4-km cycling time trial (TT). Eleven recreationally trained cyclists (V˙O2peak 54.1 ± 9.3 mL·kg·min) performed a 4-km TT 100 min after ingesting in a double-blind matter 0.15 g·kg of body mass of ammonium chloride (NH4Cl, acidosis), 0.3 g·kg of sodium bicarbonate (NaHCO3, alkalosis), or 0.15 g·kg of CaCO3 (placebo). A preliminary study (n = 7) was conducted to establish the optimal doses to promote the desirable preexercise blood pH alterations without gastrointestinal distress. Data for PO, aerobic and anaerobic energy expenditure, and blood and respiratory parameters were averaged for each 1 km and compared between conditions using two-way repeated-measures ANOVA (condition and distance factors). Gastrointestinal discomfort was analyzed qualitatively. Compared with placebo (pH 7.37 ± 0.02, [HCO3]: 27.5 ± 2.6 mmol·L), the NaHCO3 ingestion resulted in a preexercise blood alkalosis (pH +0.06 ± 0.04, [HCO3]: +4.4 ± 2.0 mmol·L, P 0.05). Minimal gastrointestinal distress was noted in all conditions. Preexercise acidosis, but not alkalosis, affects anaerobic metabolism and PO during a 4-km cycling TT.

Roles of renal ammonia metabolism other than in acid-base homeostasis.

Science.gov (United States)

Weiner, I David

2017-06-01

The importance of renal ammonia metabolism in acid-base homeostasis is well known. However, the effects of renal ammonia metabolism other than in acid-base homeostasis are not as widely recognized. First, ammonia differs from almost all other solutes in the urine in that it does not result from arterial delivery. Instead, ammonia is produced by the kidney, and only a portion of the ammonia produced is excreted in the urine, with the remainder returned to the systemic circulation through the renal veins. In normal individuals, systemic ammonia addition is metabolized efficiently by the liver, but in patients with either acute or chronic liver disease, conditions that increase the addition of ammonia of renal origin to the systemic circulation can result in precipitation and/or worsening of hyperammonemia. Second, ammonia appears to serve as an intrarenal paracrine signaling molecule. Hypokalemia increases proximal tubule ammonia production and secretion as well as reabsorption in the thick ascending limb of the loop of Henle, thereby increasing delivery to the renal interstitium and the collecting duct. In the collecting duct, ammonia decreases potassium secretion and stimulates potassium reabsorption, thereby decreasing urinary potassium excretion and enabling feedback correction of the initiating hypokalemia. Finally, the stimulation of renal ammonia metabolism by hypokalemia may contribute to the development of metabolic alkalosis, which in turn can stimulate NaCl reabsorption and contribute to the intravascular volume expansion, increased blood pressure and diuretic resistance that can develop with hypokalemia. The evidence supporting these novel non-acid-base roles of renal ammonia metabolism is discussed in this review.

Metabolic alkalosis secondary to baking soda treatment of a diaper rash.

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Gonzalez, J; Hogg, R J

1981-06-01

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

The effect of metabolic alkalosis on the ventilatory response in healthy subjects.

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Oppersma, E; Doorduin, J; van der Hoeven, J G; Veltink, P H; van Hees, H W H; Heunks, L M A

2018-02-01

Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation. In an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days. Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO 2 pressure during the HCVR test, RR, V t , Pdi, EAdi and V E increased. The clinical ratio ΔV E /ΔP et CO 2 remained unchanged, but Pdi, EAdi and V E were significantly lower after bicarbonate administration for similar levels of inspired CO 2 . This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO 2 . Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

A case report of uncompensated alkalosis induced by daily plasmapheresis in a patient with thrombotic thrombocytopenic purpura.

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Nagai, Yoshiko; Itabashi, Mitsuyo; Mizutani, Mayuko; Ogawa, Tetsuya; Yumura, Wako; Tsuchiya, Ken; Nitta, Kosaku

2008-02-01

Plasmapheresis (PP) is widely known as the standard therapy for thrombotic thrombocytopenic purpura (TTP). Citrate is used as an anticoagulant in fresh frozen plasma, and the large amount of citrate infused during PP induces metabolic alkalosis. A 29-year-old woman was diagnosed with TTP associated with systemic lupus erythematosus, and was treated by daily PP in addition to a steroid, an immunosuppressant, vincristine, and cyclophosphamide. Uncompensated alkalosis caused by a combination of metabolic and respiratory alkalosis developed after artificial ventilation was discontinued. Her metabolic status improved after controlling her respiratory status and the activity of the TTP. Metabolic alkalosis is a common complication in TTP patients treated by frequent PP, but several factors that affect metabolic status may aggravate the alkalosis and induce uncompensated alkalosis.

Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis.

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Wood, C M; Milligan, C L; Walsh, P J

1999-08-01

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA.

Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Hyperaldosternoism: A Case Report.

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Hsiao, Yu-Hsin; Fang, Yu-Wei; Leu, Jyh-Gang; Tsai, Ming-Hsein

2017-01-04

BACKGROUND Thyrotoxic periodic paralysis (TPP) is commonly observed in patients with acute paralysis and hyperthyroidism. However, there is a possibility of secondary causes of hypokalemia in such a setting. CASE REPORT Herein, we present the case of a 38-year-old woman with untreated hypertension and hyperthyroidism. She presented with muscle weakness, nausea, vomiting, and diarrhea since one week. The initial diagnosis was TPP. However, biochemistry tests showed hypokalemia with metabolic alkalosis and renal potassium wasting. Moreover, a suppressed plasma renin level and a high plasma aldosterone level were noted, which was suggestive of primary aldosteronism. Abdominal computed tomography confirmed this diagnosis. CONCLUSIONS Therefore, it is imperative to consider other causes of hypokalemia (apart from TPP) in a patient with hyperthyroidism but with renal potassium wasting and metabolic alkalosis. This can help avoid delay in diagnosis of the underlying disease.

[Self-treatment with baking soda can lead to severe metabolic alkalosis].

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Jensen, Sara; Skriver, Signe

2014-12-15

This case report describes a 66-year-old man, previously healthy besides mild hypertension. He ingested a self-made folk remedy consisting of baking soda and water against acid reflux in dosages that resulted in severe metabolic alkalosis (pH 7.8). Diagnosing and treating MA is easy and cheap, but if the condition is not treated, consequences can be severe. The challenge is to uncover patients' use of non prescription medications and folk remedies in the diagnostic process. Having this information it is possible to prevent MA in both high- and low-risk patients.

Neonatal hypokalemia

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Sarici D

2012-03-01

Full Text Available Dilek Sarici1, S Umit Sarici21Kecioren Research and Education Hospital, Kecioren, Ankara, 2Chief of Division of Neonatology, Division of Neonatology, Department of Pediatrics, Gulhane Military Medical Academy, Ankara, TurkeyAbstract: In this article, distribution of potassium (K+ in body fluids, pathophysiology, causes, clinical signs and symptoms, and the evaluation and treatment of neonatal hypokalemia are reviewed. K+ is the most important intracellular cation and normal serum K+ is stabilized between 3.5 and 5.5 mEq/L. Hypokalemia may be caused by increased renal losses, increased extrarenal (gastrointestinal losses, redistribution or prolonged insufficient K+ intake. Clinical signs and symptoms occur as the result of functional changes in striated muscle, smooth muscle, and the heart. Hypokalemia is usually asymptomatic when K+ levels are between 3.0 and 3.5 mEq/L; however, there may sometimes be slight muscle weakness. Moderate hypokalemia is observed when serum K+ is between 2.5 and 3.0 mEq/L. Proximal muscle weakness is observed most commonly in lower extremities; cranial muscles are normal, but constipation and distention are prominent. Severe hypokalemia develops when serum K+ falls below 2.5 mEq/L. Rhabdomyolysis, myoglobinuria, severe muscle weakness, paralysis, respiratory distress, and respiratory arrest are observed. The clinical signs and symptoms may be unremarkable in cases of chronically developing hypokalemia; however, appropriate treatment is essential when serum K+ level falls below 2.5 mEq/L as the most dangerous complication of hypokalemia is fatal cardiac arrythmia, and changes visible with electrocardiography may not always correlate with the level of hypokalemia. Sodium (Na+, K+, chloride (Cl-, bicarbonate, creatinine, blood sugar, magnesium (Mg, plasma renin activity, aldosterone, and blood gases should be investigated by laboratory testing. Aspartate aminotransferase, alanine aminotransferase, creatinine kinase, and

Hypernatremia and metabolic alkalosis as a consequence of the therapeutic misuse of baking soda.

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Fuchs, S; Listernick, R

1987-12-01

When used appropriately, baking soda (sodium bicarbonate, USP) is a nontoxic, readily available, multipurpose product found in many households. We report an infant who presented with hypernatremia and metabolic alkalosis due to the addition of baking soda to her water. This case represents the possible dangerous use of a common household product in infants owing to the lack of proper warning labels.

Respiratory alkalosis

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Alkalosis - respiratory ... leads to shortness of breath can also cause respiratory alkalosis (such as pulmonary embolism and asthma). ... Treatment is aimed at the condition that causes respiratory alkalosis. Breathing into a paper bag -- or using ...

Diuretics and Hypokalemia

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Ali A. Handjani

1970-01-01

Full Text Available We have studied hypokalemic action of different diuretics in a cooperative study on 28 patients and our results are as follows: I. 28 patients (18 male and 10 female were the subject of our present study. 2. E. C. G. was taken systematically on all individuals. 3. Clinical signs and symptoms of hypokalemia was looked for in d lily examination of the patients. 4. Dietary K, Na, and CI could not be determined because of lack facilities. 5. Determination ed out in all patients. We strongly believe that small amount of potassium added to diuretics has no beneficial effect on delaying hypokalemia caused by these diuretics. 7. A rich diet containing adequate amount of potassium can sat, isfactorily prevent hypokalemia. 8. Furosemide and mercurial diuretics similarly cause hyponatremia rather than hypokalemia. 9. Thiazides cause hypokalemia rather than hyponatremia. 10. Addition of triamterene can delay the occurance of hypokale; mia in those patients taking thiazides,

Effects of respiratory alkalosis on human skeletal muscle metabolism at the onset of submaximal exercise.

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LeBlanc, P J; Parolin, M L; Jones, N L; Heigenhauser, G J F

2002-10-01

The purpose of this study was to examine the effects of respiratory alkalosis on human skeletal muscle metabolism at rest and during submaximal exercise. Subjects exercised on two occasions for 15 min at 55 % of their maximal oxygen uptake while either hyperventilating (R-Alk) or breathing normally (Con). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to R-Alk. In the first minute of exercise, there was a delayed activation of pyruvate dehydrogenase (PDH) in R-Alk compared with Con, resulting in a reduced rate of pyruvate oxidation. Also, glycogenolysis was higher in R-Alk compared with Con, which was attributed to a higher availability of the monoprotonated form of inorganic phosphate (P(i)), resulting in an elevated rate of pyruvate production. The mismatch between pyruvate production and its oxidation resulted in net lactate accumulation. These effects were not seen after 15 min of exercise, with no further differences in muscle metabolism between conditions. The results from the present study suggest that respiratory alkalosis may play an important role in lactate accumulation during the transition from rest to exercise in acute hypoxic conditions, but that other factors mediate lactate accumulation during steady-state exercise.

Clinical characterization and diagnosis of cystic fibrosis through exome sequencing in Chinese infants with Bartter-syndrome-like hypokalemia alkalosis.

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Qiu, Liru; Yang, Fengjie; He, Yonghua; Yuan, Huiqing; Zhou, Jianhua

2018-03-09

Cystic fibrosis (CF) is a fatal autosomal-recessive disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. CF is characterized by recurrent pulmonary infection with obstructive pulmonary disease. CF is common in the Caucasian population but is rare in the Chinese population. The symptoms of early-stage CF are often untypical and may sometimes manifest as Bartter syndrome (BS)-like hypokalemic alkalosis. Therefore, the ability of doctors to differentiate CF from BS-like hypokalemic alkalosis in Chinese infants is a great challenge in the timely and accurate diagnosis of CF. In China, sporadic CF has not been diagnosed in children younger than three years of age to date. Three infants, who were initially admitted to our hospital over the period of June 2013 to September 2014 with BS-like hypokalemic alkalosis, were diagnosed with CF through exome sequencing and sweat chloride measurement. The compound heterozygous mutations of the CFTR gene were detected in two infants, and a homozygous missense mutation was found in one infant. Among the six identified mutations, two are novel point mutations (c.1526G > C and c.3062C > T) that are possibly pathogenic. The three infants are the youngest Chinese patients to have been diagnosed with sporadic CF at a very early stage. Follow-up examination showed that all of the cases remained symptom-free after early intervention, indicating the potential benefit of very early diagnosis and timely intervention in children with CF. Our results demonstrate the necessity of distinguishing CF from BS in Chinese infants with hypokalemic alkalosis and the significant diagnostic value of powerful exome sequencing for rare genetic diseases. Furthermore, our findings expand the CFTR mutation spectrum associated with CF.

Low Potassium (Hypokalemia)

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Symptoms Low potassium (hypokalemia) By Mayo Clinic Staff Low potassium (hypokalemia) refers to a lower than normal potassium level ... 2 millimoles per liter (mmol/L). A very low potassium level (less than 2.5 mmol/L) ...

Uteroplacental blood flow during alkalosis in the sheep

International Nuclear Information System (INIS)

Buss, D.D.; Bisgard, G.E.; Rawlings, C.A.; Rankin, J.H.G.

1975-01-01

Uteroplacental blood flow was measured by the radioactive-microsphere technique in eight near-term pregnant ewes during a normal control period and during maternal metabolic alkalosis. All measurements were made on awake, unanesthetized animals. Alkalosis, defined for this study as an arterial pH of 7.60 or greater, was produced by the oral administration of sodium bicarbonate, 3 g/kg body wt. The rise in pH thus produced was unaccompanied by significant changes in systemic arterial blood pressure and cardiac output, while maternal arterial P/sub CO 2 / rose slightly from control levels. Cotyledonary blood flow declined from a control value of 1.177 ml/min to 1.025 ml/min during alkalosis. This decline of 13 percent in cotyledonary blood flow is significant (P less than 0.02). Blood flow to the remaining uterine tissue, or noncotyledonary uterus, did not change with alkalosis, being maintained at approximately 195 ml/min. It is concluded that maternal alkalosis, unaccompanied by major changes in P /sub CO 2 / and systemic arterial pressure, causes a small increase in the resistance of the uteroplacental circulation

Journal of Special Operation Medicine: A Peer Reviewed Journal for SOF Medical Professionals. Training Supplement, Winter 10

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2010-01-01

respiratory alkalosis o Hypocalcemia o Hypokalemia o Hypernatremia Pregnancy Category C Side-effects/precautions: o Metabolic alkalosis may occur...altitude, HAPE is the most common cause of death from altitude illness. 2. Usually occurs above 8,000ft. Respiratory distress at high altitude is HAPE...they may depress respiratory drive and worsen high altitude illness. 6. Treat per Nausea and Vomiting Protocol 7. For signs or symptoms of either

Gitelman syndrome.

NARCIS (Netherlands)

Knoers, N.V.A.M.; Levtchenko, E.N.

2008-01-01

Gitelman syndrome (GS), also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence

A patient with cystinosis presenting like bartter syndrome and review of literature.

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Ertan, Pelin; Evrengul, Havva; Ozen, Serkan; Emre, Sinan

2012-12-01

Nephropathic cystinosis is an autosomal recessively inherited metabolic disorder presenting with metabolic acidosis, Fanconi syndrome and renal failure. We present a 6-year-old girl with severe growth failure, hyponatremia and hypokalemia. Her parents were 4(th) degree relatives. Two relatives were diagnosed as end stage renal failure. She also had persistant hypokalemic hypochloremic metabolic alkalosis. Her renal function was normal at presentation. She was thought to have Bartter syndrome with supporting findings of elevated levels of renin and aldosterone with normal blood pressure, and hyperplasia of juxtaglomerular apparatus. Her metabolic alkalosis did not resolve despite supportive treatment. At 6(th) month of follow-up proteinuria, glucosuria and deterioration of renal function developed. Diagnosis of cystinosis was made with slit lamp examination and leukocyte cystine levels. At 12(th) month of follow-up her metabolic alkalosis has converted to metabolic acidosis. In children presenting with persistant metabolic alkalosis, with family history of renal failure, and parental consanguinity, cystinosis should always be kept in mind as this disease is an important cause of end stage renal failure which may have features mimmicking Bartter syndrome.

[An unexpected stage of alkalosis in the dynamics of the early posthemorrhagic period].

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Beliaev, A V

2000-01-01

A study was made on acid-base metabolism in early posthemorrhagic period as exemplified by examination of patients presenting with gastrointestinal hemorrhage. It has been ascertained that hemorrhage is accompanied by a mixed variant of the acid-base state (ABS) deviation, namely metabolic lactate-acidosis and respiratory alkalosis. In the time-related course of posthemorrhagic period such deviations persist in patients with lethal outcome; with the disease running a favourable course the above deviations are found to return to normal quite soon. The development of complications leads to staging in ABC, its stages being as follows: stage I--the initial stage, stage II--persisting metabolic acidosis and respiratory alkalosis, stage III--alkalosis, stage IV--normalization, with stage III of ABS being encouraged by hypocapnia caused by function disorders of the lungs in early posthemorrhagic period, normalization of cell metabolism, increase in the rate of urination as a reflection of the third earlier identified stage of water metabolism, with the H+ excretion in the urine at the previous level. The identified ABS stage III threatens coming trouble, being accompanied by metabolic deviations together with a risk of function disorder of the myocardium.

Bartter syndrome Type III and congenital anomalies of the kidney and urinary tract: an antenatal presentation

NARCIS (Netherlands)

Westland, R.; Hack, W.W.; van der Horst, H.J.; Uittenbogaard, L.B.; van Hagen, J.M.; van der Valk, P.; Kamsteeg, E.J.; Heuvel, L.P.W.J. van den; van Wijk, J.A.

2012-01-01

Bartter syndrome encompasses a variety of inheritable renal tubular transport disorders characterized by hypokalemia and hypochloremic metabolic alkalosis. Bartter syndrome Type III is caused by genetic alterations in the chloride channel kidney B (CLCNKB) gene and often presents in the first 2

Delay in onset of metabolic alkalosis during regional citrate anti-coagulation in continous renal replacement therapy with calcium-free replacement solution

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See Kay

2009-01-01

Full Text Available Regional citrate anti-coagulation for continuous renal replacement therapy chelates calcium to produce the anti- coagulation effect. We hypothesise that a calcium-free replacement solution will require less citrate and produce fewer metabolic side effects. Fifty patients, in a Medical Intensive Care Unit of a tertiary teaching hospital (25 in each group, received continuous venovenous hemofiltration using either calcium-containing or calcium-free replacement solutions. Both groups had no significant differences in filter life, metabolic alkalosis, hypernatremia, hypocalcemia, and hypercalcemia. However, patients using calcium-containing solution developed metabolic alkalosis earlier, compared to patients using calcium-free solution (mean 24.6 hours,CI 0.8-48.4 vs. 37.2 hours, CI 9.4-65, P = 0.020. When calcium-containing replacement solution was used, more citrate was required (mean 280ml/h, CI 227.2-332.8 vs. 265ml/h, CI 203.4-326.6, P = 0.069, but less calcium was infused (mean 21.2 ml/h, CI 1.2-21.2 vs 51.6ml/h, CI 26.8-76.4, P ≤ 0.0001.

Anesthetic management of a patient with sustained severe metabolic alkalosis and electrolyte abnormalities caused by ingestion of baking soda.

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Soliz, Jose; Lim, Jeffrey; Zheng, Gang

2014-01-01

The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

Fanconi syndrome and severe polyuria: an uncommon clinicobiological presentation of a Gitelman syndrome.

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Bouchireb, Karim; Boyer, Olivia; Mansour-Hendili, Lamisse; Garnier, Arnaud; Heidet, Laurence; Niaudet, Patrick; Salomon, Remi; Poussou, Rosa Vargas

2014-08-11

Gitelman syndrome is an autosomal recessive tubulopathy characterized by hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. The majority of patients do not present with symptoms until late childhood or adulthood, and the symptoms are generally mild. We report here the first case of Gitelman syndrome presenting with the biological features of Fanconi syndrome and an early polyuria since the neonatal period. We discuss in this article the atypical electrolytes losses found in our patient, as well as the possible mechanisms of severe polyuria. A 6-year-old Caucasian girl was admitted via the Emergency department for vomiting, and initial laboratory investigations found hyponatremia, hypokalemia, metabolic acidosis with normal anion gap, hypophosphatemia, and hypouricemia. Urinalysis revealed Na, K, Ph and uric acid losses. Thus, the initial biological profile was in favor of a proximal tubular defect. However, etiological investigations were inconclusive and the patient was discharged with potassium chloride and phosphorus supplementation. Three weeks later, further laboratory analysis indicated persistent hypokalemia, a metabolic alkalosis, hypomagnesemia, and hypocalciuria. We therefore sequenced the SLC12A3 gene and found a compound heterozygosity for 2 known missense mutations. Gitelman syndrome can have varying and sometimes atypical presentations, and should be suspected in case of hypokalemic tubular disorders that do not belong to any obvious syndromic entity. In this case, the proximal tubular dysfunction could be secondary to the severe hypokalemia. This report emphasizes the need for clinicians to repeat laboratory tests in undiagnosed tubular disorders, especially not during decompensation episodes.

Anesthetic Management of a Patient with Sustained Severe Metabolic Alkalosis and Electrolyte Abnormalities Caused by Ingestion of Baking Soda

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Jose Soliz

2014-01-01

Full Text Available The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

Hyperventilation of pregnancy presenting with flaccid quadriparesis due to hypokalaemia secondary to respiratory alkalosis.

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Santra, Gouranga; Paul, Rudrajit; Das, Shubhabrata; Pradhan, Sourav

2014-06-01

Hyperventilation in pregnancy is a cause of chronic respiratory alkalosis. Alkalosis either metabolic or respiratory may cause intracellular shift of potassium ions that may lead to hypokalaemia. However, the resultant hypokalaemia in respiratory alkalosis is usually mild and does not cause much clinical features. A five-months-pregnant female of the age 25 years presented with sudden onset flaccid weakness of both lower limbs associated with thigh muscle pain followed by weakness of both upper limbs within three days. Subsequent investigation revealed severe hypokalaemia due to acute exacerbation of chronic respiratory alkalosis secondary to hyperventilation of pregnancy, other causes of hypokalaemia being ruled out. Respiratory alkalosis causes tetany and other clinical manifestations. But hypokalaemia and such weakness is rarely found. Thisis probably the first report of this type from India.

[Pseudo-Bartter syndrome as manifestation of cystic fibrosis with DF508 mutation].

Science.gov (United States)

Galaviz-Ballesteros, María de Jesús; Acosta-Rodríguez-Bueno, Carlos Patricio; Consuelo-Sánchez, Alejandra; Franco-Álvarez, Isidro; Olalla-Mora, Odilo Iván; Vázquez-Frias, Rodrigo

Pseudo Bartter syndrome (PBS) is defined as hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. Children with cystic fibrosis (CF) are at risk of developing electrolyte abnormalities and even PBS may occur. 5 months old female infant with a history of two events of dehydration with vomit, refusal to eat, chronic cough, polyuria, malnutrition, metabolic alkalosis, hypokalemia, hyponatremia, hypochloremia and acute renal failure. Chronic cough study was performed, discarding pulmonary tuberculosis, gastroesophageal reflux disease and impaired swallowing. PBS was diagnosed due to hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. CF was corroborated by electrolytes in sweat and through molecular analysis of the delta F508 mutation. This is one of the few reported cases linking PBS and this mutation. In patients with hyponatremic dehydration episodes with hypokalaemic hypochloraemic metabolic alkalosis, PBS should be considered as differential diagnosis. CF could be presented as PBS, mainly in patients younger than 2 years. Copyright © 2016 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.

Hypokalemia-associated catastrophic rhabdomyolysis in ulcerative colitis

International Nuclear Information System (INIS)

Tzvetanov, G.

2009-01-01

A case of catastrophic hypokalemia-associated rhabdomyolysis in patient with ulcerative colitis (UC) is reported. A 60-year-old man presented with an exacerbation of UC and hypokalemia due to long-term diarrhea. While in the hospital, rhabdomyolysis developed in association with worsening hypokalemia. The hypokalemia was refractory to treatment and progressive course. Patient developed painful cramps of the masticatory and facial musculature associated with a moderated weakness in distal muscle groups. The weakness extended to intercostals and diaphragm muscles and led to respiratory deficiency. Serum concentration of creatine kinase was highly increased. Patient died from advancing and insurmountable cardiovascular deficiency. The causative role of hypokalemia for muscle involvement and rhabdomyolysis in patients with inflammatory bowel diseases was discussed. (author)

Regional anesthesia is safe and effective for lower limb orthopedic surgery in patient with renal tubular acidosis and hypokalemia

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Indira Gurajala

2018-01-01

Full Text Available Renal tubular acidosis (RTA with hypokalemia may precipitate acute respiratory failure and potentially fatal arrhythmias like ventricular fibrillation. Though there are random reports of respiratory failure needing mechanical ventilation and sudden death in patients with RTA and hypokalemia, the anesthetic management of these patients has not been clearly elucidated. Acidosis and hypokalemia have significant interactions with both general and local anesthetics and alter their effect substantially. Proper preoperative planning and optimization are required for the safe conduct of anesthesia in this subset of patients. We describe a case of distal RTA, hypokalemia, and metabolic bone disease in whom central neuraxial anesthesia was effectively used for lower limb orthopedic surgery with no complications.

17-α-Hydroxylase deficiency: An unusual case with primary amenorrhea and hypertension

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Sunil Kumar Kota

2011-01-01

Full Text Available A 14-year-old girl presented with acute onset quadriparesis and newly detected hypertension. Parental consanguinity, delayed puberty with normal stature form the additional information. Hypokalemia with metabolic alkalosis, low cortisol, high ACTH and FSH pointed to the possibility of CAH with 17α hydroxylase deficiency. 46XX karyotype and high progesterone supported this. Normalization of hypokalemia and hypertension with glucocorticoid treatment confirmed the diagnosis. In summary, the possibility of 17 OHD should be suspected in patients with hypokalemic myopathy, Hypertension and hypogonadism so that appropriate therapy can be implemented.

[Metabolic alkalosis despite hyperlactatemia and hypercapnia. Interpretation and therapy with help of the Stewart concept].

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Chappell, D; Hofmann-Kiefer, K; Jacob, M; Conzen, P; Rehm, M

2008-02-01

Acid-base disturbances are commonly found in critically ill patients and are often associated with fatal complications. The basis of a successful treatment is a thorough understanding of the causes of these disorders. The "classical methods" to explain acid-base disorders--pH, base excess and bicarbonate concentration--mostly do not provide a causal correlation to the underlying pathology. An unusual case of a combined respiratory-metabolic disorder with hyperlactatemia and hypercapnia is presented. An acidosis masked by hypochloremic and hypoalbuminemic alkalosis was identified with the help of Stewart's concept and finally permitted a successful therapy. The modern Stewart concept provides enhanced information, enabling an exact diagnosis and causal therapy even in complex cases.

Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

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Adeva-Andany, María M.; Fernández-Fernández, Carlos; Mouriño-Bayolo, David; Castro-Quintela, Elvira; Domínguez-Montero, Alberto

2014-01-01

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated. PMID:25405229

Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

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María M. Adeva-Andany

2014-01-01

Full Text Available Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Chayote (Sechium edule) causing hypokalemia in pregnancy.

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Jensen, L P; Lai, A R

1986-11-01

A case of severe hypokalemia in pregnancy is presented. Chayote, a subtropical vegetable with potent diuretic action, is implicated, as the potassium level returned to normal, without recurrence of hypokalemia, once the ingestion was stopped.

Hypokalemia-induced pseudoischemic electrocardiographic changes and quadriplegia.

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Mirijello, Antonio; Rinninella, Emanuele; De Leva, Francesca; Tosoni, Alberto; Vassallo, Gabriele; Antonelli, Mariangela; Addolorato, Giovanni; Landolfi, Raffaele

2014-03-01

Hypokalemia is a common biochemical abnormality. Severe hypokalemia can produce cardiac rhythm alterations and neurologic manifestations. Early detection and treatment allow clinician to prevent morbidity and mortality from cardiac arrhythmias and respiratory failure. Here, we describe a case of severe hypokalemia inducing pseudoischemic electrocardiographic (ECG) alterations and quadriplegia, in a patient affected by chronic diarrhea. Electrocardiographic alterations and neurologic manifestations completely disappeared after potassium replacement; however, prolonged potassium supplementation was required to achieve the normalization of plasmatic potassium levels. Consecutive figures show ECG improvement until normalization of ECG findings.

Metabolic Alkalosis, Acute Renal Failure and Epileptic Seizures as Unusual Manifestations of an Upside-Down Stomach

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Johannes Stephani

2012-07-01

Full Text Available Upside-down stomach represents a critical and rare manifestation of hiatal hernias. Here we report on a 60-year-old male patient who was admitted to our hospital with epileptic seizures and dehydration. Laboratory tests revealed severe metabolic alkalosis (pH 7.56 with low potassium (2.7 mmol/l, hypochloremia (<60 mmol/l, increased hematocrit (53% and high levels of serum creatinine (651 µmol/l. Based on a history of recurrent vomiting, gastroscopy and computed tomography were performed. Both diagnostics showed an upside-down stomach with signs of incarceration. Upon infusion of sodium chloride 0.9%, acid-base state, electrolyte balance and renal function became improved. Subsequently, the patient was referred to the department of surgery for hiatoplasty with fundoplication. This case report highlights severe metabolic and neurological disorders as unusual and life-threatening complications of an upside-down stomach.

Pregnancy predisposes to rhabdomyolysis due to hypokalemia

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Muthukrishnan Jayaraman

2010-01-01

Full Text Available Increased predilection for hypokalemia-induced rhabdomyolysis has been noted in pregnant women. We managed a woman with distal renal tubular acidosis (RTA with persistent hypokalemia who presented with recurrent rhabdomyolysis in her consecutive pregnancies despite adequate potassium citrate therapy.

Respiratory alkalosis in children with febrile seizures.

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Schuchmann, Sebastian; Hauck, Sarah; Henning, Stephan; Grüters-Kieslich, Annette; Vanhatalo, Sampsa; Schmitz, Dietmar; Kaila, Kai

2011-11-01

Febrile seizures (FS) are the most common type of convulsive events in children. FS are suggested to result from a combination of genetic and environmental factors. However, the pathophysiologic mechanisms underlying FS remain unclear. Using an animal model of experimental FS, it was demonstrated that hyperthermia causes respiratory alkalosis with consequent brain alkalosis and seizures. Here we examine the acid-base status of children who were admitted to the hospital for FS. Children who were admitted because of gastroenteritis (GE), a condition known to promote acidosis, were examined to investigate a possible protective effect of acidosis against FS. We enrolled 433 age-matched children with similar levels of fever from two groups presented to the emergency department. One group was admitted for FS (n = 213) and the other for GE (n = 220). In the FS group, the etiology of fever was respiratory tract infection (74.2%), otitis media (7%), GE (7%), tonsillitis (4.2%), scarlet fever (2.3%) chickenpox (1.4%), urinary tract infection (1.4%), postvaccination reaction (0.9%), or unidentified (1.4%). In all patients, capillary pH and blood Pco(2) were measured immediately on admission to the hospital. Respiratory alkalosis was found in children with FS (pH 7.46 ± 0.04, [mean ± standard deviation] Pco(2) 29.5 ± 5.5 mmHg), whereas a metabolic acidosis was seen in all children admitted for GE (pH 7.31 ± 0.03, Pco(2) 37.7 ± 4.3 mmHg; p respiratory alkalosis, irrespective of the severity of the underlying infection as indicated by the level of fever. The lack of FS in GE patients is attributable to low pH, which also explains the fact that children with a susceptibility to FS do not have seizures when they have GE-induced fever that is associated with acidosis. The present demonstration of a close link between FS and respiratory alkalosis may pave the way for further clinical studies and attempts to design novel therapies for the treatment of FS by controlling the

Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome.

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Chiang, Wen-Fang; Lin, Shih-Hung; Chan, Jenq-Shyong; Lin, Shih-Hua

2014-02-01

Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal < 0.22 mmol/mol), high plasma renin activity, but normal plasma aldosterone concentration. Abdominal sonography revealed neither renal stones nor nephrocalcinosis. Acquired causes of cBS such as autoimmune disease and drugs were all excluded. Molecular analysis of the CLCNKB gene, encoding ClC-Kb, and SLC12A3, encoding the thiazide-sensitive sodium chloride cotransporter (NCC), revealed compound heterozygous mutations in CLCNKB (L335P and G470E) inherited from her parents; her SLC12A3 was normal. These two mutations were not identified in 100 healthy subjects. Her plasma K+ concentration rose to 3 - 3.5 mmol/l after the addition of spironolactone. Inherited cBS may present with hypokalemic paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis.

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.

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Kazmaier, S; Weyland, A; Buhre, W; Stephan, H; Rieke, H; Filoda, K; Sonntag, H

1998-10-01

Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

An Unexpected Cause of Severe Hypokalemia

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Fernando Caravaca-Fontan

2015-01-01

Full Text Available We describe an unusual case of severe hypokalemia with electrocardiographic changes, due to licorice consumption, in a 15-year-old female student with no previous medical history. Prompt replacement of potassium and cessation of licorice ingestion resulted in a favourable outcome. We also discuss the pathophysiology and diagnosis, emphasizing the importance of a detailed anamnesis to rule out an often forgotten cause of hypokalemia as the licorice poisoning.

Quadriplegia due to celiac crisis with hypokalemia as initial presentation of celiac disease: a case report.

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Bhattacharya, Malobika; Kapoor, Seema

2012-02-01

Celiac crisis is a rare, life-threatening complication of celiac disease characterized by worsening of clinical symptoms, multiple metabolic derangements and shock. We report an 8-year-old girl with previously undiagnosed celiac disease who presented with flaccid quadriparesis secondary to severe hypokalemia associated with celiac crisis. Diagnosis was expedited by an elevated anti-tissue transglutaminase antibody titer. The patient improved with correction of hypokalemia, corticosteroids and gluten-free diet. In tropical countries such as India, where both acute flaccid paresis and diarrhea are usually of infective etiologies, this rare clinical condition should also be considered in the differential diagnosis of both.

Treatment with 17-allylamino-17-demethoxygeldanamycin ameliorated symptoms of Bartter syndrome type IV caused by mutated Bsnd in mice.

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Nomura, Naohiro; Kamiya, Kazusaku; Ikeda, Katsuhisa; Yui, Naofumi; Chiga, Motoko; Sohara, Eisei; Rai, Tatemitu; Sakaki, Sei; Uchida, Shinich

2013-11-22

Mutations of BSND, which encodes barttin, cause Bartter syndrome type IV. This disease is characterized by salt and fluid loss, hypokalemia, metabolic alkalosis, and sensorineural hearing impairment. Barttin is the β-subunit of the ClC-K chloride channel, which recruits it to the plasma membranes, and the ClC-K/barttin complex contributes to transepithelial chloride transport in the kidney and inner ear. The retention of mutant forms of barttin in the endoplasmic reticulum (ER) is etiologically linked to Bartter syndrome type IV. Here, we report that treatment with 17-allylamino-17-demethoxygeldanamycin (17-AAG), an Hsp90 inhibitor, enhanced the plasma membrane expression of mutant barttins (R8L and G47R) in Madin-Darby canine kidney cells. Administration of 17-AAG to Bsnd(R8L/R8L) knock-in mice elevated the plasma membrane expression of R8L in the kidney and inner ear, thereby mitigating hypokalemia, metabolic alkalosis, and hearing loss. These results suggest that drugs that rescue ER-retained mutant barttin may be useful for treating patients with Bartter syndrome type IV. Copyright © 2013 Elsevier Inc. All rights reserved.

Hypokalemia causing rhabdomyolysis in a patient with short bowel syndrome.

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Balhara, Kamna S; Highet, Bridget; Omron, Rodney

2015-04-01

Rhabdomyolysis, usually in the setting of trauma or drug use, is frequently seen in the emergency setting, and often leads to hyperkalemia at presentation. Hypokalemia, however, is a potentially underrecognized cause of rhabdomyolysis. We present a case of rhabdomyolysis likely due to hypokalemia in the setting of short bowel syndrome. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Although less common, hypokalemia can be a significant cause of rhabdomyolysis via its effects on muscle. This scenario should be considered in the differential diagnosis of patients at risk for hypokalemia who present with weakness. Rapid recognition of this relationship and rapid correction of hypokalemia may prove very important in preventing the deleterious effects of rhabdomyolysis. Copyright © 2015 Elsevier Inc. All rights reserved.

Hypokalemia in acute medical patients

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Jensen, Helene Christine Kildegaard; Brabrand, Mikkel; Vinholt, Pernille Just

2015-01-01

. METHODS: We conducted a prospective cohort study involving all first time admissions (n=11988) to the Acute Medical Department at Odense University Hospital linking potassium level at admission with registry data on patient characteristics, laboratory data, redeemed prescriptions and time of death......: Hypokalemia occurred in 16.8% of first time admissions (n=2011). It was associated with an adjusted hazard ratio [HR] of 1.34 (95% confidence interval [CI], 0.98-1.85) for 7-day mortality and 1.56 (CI, 1.18-3.06) for 8-30 day mortality. Among patients with more severe hypokalemia (plasma [K(+)

Antenatal Bartter syndrome presenting as hyperparathyroidism with hypercalcemia and hypercalciuria: a case report and review.

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Gross, Itai; Siedner-Weintraub, Yael; Simckes, Ari; Gillis, David

2015-07-01

Antenatal type I Bartter syndrome (ABS) is usually identified by the presence of polyhydramnios, premature delivery, hypokalemia, metabolic alkalosis, hypercalciuria, and nephrocalcinosis caused by mutations in the Na-K-2Cl cotransporter (NKCC2)-encoding SLC12A1 gene. In this report, we describe a novel presentation of this syndrome with hypercalcemic hypercalciuric hyperparathyroidism, and review the literature of the variable atypical presentations of ABS.

Intracellular sodium concentration and transport in red cells in essential hypertension, hyperthyroidism, pregnancy and hypokalemia.

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Gless, K H; Sütterlin, U; Schaz, K; Schütz, V; Hunstein, W

1986-01-01

Intracellular sodium content ([Nai]), ouabain-sensitive ('Na-K ATPase') and ouabain-insensitive ('passive permeability') sodium efflux, Na-K cotransport and Na-Li ('Na-Na') countertransport were estimated in erythrocytes in 39 control subjects, 20 patients with essential hypertension, 14 patients with hypokalemia of renal or unknown etiology, 13 hyperthyroid patients and 19 pregnant women. In normokalemic essential hypertension there was only a moderate, but significant elevation of the activity of the Na-Li countertransport system. In the group of patients with hypokalemia, there was a significant increase of [Nai], ouabain-insensitive sodium efflux and Na-Li countertransport. In hyperthyroidism, a marked decrease of Na-Li countertransport was associated with a marked elevation of [Nai], in pregnancy an elevation of the Na-Li countertransport with a [Nai] 43% lower than the control values. The ouabain-sensitive sodium efflux was elevated in hyperthyroidism and hypokalemia, in which [Nai] was increased. In the control subjects there was a positive linear correlation between ouabain-sensitive sodium efflux and [Nai]. The sodium component of the Na-K cotransport was decreased to about one third of the unchanged furosemide-sensitive potassium component during pregnancy. The changes of cellular sodium metabolism in essential hypertension are of minor degree as compared to those in the other conditions studied. Cellular sodium metabolism in blood cells is influenced by thyroid hormones and metabolic disorders. Na-Li countertransport, i.e. Na-Na countertransport, seems to be involved in the regulation of [Nai]: an increase of its activity diminishes [Nai] (pregnancy); a decrease elevates [Nai] (hyperthyroidism). Ouabain-sensitive sodium efflux, i.e. 'Na-K ATPase', is mainly regulated by its substrate, [Nai].

Torsade de Pointes Induced by Hypokalemia from Imipenem and Piperacillin

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Varun Kumar

2017-01-01

Full Text Available Imipenem-cilastatin and piperacillin-tazobactam are two antibiotics with broad antimicrobial coverage. Besides the many well established adverse effects of these drugs, there have been few case reports of hypokalemia. Here we present an interesting case of resistant hypokalemia caused by these drugs leading to Torsades de Pointes which has never been reported in the past. Hypokalemia resolved with discontinuation of piperacillin.

Bartter's and Gitelman's syndromes: from gene to clinic

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Naesens, Maarten; STEELS, Paul; Verberckmoes, René; Vanrenterghem, Yves; Kuypers, Dirk

2004-01-01

Bartter's and Gitelman's syndromes are characterized by hypokalemia, normal to low blood pressure and hypochloremic metabolic alkalosis. Recently, investigators have been able to demonstrate mutations of six genes encoding several renal tubular transporters and ion channels that can be held responsible for Bartter's and Gitelman's syndromes. Neonatal Bartter's syndrome is caused by mutations of NKCC2 or ROMK, classic Bartter's syndrome by mutations of ClC-Kb, Bartter's syndrome associated wit...

Association of Amelogenesis Imperfecta and Bartter's Syndrome.

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Kumar, A C V; Alekya, V; Krishna, M S V V; Alekya, K; Aruna, M; Reddy, M H K; Sangeetha, B; Ram, R; Kumar, V S

2017-01-01

Bartter's syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. Bartter's syndrome is associated with hypercalciuria and nephrocalcinosis. Amelogenesis imperfecta (AI) is a group of hereditary disorders that affect dental enamel. AI could be part of several syndromes. The enamel renal syndrome is the association of AI and nephrocalcinosis. We report two patients of AI with Bartter's syndrome.

Tetany: quantitative interrelationships between calcium and alkalosis.

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Edmondson, J W; Brashear, R E; Li, T K

1975-04-01

Tetany occurs with hypocalcemia and alkalosis or both. The interrelationship of calcium and acid-base balance necessary for inducing tetany, the role of the central nervous system, and the rate of development of hypocalcemia have been investigated. Tetany occurred in less than 50 percent of one group of dogs made alkalotic by hyperventilation or made hypocalcemic by infusion of ethylene glycol-bis(beta-amino ethyl ether) N, N'-tetraacetate. In contrast, hypocalcemia combined with hypocapnic alkalosis always produced tetany. Slowly evolving hypocalcemia was achieved inanother group of dogs by thyroparathyroidectomy, and tetany was induced postoperatively by hypocapnic alkalosis. An identical relationship between serum calcium ion concentration and arterial pH or CO2 tension was found in both groups. Tetany could not be related to the cerebrospinal fluid (CSF) calcium ion content in either group. Hypocalcemia and alkalosis are therefore coparticipants in the development of tetany and are independent of the rate of development of hypocalcemia and of CSF calcium ion concentration. The importance of alkalosis in tetany with hypoparathyroidism is emphasized.

Evaluation and treatment of respiratory alkalosis.

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Palmer, Biff F

2012-11-01

Respiratory alkalosis is the most frequent acid-base disturbance encountered in clinical practice. This is particularly true in critically ill patients, for whom the degree of hypocapnia directly correlates with adverse outcomes. Although this acid-base disturbance often is considered benign, evidence suggests that the alkalemia of primary hypocapnia can cause clinically significant decreases in tissue oxygen delivery. Mild respiratory alkalosis often serves as a marker of an underlying disease and may not require therapeutic intervention. In contrast, severe respiratory alkalosis should be approached with a sense of urgency and be aggressively corrected. Copyright © 2012 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus

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Gianluca Vergine

2018-01-01

Full Text Available Bartter syndrome (BS type 1 (OMIM #601678 is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management.

Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus.

Science.gov (United States)

Vergine, Gianluca; Fabbri, Elena; Pedini, Annalisa; Tedeschi, Silvana; Borsa, Niccolò

2018-01-01

Bartter syndrome (BS) type 1 (OMIM #601678) is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management.

Calcium Unresponsive Hypocalcemic Tetany: Gitelman Syndrome with Hypocalcemia

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Madhav Desai

2013-01-01

Full Text Available Introduction. Gitelman’s syndrome (GS is autosomal recessive renal tubular disorder characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis, and hyperreninemic hyperaldosteronism. It is usually associated with normal serum calcium. We report a patient presented with hypocalcemic tetany, and evaluation showed Gitelman’s syndrome with hypocalcemia. Case Report. A 28-year-old woman presented with cramps of the arms, legs, fatigue, and carpal spasms of one week duration. She has history of similar episodes on and off for the past two years. Her blood pressure was 98/66 mmHg. Chvostek’s sign and Trousseau’s sign were positive. Evaluation showed hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Self-medication, diuretic use, laxative abuse, persistent vomiting, and diarrhoea were ruled out. Urinary prostaglandins and genetic testing could not be done because of nonavailability. To differentiate Gitelman syndrome from Bartter’s syndrome (BS, thiazide loading test was done. It showed blunted fractional chloride excretion. GS was confirmed and patient was treated with spironolactone along with magnesium, calcium, and potassium supplementation. Symptomatically, she improved and did not develop episodes of tetany again. Conclusion. In tetany patient along with serum calcium measurement, serum magnesium, serum potassium, and arterial blood gases should be measured. Even though hypocalcemia in Gitelman syndrome is rare, it still can occur.

Gitelman′s syndrome presenting with hypocalcemic tetany and hypokalemic periodic paralysis

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Kunal Gandhi

2016-01-01

Full Text Available Gitelman′s syndrome is an autosomal recessive renal tubular disorder characterized by hypomagnesemia, hypokalemia, hypocalciuria, and metabolic alkalosis. Hypocalcemic tetany as a presentation of Gitelman′s syndrome has rarely been reported in literature. We report a rare case of Gitelman′s syndrome presenting with hypocalcemic tetany along with hypokalemic periodic paralysis. A 17-year-old female was admitted to our hospital with a history of perioral numbness and carpal spasms of five days duration with progressive quadriparesis developing over a period of few hours. Past history was significant for three episodes of transient lower limb weakness. On examination, blood pressure was 110/70 mm Hg. Chvostek′s sign and Trousseau′s sign were positive. Neurologically, she was fully oriented. She had Grade 3 power in all the four limbs with intact sensation. Laboratory tests showed hypocalcemia (7.8 mg/dL, hypokalemia (2.2 mEq/L, hypomagnesemia (0.9 mEq/L, and hypocalciuria (104 mg/day. Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Thus, a clinical diagnosis of GS was made. The patient made a remarkable recovery after the correction of electrolyte imbalance. The aim of this case report is to re-emphasize the fact that hypocalcemia can rarely occur in Gitelman′s syndrome.

A patient with Dent disease and features of Bartter syndrome caused by a novel mutation of CLCN5.

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Okamoto, Takayuki; Tajima, Toshihiro; Hirayama, Tomoya; Sasaki, Satoshi

2012-02-01

Dent disease is an X-linked tubulopathy mainly caused by inactivating mutations of CLCN5. Features of Bartter syndrome such as hypokalemic metabolic alkalosis are rarely observed in patients with Dent disease. We report a Japanese male patient with Dent disease who also manifested features of Bartter syndrome. At the age of 3 years, he was diagnosed with Dent disease based on low molecular weight proteinuria and hypercalciuria. One year later, he was found to have features of Bartter syndrome, i.e., hypokalemia and metabolic alkalosis, and high levels of plasma renin activity and aldosterone with a normal blood pressure. Despite medical interventions, he developed chronic kidney disease stage 3 at the age of 21 years. To investigate the molecular basis of his disease, CLCN5, KCNJ1, SLC12A1, and CLCkb were analyzed and a novel mutation (Y567X) in CLCN5 was identified. Hypokalemic metabolic alkalosis is a rare manifestation in Dent disease. It is speculated that Dent patients with features of Bartter syndrome are susceptible to progression to renal failure. To study this hypothesis, additional observations and long-term follow-up of such patients are necessary.

Acquired Bartter syndrome following gentamicin therapy.

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Singh, J; Patel, M L; Gupta, K K; Pandey, S; Dinkar, A

2016-01-01

Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS), or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7 th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

Association of amelogenesis imperfecta and Bartter's syndrome

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A. C. V. Kumar

2017-01-01

Full Text Available Bartter's syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. Bartter's syndrome is associated with hypercalciuria and nephrocalcinosis. Amelogenesis imperfecta (AI is a group of hereditary disorders that affect dental enamel. AI could be part of several syndromes. The enamel renal syndrome is the association of AI and nephrocalcinosis. We report two patients of AI with Bartter's syndrome.

Hypercholermic metabolic alcalsosis as a presentation of cystic fibrosis: presentation of two cases = Alcalosis metabólica hipoclorémica como presentación de la fibrosis quística. Informe de dos casos

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Olga Lucía Morales Múnera

2013-07-01

Full Text Available Introduction: We describe two cases of patients with hyperchloremic metabolic acidosis as an initial presentation of cystic fibrosis (CF or as part of a second CF exacerbation. Clinical Cases: Two patients, 6 and 9 months old, consulted for cough, fever, and dyspnea. The first had syndrome of recurrent bronchial obstruction, without a diagnosis of CF on admission. Both presented with difficulty breathing, dehydration, and malnutrition. Arterial blood gases showed metabolic acidosis, hypokalemia, and severe hypochloremia. Treatment with sodium chloride and potassium improved their electrolyte balance and acid-base status. They did not present with renal or gastrointestinal losses of chloride. CF and pseudo-Barter’s Syndrome were diagnosed. Conclusion: Metabolic alkalosis can present as an initial manifestation of CF in infants with recurrent bronchiolitis and short stature suspected of having CF: equally it can be an acute exacerbation in patients with known CF. Your recognition and treatment are an opportunity to decrease morbidity.

Hypokalemia and agitation in acute psychotic patients.

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Hatta, K; Takahashi, T; Nakamura, H; Yamashiro, H; Asukai, N; Yonezawa, Y

1999-04-19

Hypokalemia is caused partly by intensive exercise. Some evidence suggests that psychological distress may cause hypokalemia. The relationship between the decline of serum potassium concentration and the level of symptoms of acute agitation, which was defined as a total score on a subset of six categories on the 18-item Brief Psychiatric Rating Scale (anxiety, tension, mannerism and posturing, hostility, uncooperativeness, psychomotor excitement), was examined in 313 schizophrenic men, admitted on an emergency basis during a 24-month period. In addition, change in serum potassium concentration after sedation was investigated. Serum potassium concentration in the severely agitated group was lower than that in the mild group. There was a significant correlation between serum potassium concentration and the level of symptoms of acute agitation (r = -0.30, P < 0.0001). Although the decline of serum potassium concentration in the patients who were sufficiently sedated improved within 8 h, that in the patients showing high scores on the acute agitation subset even 8 h after emergency admission was prolonged. Results indicate that sedation improves acute agitation-induced hypokalemia. rights

Acquired Bartter syndrome following gentamicin therapy

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J Singh

2016-01-01

Full Text Available Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS, or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7 th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

Status epilepticus as the only presentation of the neonatal Bartter syndrome.

Science.gov (United States)

Patra, Soumya; Konar, Mithun C; Basu, Rajarshi; Khaowas, Ajoy K; Dutta, Soumyadeep; Sarkar, Debanjali

2012-03-01

Bartter syndrome is a rare hereditary (autosomal recessive) salt-losing tubulopathy characterized by hypokalemia, hypochloremia, metabolic alkalosis, and normal blood pressure with hyperreninemia, The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. We report a case of a four-month-old infant with neonatal Bartter syndrome, who presented only with status epilepticus. To the best of our present knowledge, there is no reported case of Bartter syndrome who presented with status epilepticus.

Reversible Hypokalemia and Bartter-Like Syndrome during Prolonged Systemic Therapy with Colistimethate Sodium in an Adult Patient.

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Kamal Eldin, Tarek; Tosone, Grazia; Capuano, Alfredo; Orlando, Raffaele

2017-12-01

We present the case of a 58-year-old woman who developed hypokalaemia and metabolic alkalosis 2 weeks after therapy with colistimethate sodium for the treatment of chronic lower limb ulcer infection by extensively drug-resistant (XDR) Pseudomonas aeruginosa. The metabolic changes observed resembled Bartter syndrome, a group of congenital disorders affecting the distal segments of the renal tubules. The metabolic abnormalities reversed spontaneously 6 days after drug discontinuation. Acquired forms of Bartter syndrome have been reported during courses of antibiotic therapy; however, to our knowledge, this is the first documented case associated with colistimethate therapy in an adult.

Status epilepticus as the only presentation of the neonatal Bartter syndrome

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Soumya Patra

2012-01-01

Full Text Available Bartter syndrome is a rare hereditary (autosomal recessive salt-losing tubulopathy characterized by hypokalemia, hypochloremia, metabolic alkalosis, and normal blood pressure with hyperreninemia, The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. We report a case of a four-month-old infant with neonatal Bartter syndrome, who presented only with status epilepticus. To the best of our present knowledge, there is no reported case of Bartter syndrome who presented with status epilepticus.

Anesthetic management of a patient with Bartter’s syndrome: A case report

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Harun Aydoğan

2012-09-01

Full Text Available Bartter’s syndrome is a rare disorder characterized bysevere hypochloremic metabolic alkalosis, hypokalemia,hyponatremia, hyperaldosteronism, elevation in plasmarenin activity and insensitivity to angiotensin II. Electrolyteimbalances such as hypomagnesemia, hyponatremiamight make anesthetic management difficult in Barttersyndrome. A 4 years old patient underwent surgery foringuinal hernia with caudal anesthesia using bupivacaine0.25%. In this case report, it was aimed to discuss the anestheticmanagement of a patient with Bartter syndrome.Key words: Regional anesthesia, Bartter syndrome, inguinalhernia surgery, pediatric anesthesia

Furosemide Induced Electrolyte Imbalance: A Real Danger of Overdiuresis in Patients with Heart Failure

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Yaseen Ali

2014-12-01

Full Text Available Background: Chronic heart failure is one of the most common reasons for hospital admissions in the United States. There have been several approaches for treating heart failure but loop diuretics has been at the forefront to alleviate the symptoms. Loop diuretics have their own side effects as with any medication use, and a lesser known and monitored one is metabolic alkalosis. Case report: The patient was a 76 years old female with past medical history of diabetes, hypertension, chronic kidney disease, dyslipidemia and chronic heart failure who came to the hospital with progressive shortness of breath for the past few days and was started on aggressive diuresis with intravenous loop diuretics and well responded. On the morning of d 6 of her admission, she was kept on the floor and started on BIPAP to correct hypercarbia and respiratory acidosis due to metabolic alkalosis and back to baseline with normal mentation by the middle of the day. Conclusion: Hypokalemia due to the diuretic effect can cause alkalosis by resulting in the shift of hydrogen ions intracellularly, stimulating the apical H+/K+ ATPase in the collecting duct, stimulating renal ammonia genesis, reabsorption, and secretion, leading to impaired chloride ion reabsorption in the distal nephron and reducing the glomerular filtration rate (GFR. The patient improved after being started on oxygen therapy and switched to acetazolamide as an alternative diuretic, indicating that acetazolamide corrected the effect of metabolic alkalosis by causing metabolic acidosis due to decrease reclamation of bicarbonate at the level of proximal convoluted tubule.

Bartter syndrome and growth hormone deficiency: three cases.

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Buyukcelik, Mithat; Keskin, Mehmet; Kilic, Beltinge Demircioglu; Kor, Yilmaz; Balat, Ayse

2012-11-01

Bartter syndrome is a rare autosomal recessive disorder characterized by hypokalemia, salt loss, and metabolic alkalosis. Short stature is one of the clinical manifestations in these children. Although polyuria, polydipsia, hypokalemia, and salt loss may be responsible for growth retardation, the exact pathogenesis of short stature in Bartter syndrome is not known. In this study, we present three children diagnosed as having Bartter syndrome with short stature and growth hormone (GH) deficiency. After recombinant human growth hormone therapy (rhGH), their growth velocities were improved. These results indicate that GH deficiency may contribute to short stature in children with Bartter syndrome, and rhGH therapy would be an excellent adjunctive treatment for short children with this syndrome whose condition is resistant to conventional therapies in terms of growth.

Neonatal Bartter syndrome with cholelithiasis and hydrocephalus: Rare association.

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Özdemir, Özmert Ma; Çıralı, Ceren; Yılmaz Ağladıoğlu, Sebahat; Evrengül, Havva; Tepeli, Emre; Ergin, Hacer

2016-09-01

Neonatal Bartter syndrome (NBS) is a rare autosomal recessive renal tubular disorder. This disease is characterized by hypokalemia, hypochloremia, and metabolic alkalosis that is often associated with failure to thrive and recurrent episodes of dehydration. The combination of BS and cholelithiasis in an infant is very rare. Herein, we report a premature male infant with NBS who developed cholelithiasis and hydrocephalus on clinical follow up. We recommend that periodic routine hepatobiliary ultrasonograpic screening for cholelithiasis should be performed in patients with NBS. © 2016 Japan Pediatric Society.

Hypokalemia and sudden cardiac death

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Kjeldsen, Keld

2010-01-01

Worldwide, approximately three million people suffer sudden cardiac death annually. These deaths often emerge from a complex interplay of substrates and triggers. Disturbed potassium homeostasis among heart cells is an example of such a trigger. Thus, hypokalemia and, also, more transient...... of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis....

Pathophysiological aspect of metabolic acid-base disorders

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Nešović-Ostojić Jelena

2016-01-01

Full Text Available Maintaing the arterial pH values (in normal range of 7,35-7,45 is one of the main principles of homeostasis. Regulatory responses, including chemical buffering (extracellular, intracellular, sceletal, the regulation of pCO2 by the respiratory system, and the regulation of [HCO3-] by the kidneys, act in concert to maintain normal arterial pH value. The main extracellular chemical buffer is bicarbonate-carbonic acid buffer system. The kidneys contribute to the regulation of hydrogen (and bicarbonate in body fluids in two ways. Proximal tubules are important in bicarbonate reabsorption and distal tubules excrete hydrogen ion (as ammonium ion or titratable acid. There are four simple acid-base disorders: metabolic acidosis and metabolic alkalosis; respiratory acidosis and respiratory alkalosis. Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids, loss of bicarbonate (as in diarrhea, or accumulation of endogenous acids (as in renal failure. Metabolic acidosis can also be with high and normal (hyperchloremic metabolic acidosis anion gap. Renal tubular acidosis (RTA is a form of hyperchloremic metabolic acidosis which occurs when the renal damage primarily affects tubular function. The main problem in distal RTA is reduced H+ excretion in distal tubule. Type 2 RTA is also called proximal RTA because the main problem is greatly impaired reabsorption of bicarbonate in proximal tubule. Impaired cation exchange in distal tubule is the main problem in RTA type 4. Metabolic alkalosis occurs as a result of net gain of [HCO3-] or loss of nonvolatile acid from extracellular fluids. Metabolic alkalosis can be associated with reduced or increased extracellular volume.

Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production.

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Ueda, Yoshiyasu; Aizawa, Masayo; Takahashi, Atsushi; Fujii, Masamitsu; Isaka, Yoshitaka

2009-03-01

In acute respiratory alkalosis, the severity of alkalaemia is ameliorated by a decrease in plasma [HCO(3)(-)] of 0.2 mEq/L for each 1 mmHg decrease in PaCO(2). Although hyperventilation in panic disorder patients is frequently encountered in outpatients, the drop in plasma [HCO(3)(-)] sometimes surpasses the expectation calculated from the above formula. The quantitative relationship between reduced PaCO(2) and plasma [HCO(3)(-)] in acute respiratory alkalosis has not been studied in panic disorder patients. Our objective was to provide reference data for the compensatory metabolic changes in acute respiratory alkalosis in panic disorder patients. In 34 panic disorder patients with hyperventilation attacks, we measured arterial pH, PaCO(2), plasma [HCO(3)(-)] and lactate on arrival at the emergency room. For each decrease of 1 mmHg in PaCO(2), plasma [HCO(3)(-)] decreased by 0.41 mEq/L. During hypocapnia, panic disorder patients exhibited larger increases in serum lactate levels (mean +/- SD; 2.59 +/- 1.50 mmol/L, range; 0.78-7.78 mmol/L) than previously reported in non-panic disorder subjects. Plasma lactate accumulation was correlated with PaCO(2) (P respiratory alkalosis is exaggerated by increased lactic acid production in panic disorder patients. Here, we call attention to the diagnosis of acid-base derangements by means of plasma [HCO(3)(-)] and lactate concentration in panic disorder patients.

Delayed Awakening from Anesthesia Following Electrolyte and Acid-Base Disorders, Two Cases

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Razavi M

2014-01-01

Full Text Available Introduction: Delayed awakening from anesthesia remains one of the biggest challenges that involve anesthesiologists. Most commonly, delayed awakening is due to drugs effects persistence. Metabolic (like hypo- hyperglycemia, electrolyte, acid-base disorders and hypothermia may cause delayed emergence from anesthesia. Structural disorders of cerebral nervous system (like increase in intracranial pressure, brain ischemia and psychological disorders can be regarded as other uncommon causes of this condition. Hypokalemia is induced by low potassium intake, excessive excretion from gastrointestinal (GI and kidneys (like using diuretics or a shift from extracellular space into intracellular space. Cases:  In these two reported cases, although proper measures had been taken to reverse the effects of anesthetic drugs, the patients did not regain their consciousness as fast as expected. The only significant finding in postoperative tests, along with respiratory alkalosis, was low serum potassium level (K=2.5 and K=2.9 in the first and the second patients, respectively. Correction of serum potassium (to K=3.3 and K=3.2 in the first and the second, respectively improved patients level of consciousness, and they were discharged from intensive care unit (ICU with good general condition. Conclusion: During surgery; pain, stress, sympathetic increase, catecholamine release and the consequent β-stimulation, certain drugs, and respiratory alkalosis due to hyperventilation may cause acute shift of potassium into the cells, which will be intensified in the patients with preoperative hypokalemia. Hypokalemia induces consciousness impairment and increases muscle relaxation, both of which affect patient awakening. Serum potassium evaluation is recommended in cases of delayed emergence from anesthesia.

The hemodynamic effects of prolonged respiratory alkalosis in anesthetized newborn piglets.

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Jundi, K; Barrington, K J; Henderson, C; Allen, R G; Finer, N N

2000-04-01

To test the hypothesis that prolonged alkalosis decreases cardiac output and, furthermore, exacerbates hypoxic pulmonary vasoconstriction, as respiratory alkalosis is frequently induced as a therapy for persistent pulmonary hypertension of the newborn despite a lack of controlled evidence of improved outcomes. Potential adverse effects of prolonged alkalosis have been demonstrated. Two groups (control, n = 6, and hypocapnic alkalosis, n = 6) of 1-3 day old fentanyl-anesthetized, vecuronium-paralyzed piglets were instrumented to measure cardiac index (CI) and mean systemic (MAP) and pulmonary (PAP) arterial pressures. Baseline values were recorded. Alveolar hypoxia was then induced to achieve an arterial oxygen saturation of between 50 and 60% for 15 min. Respiratory alkalosis was then induced, by increasing ventilation to achieve a pH between 7.55-7.60, and was continued for 240 min. Inspired carbon dioxide was used with hyperventilation in the control group to maintain pressure of arterial carbon dioxide (PaCO2) at 35-45 mmHg and pH of 7.35-7.45. Hypoxia was induced again at 15 and 240 min. Pulmonary and systemic vascular resistances (PVR and SVR) were calculated. Prolonged alkalosis led to a significant and progressive fall in mean MAP from 61 (SD 7) mmHg at the start of the study falling to 50 (SD 6.9, p = 0.043), with no effect on CI. Calculated SVR decreased (0.45 SD 0.03 vs 0.36 SD 0.05). There were no statistically significant changes in any of the variables in the control group. Neither acute nor prolonged respiratory alkalosis had a significant effect on hypoxic pulmonary vasoconstriction. Prolonged hyperventilation leads to systemic hypotension, however it does not exacerbate hypoxic pulmonary vasoconstriction.

Time course of hemolysis in respiratory alkalosis

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A. Babaknia

1969-01-01

Full Text Available Blood pH and plasma hemoglobin concentration were measured in dog undergoing hyperventilation with or without 6 %CO 2. Blood pH rose in the first minutes in the alkalotic group and hemolysis appeared mostly during second hour after alkalosis was established. It increased gradually during the following hours of hyperventilation. No hemolysis was observed in the group undergoing hyperventilation with 6% C02. It is concluded thal hemolysis is unrelated to mechanical action of hyperventilatroi n and in due to alkalosis. the possible cause of hemo lysis and related Iitrature is discussed.

Primary Molecular Disorders and Secondary Biological Adaptations in Bartter Syndrome

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Deschênes, Georges; Fila, Marc

2011-01-01

Bartter syndrome is a hereditary disorder that has been characterized by the association of hypokalemia, alkalosis, and the hypertrophy of the juxtaglomerular complex with secondary hyperaldosteronism and normal blood pressure. By contrast, the genetic causes of Bartter syndrome primarily affect molecular structures directly involved in the sodium reabsorption at the level of the Henle loop. The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. These secondary biological adaptations lead to hypokalemia and alkalosis, illustrating a close integration of the solutes regulation in the tubular structures. PMID:21941653

Primary Molecular Disorders and Secondary Biological Adaptations in Bartter Syndrome

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Georges Deschênes

2011-01-01

Full Text Available Bartter syndrome is a hereditary disorder that has been characterized by the association of hypokalemia, alkalosis, and the hypertrophy of the juxtaglomerular complex with secondary hyperaldosteronism and normal blood pressure. By contrast, the genetic causes of Bartter syndrome primarily affect molecular structures directly involved in the sodium reabsorption at the level of the Henle loop. The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. These secondary biological adaptations lead to hypokalemia and alkalosis, illustrating a close integration of the solutes regulation in the tubular structures.

Life-threatening hypokalemia following rapid correction of respiratory acidosis.

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Hammond, Kendra; You, David; Collins, Eileen G; Leehey, David J; Laghi, Franco

2013-01-01

A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because of progressive deterioration of respiratory muscle function, severe respiratory acidosis, obtundation and hypotension. Upon transfer to the ICU, arterial blood gas revealed severe acute-on-chronic respiratory acidosis (pH 7.00, PCO2 120 mm Hg, PO2 211 mm Hg). The patient was immediately intubated and mechanically ventilated. Intravenous fluid boluses of normal saline (10.5 L in about 24 h) and vasopressors were started with rapid correction of hypotension. In addition, she was given hydrocortisone. Within 40 min of initiation of mechanical ventilation, there was improvement in acute respiratory acidosis. Sixteen hours later, however, the patient developed life-threatening hypokalemia (K(+) of 2.1 mEq/L) and hypomagnesemia (Mg of 1.4 mg/dL). Despite aggressive potassium supplementation, hypokalemia continued to worsen over the next several hours (K(+) of 1.7 mEq/L). Urine studies revealed renal potassium wasting. We reason that the recalcitrant life-threatening hypokalemia was caused by several mechanisms including total body potassium depletion (chronic respiratory acidosis), a shift of potassium from the extracellular to intracellular space (rapid correction of respiratory acidosis with mechanical ventilation), increased sodium delivery to the distal nephron (normal saline resuscitation), hyperaldosteronism (secondary to hypotension plus administration of hydrocortisone) and hypomagnesemia. We conclude that rapid correction of respiratory acidosis, especially in the setting of hypotension, can lead to life-threatening hypokalemia. Serum potassium levels must be monitored closely in these patients, as failure to do so can lead to potentially lethal consequences

Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients.

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Fontana, V; Santinelli, S; Internullo, M; Marinelli, P; Sardo, L; Alessandrini, G; Borgognoni, L; Ferrazza, A M; Bonini, M; Palange, P

2016-01-01

Non-invasive ventilation (NIV) is an effective treatment in patients with acute exacerbation of COPD (AECOPD). However, it may induce post-hypercapnic metabolic alkalosis (MA). This study aims to evaluate the effect of acetazolamide (ACET) in AECOPD patients treated with NIV. Eleven AECOPD patients, with hypercapnic respiratory failure and MA following NIV, were treated with ACET 500 mg for two consecutive days and compared to a matched control group. Patients and controls were non invasively ventilated in a bilevel positive airway pressure (BiPAP) mode to a standard maximal pressure target of 15-20 cmH2O. ACET intra-group analysis showed a significant improvement for PaCO2 (63.9 ± 9.8 vs. 54.9 ± 8.3 mmHg), HCO3- (43.5 ± 5.9 vs. 36.1 ± 5.4 mmol/L) and both arterial pH (7.46 ± 0.06 vs. 7.41 ± 0.06) and urinary pH (6.94 ± 0.77 vs 5.80 ± 0.82), already at day 1. No significant changes in endpoints considered were observed in the control group at any time-point. Inter-group analysis showed significant differences between changes in PaCO2 and HCO3- (delta), both at day 1 and 2. Furthermore, the length of NIV treatment was significantly reduced in the ACET group compared to controls (6 ± 8 vs. 19 ± 19 days). No adverse events were recorded in the ACET and control groups. ACET appears to be effective and safe in AECOPD patients with post-NIV MA.

Pulmonary vascular responses during acute and sustained respiratory alkalosis or acidosis in intact newborn piglets.

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Gordon, J B; Rehorst-Paea, L A; Hoffman, G M; Nelin, L D

1999-12-01

Acute alkalosis-induced pulmonary vasodilation and acidosis-induced pulmonary vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro studies have found that relatively brief periods of sustained alkalosis can enhance, and sustained acidosis can decrease, vascular reactivity. In this study of intact newborn piglets, effects of acute (20 min) and sustained (60-80 min) alkalosis or acidosis on baseline (35% O2) and hypoxic (12% O2) pulmonary vascular resistance (PVR) were compared with control piglets exposed only to eucapnia. Acute alkalosis decreased hypoxic PVR, but sustained alkalosis failed to attenuate either baseline PVR or the subsequent hypoxic response. Acute acidosis did not significantly increase hypoxic PVR, but sustained acidosis markedly increased both baseline PVR and the subsequent hypoxic response. Baseline PVR was similar in all piglets after resumption of eucapnic ventilation, but the final hypoxic response was greater in piglets previously exposed to alkalosis than in controls. Thus, hypoxic pulmonary vasoconstriction was not attenuated during sustained alkalosis, but was accentuated during sustained acidosis and after the resumption of eucapnia in alkalosis-treated piglets. Although extrapolation of data from normal piglets to infants and children with pulmonary hypertension must be done with caution, this study suggests that sustained alkalosis may be of limited efficacy in treating acute hypoxia-induced pulmonary hypertension and the risks of pulmonary hypertension must be considered when using ventilator strategies resulting in permissive hypercapnic acidosis.

Does hypokalemia contribute to acute kidney injury in chronic laxative abuse?

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Eun-Young Lee

2015-06-01

Full Text Available Prolonged hypokalemia from chronic laxative abuse is recognized as the cause of chronic tubulointerstitial disease, known as “hypokalemic nephropathy,” but it is not clear whether it contributes to acute kidney injury (AKI. A 42-year-old woman with a history of chronic kidney disease as a result of chronic laxative abuse from a purging type of anorexia nervosa (AN-P, developed an anuric AKI requiring hemodialysis and a mild AKI 2 months later. Both episodes of AKI involved severe to moderate hypokalemia (1.2 and 2.7 mmol/L, respectively, volume depletion, and mild rhabdomyolysis. The histologic findings of the first AKI revealed the remnants of acute tubular necrosis with advanced chronic tubulointerstitial nephritis and ischemic glomerular injury. Along with these observations, the intertwined relationship among precipitants of recurrent AKI in AN-P is discussed, and then we postulate a contributory role of hypokalemia involved in the pathophysiology of the renal ischemia-induced AKI.

Conn syndrome and Crohn disease in a pediatric case: an interesting parallel.

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Rodriguez, Manuel A; Alkhoury, Fuad; Malvezzi, Leopoldo; Diaz, Alejandro

2013-01-01

Conn syndrome is characterized by surreptitious secretion of aldosterone in which patients are found to have hypertension, hypokalemia, and metabolic alkalosis. Although rare, the most common presentation in the pediatric population is bilateral hyperplasia of the adrenal glands as opposed to an adenoma. Crohn disease is part of the spectrum of inflammatory bowel disease, which manifests in children as flare-ups of bloody diarrhea and abdominal pain. The association of concurrent Conn syndrome and Crohn disease has been previously presented in two cases in adults. This is the first pediatric case to be reported in the literature.

Hyperthermic-induced hyperventilation and associated respiratory alkalosis in humans.

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Abbiss, Chris R; Nosaka, Kazunori; Laursen, Paul B

2007-05-01

The purpose of this study was to determine if increased environmental heat leads to hyperthermic-induced hypocapnia and associated alkalosis during prolonged self-paced cycling. Nine male cyclists completed three 100 km stochastic time trials in hot (34 degrees C), neutral (22 degrees C) and cold (10 degrees C) environments. Intermittent measurements of rectal and skin temperature, expired gases, blood pH, PaCO(2), PaO(2), and bicarbonate were made throughout. Rectal temperature increased significantly throughout all trials (P respiratory alkalosis.

Hypokalemia, its contributing factors and renal outcomes in patients with chronic kidney disease.

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Hsiao-Han Wang

Full Text Available BACKGROUND: In the chronic kidney disease (CKD population, the impact of serum potassium (sK on renal outcomes has been controversial. Moreover, the reasons for the potential prognostic value of hypokalemia have not been elucidated. DESIGN PARTICIPANTS & MEASUREMENTS: 2500 participants with CKD stage 1-4 in the Integrated CKD care program Kaohsiung for delaying Dialysis (ICKD prospective observational study were analyzed and followed up for 2.7 years. Generalized additive model was fitted to determine the cutpoints and the U-shape association between sK and end-stage renal disease (ESRD. sK was classified into five groups with the cutpoints of 3.5, 4, 4.5 and 5 mEq/L. Cox proportional hazard regression models predicting the outcomes were used. RESULTS: The mean age was 62.4 years, mean sK level was 4.2±0.5 mEq/L and average eGFR was 40.6 ml/min per 1.73 m(2. Female vs male, diuretic use vs. non-use, hypertension, higher eGFR, bicarbonate, CRP and hemoglobin levels significantly correlated with hypokalemia. In patients with lower sK, nephrotic range proteinuria, and hypoalbuminemia were more prevalent but the use of RAS (renin-angiotensin system inhibitors was less frequent. Hypokalemia was significantly associated with ESRD with hazard ratios (HRs of 1.82 (95% CI, 1.03-3.22 in sK 5 mEq/L conferred 1.6-fold (95% CI,1.09-2.34 increased risk of ESRD compared with sK = 4.5-5 mEq/L. Hypokalemia was also associated with rapid decline of renal function defined as eGFR slope below 20% of the distribution range. CONCLUSION: In conclusion, both hypokalemia and hyperkalemia are associated with increased risk of ESRD in CKD population. Hypokalemia is related to increased use of diuretics, decreased use of RAS blockade and malnutrition, all of which may impose additive deleterious effects on renal outcomes.

Acute respiratory acidosis and alkalosis – A modern quantitative interpretation

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Andraž Stožer

2014-03-01

Full Text Available Background: Three different approaches for assessing the acid-base status of a patient exist, i.e. the Boston, Copenhagen, and Stewart´s approach, and they employ different parameters to assess a given acid-base disturbance. Students, researchers, and clinicians are getting confused by heated debates about which of these performs best and by the fact that during their curricula, they typically get acquainted with one of the approaches only, which prevents them to understand sources employing other approaches and to critically evaluate the advantages and drawbacks of each approach. In this paper, the authors introduce and define the basic parameters characterizing each of the approaches and point out differences and similarities between them. Special attention is devoted to how the different approaches assess the degree of change in the concentration of plasma bicarbonate that occurs during primary respiratory changes; proper understanding of these is necessary to correctly interpret chronic respiratory and metabolic acid-base changes.Conclusion: During acute respiratory acidosis the concentration of bicarbonate rises and during acute respiratory alkalosis it falls, depending on the buffering strength of non-bicarbonate buffers. During acute respiratory acid-base disturbances, buffer base (employed by the Copenhagen approach, apparent and effective strong ion difference, as well as strong ion gap (employed by the Stewart approach remain unchanged; the anion gap (employed by the Boston and Copenhagen approach falls during acute respiratory acidosis and rises during acute respiratory alkalosis.

Inconceivable Hypokalemia: A Case Report of Acute Severe Barium Chloride Poisoning

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Haibo Tao

2016-01-01

Full Text Available Barium is a heavy divalent alkaline earth metal that has been known as a muscle poison. Barium can cause human toxicity, which may lead to significant hypokalemia and have serious consequences. This paper reports a case of unprecedented barium intoxication in which the patient, who suffered from depression, swallowed at least 3.0 g barium chloride to commit suicide. On admission, the patient presented with nausea, vomiting, stomach burning feeling, dizziness, and weakness. Emergency biochemical testing showed that the patient was suffering from severe hypokalemia (K+ 1.7 mmol/L. His electrocardiogram (ECG prompted atrioventricular blocking, ventricular tachycardia, prolongation of PR interval, ST segment depression with U waves, and T wave inversion. Intravenous potassium supplements were given immediately to correct hypokalemia and regular monitoring of vital signs and fluid balance was arranged. After all-out rescue of our hospital personnel, the condition of the patient is currently stable and he is gradually recovering. This case exemplifies the weaknesses of the management of toxic substances and the lack of mental health education for young people. We hope to get more attention for the supervision of toxic substances and the healthy development of young people.

A dangerous mixture

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Anna Piva

2014-03-01

Full Text Available A 59-year old woman was admitted for fatigue and arm paresthesias with Trousseau sign. Her medical history included thyroidectomy and hypercholesterolemia recently treated with simvastatin. Laboratory tests showed severe hypokalemia and hypocalcemia, severe increase in muscle enzymes, metabolic alkalosis; low plasma renin activity, increased thyroid-stimulating hormone, normal free thyroxine, increased parathyroid hormone, decreased vitamin D3; alterations in electrolyte urinary excretion, cortisol and aldosterone were excluded. Hypothesizing a statin-related myopathy, simvastatin was suspended; the patient reported use of laxatives containing licorice. Electrolytes normalized with intravenous supplementation. Among many biochemical alterations, none stands out as a major cause for muscular and electrolyte disorders. All co-factors are inter-connected, starting with statin-induced myopathy, worsened by hypothyroidism, secondary hyperaldosteronism and vitamin D deficiency, leading to hypocalcemia and hypokalemia, perpetrating muscular and electrolyte disorders. The importance of considering clinical conditions as a whole emerges with multiple co-factors involved. Another issue concerns herbal products and their potential dangerous effects.

Cystinosis presenting with findings of Bartter syndrome.

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Özkan, Behzat; Çayır, Atilla; Koşan, Celalettin; Alp, Handan

2011-01-01

A five-year-old boy was referred to our pediatric clinic for evaluation of failure to thrive, headache, intermittent high fever, restlessness, polyuria, and polydipsia. His weight and height measurements were under the 3rd percentile. Clinical findings consisted of frontal bossing, carious teeth, O-bain deformity of the lower extremities, and moderate dehydration. The presence of metabolic alkalosis, hypokalemia, hypochloremia, and high renin and aldosterone levels were suggestive of Bartter syndrome and a treatment regimen for Bartter syndrome was started. At follow-up, the polyuria and hyponatremia were found to persist. A reassessment of the patient revealed findings consistent with proximal renal tubular acidosis such as metabolic acidosis with a high urinary pH, proteinuria, aminoaciduria with phosphaturia and hypercalciuria. Based on the presence of parental consanguinity as well as polyuria, proteinuria, low tubular reabsorption of phosphorus, generalized aminoaciduria, light yellow skin and hair color, the probable diagnosis of cystinosis was established and was confirmed by slit-lamp examination of the cornea showing cystine crystal deposition. Our case is a good example demonstrating that development of metabolic alkalosis does not exclude cystinosis and that all findings of the patient should be thoroughly evaluated. ©Journal of Clinical Research in Pediatric Endocrinology, Published by Galenos Publishing.

Bartter's Syndrome with Type 2 Diabetes Mellitus

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Ting-Ting See

2009-02-01

Full Text Available We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patient's condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin, oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.

[A case of ammonium urate urinary stones with anorexia nervosa].

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Komori, K; Arai, H; Gotoh, T; Imazu, T; Honda, M; Fujioka, H

2000-09-01

A 27-year-old woman had been suffering from bulimia and habitual vomiting for about 7 years and was incidentally found to have right renal stones by computed tomography. She was referred to our hospital for the treatment of these caluculi. On admission, she presented with hypokalemia, hypochloremia and metabolic alkalosis and was diagnosed with anorexia nervosa. Following successful removal by percutaneous nephrolithotripsy and extracorporeal shockwave lithotripsy the stones were found to consist of pure ammonium urate. Since the urine of an anorexia nervosa patient tends to be rich in uric acid and ammonium, anorexia nervosa seems to be associated with ammonium urate urinary stones.

Anaesthesia for laparoscopic cholecystectomy in Bartter′s syndrome

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Bala S Bhaskar

2010-01-01

Full Text Available Bartter′s syndrome is a rare inherited anamoly with defect in the thick segment of the ascending limb of the loop of Henle, with reduced reabsorption of potassium. Growth is affected with worsening renal function, hypokalaemia, hypochloraemic metabolic alkalosis, hypocalcemia, hypomagnesemia, increased levels of aldosterone, renin and angiotensin without hypertension and lack of responses to vasopressors. Treatment consists of potassium supplementation along with other medications. We present the case report, probably the first, of a child suffering from Bartter′s syndrome with gall stones posted for laparoscopic cholecystectomy. The pre-operative correction of hypokalemia and successful anaesthetic and fluid and electrolyte management of the patient are discussed.

Post-prandial metabolic alkalosis in the seawater-acclimated trout: the alkaline tide comes in.

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Bucking, Carol; Fitzpatrick, John L; Nadella, Sunita R; Wood, Chris M

2009-07-01

The consequences of feeding and digestion on acid-base balance and regulation in a marine teleost (seawater-acclimated steelhead trout; Oncorhynchus mykiss) were investigated by tracking changes in blood pH and [HCO3-], as well as alterations in net acid or base excretion to the water following feeding. Additionally the role of the intestine in the regulation of acid-base balance during feeding was investigated with an in vitro gut sac technique. Feeding did not affect plasma glucose or urea concentrations, however, total plasma ammonia rose during feeding, peaking between 3 and 24 h following the ingestion of a meal, three-fold above resting control values (approximately 300 micromol ml(-1)). This increase in plasma ammonia was accompanied by an increase in net ammonia flux to the water (approximately twofold higher in fed fish versus unfed fish). The arterial blood also became alkaline with increases in pH and plasma [HCO3-] between 3 and 12 h following feeding, representing the first measurement of an alkaline tide in a marine teleost. There was no evidence of respiratory compensation for the measured metabolic alkalosis, as Pa CO2 remained unchanged throughout the post-feeding period. However, in contrast to an earlier study on freshwater-acclimated trout, fed fish did not exhibit a compensating increase in net base excretion, but rather took in additional base from the external seawater, amounting to approximately 8490 micromol kg(-1) over 48 h. In vitro experiments suggest that at least a portion of the alkaline tide was eliminated through increased HCO3- secretion coupled to Cl- absorption in the intestinal tract. This did not occur in the intestine of freshwater-acclimated trout. The marked effects of the external salinity (seawater versus freshwater) on different post-feeding patterns of acid-base balance are discussed.

Acute toxicity from baking soda ingestion.

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Thomas, S H; Stone, C K

1994-01-01

Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy -A case report-.

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Sung, Hui-Jin; Sohn, Ju-Tae; Kim, Jae-Gak; Shin, Il-Woo; Ok, Seong-Ho; Lee, Heon-Keun; Chung, Young-Kyun

2010-12-01

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy.

Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.

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Zoladz, Jerzy A; Szkutnik, Zbigniew; Duda, Krzysztof; Majerczak, Joanna; Korzeniewski, Bernard

2005-03-01

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).

Acute Metabolic Alkalosis Enhances Response of C3H Mouse Mammary Tumors to the Weak Base Mitoxantrone

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Natarajan Raghunand

2001-01-01

Full Text Available Uptake of weak acid and weak base chemotherapeutic drugs by tumors is greatly influenced by the tumor extracellular/interstitial pH (pHe, the intracellular pH (pHi maintained by the tumor cells, and by the ionization properties of the drug itself. The acid-outside plasmalemmal pH gradient in tumors acts to exclude weak base drugs like the anthracyclines, anthraquinones, and vinca alkaloids from the cells, leading to a substantial degree of “physiological drug resistance” in tumors. We have induced acute metabolic alkalosis in C3H tumor-bearing C3H/hen mice, by gavage and by intraperitoneal (i.p. administration of NaHCO3. 31P magnetic resonance spectroscopic measurements of 3-aminopropylphosphonate show increases of up to 0.6 pH units in tumor pHe, and 0.2 to 0.3 pH units in hind leg tissue pHe, within 2 hours of i.p. administration of NaHCO3. Theoretical calculations of mitoxantrone uptake into tumor and normal (hind leg tissue at the measured pH, and pHI values indicate that a gain in therapeutic index of up to 3.3-fold is possible with NaHCO3 pretreatment. Treatment of C3H tumor-bearing mice with 12 mg/kg mitoxantrone resulted in a tumor growth delay of 9 days, whereas combined NaHCO3mitoxantrone therapy resulted in an enhancement of the TGD to 16 days.

Aldosterone Response in Severe Hypokalemia and Volume Depletion: A Case Report and Review of the Recent Research

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Keiko Kai

2016-01-01

Full Text Available We report a case of severe hypokalemia and volume depletion complicated by chronic watery diarrhea resulting from chronic alcoholism in a 57-year-old man. Prompt replacement of normal saline with potassium chloride and cessation of alcohol intake resulted in a favorable outcome. We discuss the pathophysiology of the case, emphasizing the response of aldosterone in both hypokalemia and volume depletion, and provide a review of recent research.

Metabolic, respiratory, and cardiological measurements during exercise and rest

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1971-01-01

Low concentration effects of CO2 on metabolic respiration and circulation were measured during work and at rest. The relationship between heart rate and metabolic rate is examined, as well as calibration procedures, and rate measurement during submaximal and standard exercise tests. Alterations in acid base and electrolytes were found during exhaustive exercise, including changes in ECG and metabolic alkalosis effects.

[Acid-base homeostasis: metabolic acidosis and metabolic alkalosis].

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Dussol, Bertrand

2014-07-01

Acid-base homeostasis ensured by the kidneys, which maintain the equilibrium between proton generation by cellular metabolism and proton excretion in urine. This requirement is lifesaving because of the protons' ability to bind to anionic proteins in the extracellular space, modifying their structure and functions. The kidneys also regenerate bicarbonates. The kidney is not the sole organ in charge of maintaining blood pH in a very narrow range; lungs are also involved since they allow a large amount of volatile acid generated by cellular respiration to be eliminated. Copyright © 2014 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

Gitelman′s syndrome with panhypopituitarism: Reno-endocrine interplay

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Vimal Upreti

2012-01-01

Full Text Available Gitelman′s syndrome is an inherited tubulopathy affecting thiazide-sensitive sodium chloride cotransporter, which manifests with hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Recently few cases have been described having an association of Gitelman′s syndrome with pituitary abnormalities on imaging, though with normal hormonal status. We describe the first case of an adult patient having Gitelman′s syndrome and hypopituitarism with abnormal pituitary imaging. She presented to us with hypotension, hypokalemia, hypomagnesemia with alkalosis, hypothyroidism, hypocortisolism, and hypogonadism. She was treated with replacement of electrolytes and hormones, to which she showed an excellent response.

Reversed electrogenic sodium bicarbonate cotransporter 1 is the major acid loader during recovery from cytosolic alkalosis in mouse cortical astrocytes.

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Theparambil, Shefeeq M; Naoshin, Zinnia; Thyssen, Anne; Deitmer, Joachim W

2015-08-15

The regulation of H(+) i from cytosolic alkalosis has generally been attributed to the activity of Cl(-) -coupled acid loaders/base extruders in most cell types, including brain cells. The present study demonstrates that outwardly-directed sodium bicarbonate cotransport via electrogenic sodium bicarbonate cotransporter 1 (NBCe1) mediates the major fraction of H(+) i regulation from cytosolic alkalosis in mouse cortical astrocytes. Cl(-) -coupled acid-loading transporters play only a minor role in the regulation of H(+) i from alkalosis in mouse cortical astrocytes. NBCe1-mediated H(+) i regulation from alkalosis was dominant, with the support of intracellular carbonic anhydrase II, even when the intra- and extracellular [HCO3 (-) ] was very low (sodium bicarbonate cotransporter 1 (NBCe1) and for carbonic anhydrase (CA) isoform II. An acute cytosolic alkalosis was induced by the removal of either CO2 /HCO3 (-) or butyric acid, and the subsequent acid loading was analysed by monitoring changes in cytosolic H(+) or Na(+) using ion-sensitive fluorescent dyes. We have identified that NBCe1 reverses during alkalosis and contributes more than 70% to the rate of recovery from alkalosis by extruding Na(+) and HCO3 (-) . After CA inhibition or in CAII-knockout (KO) cells, the rate of recovery was reduced by 40%, and even by 70% in the nominal absence of CO2 /HCO3 (-) . Increasing the extracellular K(+) concentration modulated the rate of acid loading in wild-type cells, but not in NBCe1-KO cells. Removing chloride had only a minor effect on the recovery from alkalosis. Reversal of NBCe1 by reducing pH/[HCO3 (-) ] was demonstrated in astrocytes and in Xenopus oocytes, in which human NBCe1 was heterologously expressed. The results obtained suggest that reversed NBCe1, supported by CAII activity, plays a major role in acid-loading cortical astrocytes to support recovery from cytosolic alkalosis. © 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.

Congenital chloride diarrhea misdiagnosed as pseudo-Bartter syndrome.

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Saneian, Hossein; Bahraminia, Emad

2013-09-01

Congenital chloride diarrhea (CCD) is a rare autosomal recessive disease which is characterized by intractable diarrhea of infancy, failure to thrive, high fecal chloride, hypochloremia, hypokalemia, hyponatremia and metabolic alkalosis. In this case report, we present the first female and the second official case of CCD in Iran. A 15-month-old girl referred to our hospital due to failure to thrive and poor feeding. She had normal kidneys, liver and spleen. Treating her with Shohl's solution, thiazide and zinc sulfate did not result in weight gain. Consequently, pseudo-Bartter syndrome was suspected, she was treated with intravenous (IV) therapy to which she responded dramatically. In addition, hypokalemia resolved quickly. Since this does not usually happen in patients with the pseudo-Bartter syndrome, stool tests were performed. Abnormal level of chloride in stool suggested CCD and she was thus treated with IV fluid replacement, Total parentral nutrition and high dose of oral omeprazole (3 mg/kg/day). She gained 1 kg of weight and is doing fine until present. CCD is a rare hereditary cause of intractable diarrhea of infancy. It should be considered in infants with unknown severe electrolyte disturbances.

Gitelman syndrome

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Levtchenko Elena N

2008-07-01

Full Text Available Abstract Gitelman syndrome (GS, also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence of heterozygotes is approximately 1% in Caucasian populations, making it one of the most frequent inherited renal tubular disorders. In the majority of cases, symptoms do not appear before the age of six years and the disease is usually diagnosed during adolescence or adulthood. Transient periods of muscle weakness and tetany, sometimes accompanied by abdominal pain, vomiting and fever are often seen in GS patients. Paresthesias, especially in the face, frequently occur. Remarkably, some patients are completely asymptomatic except for the appearance at adult age of chondrocalcinosis that causes swelling, local heat, and tenderness over the affected joints. Blood pressure is lower than that in the general population. Sudden cardiac arrest has been reported occasionally. In general, growth is normal but can be delayed in those GS patients with severe hypokalemia and hypomagnesemia. GS is transmitted as an autosomal recessive trait. Mutations in the solute carrier family12, member 3 gene, SLC12A3, which encodes the thiazide-sensitive NaCl cotransporter (NCC, are found in the majority of GS patients. At present, more than 140 different NCC mutations throughout the whole protein have been identified. In a small minority of GS patients, mutations in the CLCNKB gene, encoding the chloride channel ClC-Kb have been identified. Diagnosis is based on the clinical symptoms and biochemical abnormalities (hypokalemia, metabolic alkalosis, hypomagnesemia and hypocalciuria. Bartter syndrome (especially type III is the most important genetic disorder to consider in the differential diagnosis of GS. Genetic counseling is important. Antenatal diagnosis for GS

Bartter syndrome type III and congenital anomalies of the kidney and urinary tract: an antenatal presentation.

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Westland, Rik; Hack, Wilfried W; van der Horst, Henricus J R; Uittenbogaard, Lukas B; van Hagen, Johanna M; van der Valk, Paul; Kamsteeg, Erik J; van den Heuvel, Lambert P; van Wijk, Joanna A E

2012-12-01

Bartter syndrome encompasses a variety of inheritable renal tubular transport disorders characterized by hypokalemia and hypochloremic metabolic alkalosis. Bartter syndrome Type III is caused by genetic alterations in the chloride channel kidney B (CLCNKB) gene and often presents in the first 2 years of life, known as classic Bartter syndrome. However, in rare cases Bartter syndrome Type III has an antenatal presentation with polyhydramnios, premature delivery and severe dehydration in the first weeks of life. Associations between congenital anomalies of the kidney and urinary tract and Bartter syndrome are extremely rare. This case report presents a girl with Bartter syndrome Type III due to a homozygous CLCNKB mutation and bilateral congenital anomalies of the kidney and urinary tract. In addition, we describe the antenatal presentation as well as its perinatal management.

A Case of Paraneoplastic Cushing Syndrome Presenting as Hyperglycemic Hyperosmolar Nonketotic Syndrome

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Christina E. Brzezniak

2017-04-01

Full Text Available Carcinoid tumors are neuroendocrine tumors that mainly arise in the gastrointestinal tract, lungs, and bronchi. Bronchopulmonary carcinoids have been associated with Cushing syndrome, which results from ectopic adrenocorticotrophic hormone (ACTH secretion. We report the case of a 65-year-old man, a colonel in the US Air Force, with metastatic bronchopulmonary carcinoid tumors treated on a clinical trial who was hospitalized for complaints of increasing thirst, polydipsia, polyuria, weakness, and visual changes. Decompensated hyperglycemia suggested a diagnosis of hyperglycemic hyperosmolar nonketotic syndrome (HHNS. Additional findings, which included hypokalemia, hypernatremia, hypertension, metabolic alkalosis, moon facies, and striae, raised a red flag for an ectopic ACTH syndrome. Elevated ACTH levels confirmed Cushing syndrome. Treatment with a fluid replacement and insulin drip resulted in immediate symptomatic improvement. Cushing syndrome should be considered in carcinoid patients with physical stigmata such as moon facies and striae. HHNS may be the presenting clinical feature in patients with impaired glucose metabolism.

Mechanisms controlling the oxygen consumption in experimentally induced hypochloremic alkalosis in calves.

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Cambier, Carole; Clerbaux, Thierry; Amory, Hélène; Detry, Bruno; Florquin, Sandra; Marville, Vincent; Frans, Albert; Gustin, Pascal

2002-01-01

The study was carried out on healthy Friesian calves (n = 10) aged between 10 and 30 days. Hypochloremia and alkalosis were induced by intravenous administration of furosemide and isotonic sodium bicarbonate. The venous and arterial blood samples were collected repeatedly. 2,3-diphosphoglycerate (2,3-DPG), hemoglobin and plasmatic chloride concentrations were determined. The red blood cell chloride concentration was also calculated. pH, PCO2 and PO2 were measured in arterial and mixed venous blood. The oxygen equilibrium curve (OEC) was measured in standard conditions. The correspondence of the OEC to the arterial and mixed venous compartments was calculated, taking blood temperature, pH and PCO2 values into account. The oxygen exchange fraction (OEF%), corresponding to the degree of blood desaturation between the arterial and mixed venous compartments and the amount of oxygen released at the tissue level by 100 mL of blood (OEF Vol%) were calculated from the arterial and mixed venous OEC, combined with PO2 and hemoglobin concentration. Oxygen delivery (DO2) was calculated using the arterial oxygen content, the cardiac output measured by thermodilution, and the body weight of the animal. The oxygen consumption (VO2) was derived from the cardiac output, OEF Vol% and body weight values. Despite the plasma hypochloremia, the erythrocyte chloride concentration was not influenced by furosemide and sodium bicarbonate infusion. Due to the alkalosis-induced increase in the 2,3-DPG, the standard OEC was shifted to the right, allowing oxygen to dissociate from hemoglobin more rapidly. These changes opposed the increased affinity of hemoglobin for oxygen induced by alkalosis. Moreover, respiratory acidosis, hemoconcentration, and the slight decrease in the partial oxygen pressure in mixed venous blood (Pvo2) tended to improve the OEF Vol% and maintain the oxygen consumption in a physiological range while the cardiac output, and the oxygen delivery were significantly decreased

Hypokalemia during the early phase of refeeding in patients with cancer

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Grasso, Simona; Ferro, Yvelise; Migliaccio, Valeria; Mazza, Elisa; Rotundo, Stefania; Pujia, Arturo; Montalcini, Tiziana

2013-01-01

OBJECTIVE: Refeeding syndrome occurs in patients with severe malnutrition when refeeding begins after a long period of starvation. This syndrome increases the risk of clinical complications and mortality. Hypophosphatemia is considered the primary characteristic of the syndrome. The aim of our study was to investigate the presence of other electrolyte alterations in patients with cancer during the early stage of refeeding. METHODS: In this observational study, we enrolled 34 patients with cancer of the upper aerodigestive tract receiving upfront radiotherapy who were also enrolled in a nutrition program. A caloric intake assessment, anthropometric measurements and biochemical laboratory tests were performed. RESULTS: Significant weight loss (∼20%) was found in these patients. In the patients receiving artificial nutrition, we found lower levels of potassium and total protein compared with those who were fed orally (p = 0.03 for potassium and 0.02 for protein, respectively). Patients on enteral tube feeding had a higher caloric intake compared with those who were fed orally (25±5 kcal/kg/day vs. 10±2 kcal/kg/day). CONCLUSION: Hypokalemia, like hypophosphatemia, could be a complication associated with refeeding in patients with cancer. Hypokalemia was present in the early stages of high-calorie refeeding. PMID:24270952

Hypokalemia during the early phase of refeeding in patients with cancer

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Simona Grasso

2013-11-01

Full Text Available OBJECTIVE: Refeeding syndrome occurs in patients with severe malnutrition when refeeding begins after a long period of starvation. This syndrome increases the risk of clinical complications and mortality. Hypophosphatemia is considered the primary characteristic of the syndrome. The aim of our study was to investigate the presence of other electrolyte alterations in patients with cancer during the early stage of refeeding. METHODS: In this observational study, we enrolled 34 patients with cancer of the upper aerodigestive tract receiving upfront radiotherapy who were also enrolled in a nutrition program. A caloric intake assessment, anthropometric measurements and biochemical laboratory tests were performed. RESULTS: Significant weight loss (∼20% was found in these patients. In the patients receiving artificial nutrition, we found lower levels of potassium and total protein compared with those who were fed orally (p = 0.03 for potassium and 0.02 for protein, respectively. Patients on enteral tube feeding had a higher caloric intake compared with those who were fed orally (25±5 kcal/kg/day vs. 10±2 kcal/kg/day. CONCLUSION: Hypokalemia, like hypophosphatemia, could be a complication associated with refeeding in patients with cancer. Hypokalemia was present in the early stages of high-calorie refeeding.

Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation

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Terzano, Claudio; Di Stefano, Fabio; Conti, Vittoria; Di Nicola, Marta; Paone, Gregorino; Petroianni, Angelo; Ricci, Alberto

2012-01-01

Background Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Methods Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Results Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis–metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1±9.8, 36.2±8.9 and 53.3±4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (prespiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis–metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Conclusions Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated. PMID:22539963

Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

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Terzano, Claudio; Di Stefano, Fabio; Conti, Vittoria; Di Nicola, Marta; Paone, Gregorino; Petroianni, Angelo; Ricci, Alberto

2012-01-01

Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2) and PaCO(2) and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (prespiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

Sodium acetate induces a metabolic alkalosis but not the increase in fatty acid oxidation observed following bicarbonate ingestion in humans.

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Smith, Gordon I; Jeukendrup, Asker E; Ball, Derek

2007-07-01

We conducted this study to quantify the oxidation of exogenous acetate and to determine the effect of increased acetate availability upon fat and carbohydrate utilization in humans at rest. Eight healthy volunteers (6 males and 2 females) completed 2 separate trials, 7 d apart in a single-blind, randomized, crossover design. On each occasion, respiratory gas and arterialized venous blood samples were taken before and during 180 min following consumption of a drink containing either sodium acetate (NaAc) or NaHCO3 at a dose of 2 mmol/kg body mass. Labeled [1,2 -13C] NaAc was added to the NaAc drink to quantify acetate oxidation. Both sodium salts induced a mild metabolic alkalosis and increased energy expenditure (P < 0.05) to a similar magnitude. NaHCO3 ingestion increased fat utilization from 587 +/- 83 kJ/180 min to 693 +/- 101 kJ/180 min (P = 0.01) with no change in carbohydrate utilization. Following ingestion of NaAc, the amount of fat and carbohydrate utilized did not differ from the preingestion values. However, oxidation of the exogenous acetate almost entirely (90%) replaced the additional fat that had been oxidized during the bicarbonate trial. We determined that 80.1 +/- 2.3% of an exogenous source of acetate is oxidized in humans at rest. Whereas NaHCO3 ingestion increased fat oxidation, a similar response did not occur following NaAc ingestion despite the fact both sodium salts induced a similar increase in energy expenditure and shift in acid-base balance.

Experimental febrile seizures are precipitated by a hyperthermia-induced respiratory alkalosis.

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Schuchmann, Sebastian; Schmitz, Dietmar; Rivera, Claudio; Vanhatalo, Sampsa; Salmen, Benedikt; Mackie, Ken; Sipilä, Sampsa T; Voipio, Juha; Kaila, Kai

2006-07-01

Febrile seizures are frequent during early childhood, and prolonged (complex) febrile seizures are associated with an increased susceptibility to temporal lobe epilepsy. The pathophysiological consequences of febrile seizures have been extensively studied in rat pups exposed to hyperthermia. The mechanisms that trigger these seizures are unknown, however. A rise in brain pH is known to enhance neuronal excitability. Here we show that hyperthermia causes respiratory alkalosis in the immature brain, with a threshold of 0.2-0.3 pH units for seizure induction. Suppressing alkalosis with 5% ambient CO2 abolished seizures within 20 s. CO2 also prevented two long-term effects of hyperthermic seizures in the hippocampus: the upregulation of the I(h) current and the upregulation of CB1 receptor expression. The effects of hyperthermia were closely mimicked by intraperitoneal injection of bicarbonate. Our work indicates a mechanism for triggering hyperthermic seizures and suggests new strategies in the research and therapy of fever-related epileptic syndromes.

Metformin-associated respiratory alkalosis.

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Bryant, Sean M; Cumpston, Kirk; Lipsky, Martin S; Patel, Nirali; Leikin, Jerrold B

2004-01-01

We present an 84-year-old man with a history of chronic obstructive pulmonary disease, type 2 diabetes, hypertension, glaucoma, and bladder cancer who presented to the emergency department after the police found him disoriented and confused. Metformin therapy began 3 days before, and he denied any overdose or suicidal ideation. Other daily medications included glipizide, fluticasone, prednisone, aspirin, furosemide, insulin, and potassium supplements. In the emergency department, his vital signs were significant for hypertension (168/90), tachycardia (120 bpm), and Kussmaul respirations at 24 breaths per minute. Oxygen saturation was 99% on room air, and a fingerstick glucose was 307 mg/dL. He was disoriented to time and answered questions slowly. Metformin was discontinued, and by day 3, the patient's vital signs and laboratory test results normalized. He has been asymptomatic at subsequent follow-up visits. Metformin-associated lactic acidosis is a well-known phenomenon. Respiratory alkalosis may be an early adverse event induced by metformin prior to the development of lactic acidosis.

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

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Höhne, Claudia; Boemke, Willehad; Schleyer, Nora; Francis, Roland C; Krebs, Martin O; Kaczmarczyk, Gabriele

2002-05-01

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

Is the alkaline tide a signal to activate metabolic or ionoregulatory enzymes in the dogfish shark (Squalus acanthias)?

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Wood, Chris M; Kajimura, Makiko; Mommsen, Thomas P; Walsh, Patrick J

2008-01-01

Experimental metabolic alkalosis is known to stimulate whole-animal urea production and active ion secretion by the rectal gland in the dogfish shark. Furthermore, recent evidence indicates that a marked alkaline tide (systemic metabolic alkalosis) follows feeding in this species and that the activities of the enzymes of the ornithine-urea cycle (OUC) for urea synthesis in skeletal muscle and liver and of energy metabolism and ion transport in the rectal gland are increased at this time. We therefore evaluated whether alkalosis and/or NaCl/volume loading (which also occurs with feeding) could serve as a signal for activation of these enzymes independent of nutrient loading. Fasted dogfish were infused for 20 h with either 500 mmol L(-1) NaHCO3 (alkalosis + volume expansion) or 500 mmol L(-1) NaCl (volume expansion alone), both isosmotic to dogfish plasma, at a rate of 3 mL kg(-1) h(-1). NaHCO3 infusion progressively raised arterial pH to 8.28 (control = 7.85) and plasma [HCO3-] to 20.8 mmol L(-1) (control = 4.5 mmol L(-1)) at 20 h, with unchanged arterial P(CO2), whereas NaCl/volume loading had no effect on blood acid-base status. Rectal gland Na+,K+-ATPase activity was increased 50% by NaCl loading and more than 100% by NaHCO3 loading, indicating stimulatory effects of both volume expansion and alkalosis. Rectal gland lactate dehydrogenase activity was elevated 25% by both treatments, indicating volume expansion effects only, whereas neither treatment increased the activities of the aerobic enzymes citrate synthase, NADP-isocitrate dehydrogenase, or the ketone body-utilizing enzyme beta-hydroxybutyrate dehydrogenase in the rectal gland or liver. The activity of ornithine-citrulline transcarbamoylase in skeletal muscle was doubled by NaHCO3 infusion, but neither treatment altered the activities of other OUC-related enzymes (glutamine synthetase, carbamoylphosphate synthetase III). We conclude that both the alkaline tide and salt loading/volume expansion act as

A patient with Bartter syndrome accompanying severe growth hormone deficiency and focal segmental glomerulosclerosis.

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Akil, Ipek; Ozen, Serkan; Kandiloglu, Ali Riza; Ersoy, Betul

2010-06-01

Bartter syndrome is a rare autosomal recessive, salt-losing disorder characterized by hypokalemic hypochloremic metabolic alkalosis. A 10-year-old boy had severe growth retardation (height standard deviation score -8.15). He had a thin, triangular face, prominent ears and forehead, and big eyes. Megacystis, bilateral hydroureteronephrosis, and residual urine were detected in ultrasonography, but there was no vesicoureteral reflux. Lumbosacral magnetic resonance (MR) showed posterior disc bulging at L4-5. Serum sodium and chloride levels were normal, but mild hypokalemia was overlooked initially. During follow-up, hypokalemic hypochloremic metabolic alkalosis developed, with high urinary chloride and potassium excretion (52 and 43 mEq/L, respectively). The patient, with renal salt loss, was thought to have classic Bartter syndrome due to absence of nephrocalcinosis, presence of persistent hypercalciuria and sensorineural deafness, and presence of relatively mild clinical and laboratory findings, except polyuria initially. The child was treated with indomethacin, spironolactone, and oral potassium in addition to growth hormone (GH). During treatment, he had considerable increase in weight and height compared with the period of GH therapy only. We present this case because, although growth retardation is a major feature of Bartter syndrome, associated GH deficiency is rarely reported in the literature. Diagnosis of Bartter syndrome was made later, as our patient was followed for megacystis and megaureter secondary to the neurogenic bladder and GH deficiency initially; and proteinuria associated with focal segmental glomerulosclerosis responded to treatment for Bartter syndrome.

Neonatal bartter syndrome

International Nuclear Information System (INIS)

Parkash, J.; Salat, S. M.; Khan, I.A.

2006-01-01

A pre-term baby girl was born following a pregnancy complicated by severe polyhydramnios at a gestational age of 36 weeks. She was initially suffering from respiratory distress consistent with idiopathic respiratory distress syndrome, and altered electrolyte imbalance with hyponatremia, hypokalemia and hypochloremic metabolic alkalosis. However, during the third week of life when she had dehydration along with significant electrolyte imbalance, Bartter's syndrome was considered which was supported by findings of high renin and aldosterone levels. Treatment was done by correction of electrolytes and dehydration along with indomethacin. The drug was well tolerated. The infant showed correction of electrolyte imbalance. The features of this case suggest an extreme form of Bartter's syndrome presenting from the early days of life. The syndrome is reported because of it's rarity and alerts pediatricians to the antenatal and neonatal variant of Bartter's syndrome. (author)

[Clinical analysis of 6 cases of Bartter syndrome].

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Yin, Fang-mei; Zheng, Fang-qiu; Zhang, Xin; Wu, Mei-jun; Wei, Hong-yan; Ma, Zhong-shu; Lu, Biao; Qiu, Ming-cai

2011-03-01

To summarize the clinical characteristics of Bartter syndrome and investigate its pathogenesis. The clinical data of 6 cases of Bartter syndrome at our hospital from November 2006 to May 2010 were analyzed retrospectively. The onset age of Bartter syndrome was 13-35 years old. The main symptoms included weakness (6/6), paralysis (1/6), numbness (5/6) and tetany (4/6). All patients had normal blood pressure. The biochemical tests showed persistent hypokalemia, metabolic alkalosis (6/6) and hyperreninemia. The pathological examination of deltoid muscle biopsy showed the swelling, degeneration and necrosis of myocytes and the deposition of immunocomplex in myolemma. And the pathological examination of renal biopsy showed the hyperplasia of juxtaglomerular apparatus (5/6) and the deposition of immunocomplex. All symptoms were relieved after a therapy of potassium supplementation or a combination of indomethacin, spironolactone and immunosuppressant. When such clinical features as weakness, paralysis, tetany, hypokalemic alkalosis and normotension are encountered, Bartter syndrome should be suspected. Serum electrolytes, blood gas analysis and activation of the renin-angiotensin-aldosterone system should be examined for a definite diagnosis. The treatment of choice includes potassium and magnesium supplementation or in combination with prostaglandin synthetase inhibitor, aldosterone antagonist and immunosuppressant. Immunologic mechanism may participate in the course of Bartter syndrome.

Recurrent aborted sudden cardiac death with seizures and rhabdomyolysis due to bulimia-induced hypokalemia: report of one case.

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Finsterer, Josef; Stöllberger, Claudia

2014-06-01

Recurrent vomiting due to bulimia associated with abuse of furosemide and laxatives causing severe hypokalemia may result in recurrent aborted sudden cardiac death (SCD) and seizures. We report a 25-year-old female with a history of bulimia associated with abuse of furosemide and laxatives since the age of 15 years, migraine since puberty, renal abscesses at age 20 y, and rhabdomyolysis of unknown cause at age 24 y. She experienced aborted SCD due to severe hypokalemia with symptomatic seizures at 21 and 25 years of age. Bulimia patients additionally taking laxatives or furosemide are at particular risk of SCD and rhabdomyolysis and require periodic determination of electrolytes, potassium substitution, and adequate psychiatric therapy and surveillance.

Tumour genesis syndrome: severe hypophosphatemia and hypokalemia may be ominous presenting findings in childhood acute myeloid leukaemia.

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Chan, Winnie Ky; Chang, Kai On; Lau, Wing Hung

2017-08-01

We report a 16-year-old girl who was diagnosed with acute leukaemia and a marked leucocytosis >200 × 10 9 /L. She presented with marked hypophosphatemia, hypokalemia, acute renal failure and acute respiratory failure. These electrolytes disturbances may indicate rapid tumour genesis. These ominous findings required urgent treatment to halt the crises of rapid leukemic cell proliferation. Mark hypophosphatemia and hypokalemia may be presenting electrolyte abnormalities in a patient with acute leukaemia, and these may be indicators of aggressive tumour genesis. What is known: • Mild electrolyte disturbances are common in oncology patients • Tumour lysis syndrome is well recognized by paediatriaticians What is new: • Life-threatening hypophosphatemia is an uncommon presentation • These electrolytes disorders may indicate an aggressive tumour genesis process even at presentation and require urgent treatment.

Hypokalemic paralysis and respiratory failure due to excessive intake of licorice syrup

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Mehmet Oguzhan Ay

2014-04-01

Full Text Available Licorice is the root of Glycyrrhiza glabra, which has a herbal ingredient, glycyrrhizic acid. Excessive intake of licorice may cause a hypermineralocorticoidism-like syndrome characterized by sodium and water retention, hypokalemia, hypertension, metabolic alkalosis, low-renin activity, and hypoaldosteronism. In this paper, an 34 years old man who admitted to the emergency department with respiratory failure and marked muscle weakness of all extremities that progressed to paralysis after excessive intake of licorice syrup was presented. It was aimed to draw attention to the necessity of questioning whether there is excessive intake of licorice or not in patients who admitted to emergency department with paralysis and dyspnea. Plasma potassium concentration of the patient was 1.4 mmol/L. The patient\\'s respiratory distress and loss of muscle strength recovered completely after potassium replacement. [Cukurova Med J 2014; 39(2.000: 387-391

Amikacin-induced type 5 Bartter-like syndrome with severe hypocalcemia

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Chrispal A

2009-01-01

Full Text Available Aminoglycoside-induced renal toxicity is well known and may manifest with nonoliguric renal failure or renal tubular dysfunction. Aminoglycoside-induced renal tubular dysfunction could result in diffuse damage or manifest as a Fanconi-like syndrome, Bartter-like syndrome, or distal renal tubular acidosis. We discuss a patient who developed severe renal tubular dysfunction secondary to short-term therapy with Amikacin, resulting in refractory hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and polyuria. This constellation of biochemical abnormalities mimic Type 5 Bartter′s syndrome, where there is activating mutation of the calcium sensing receptor in the thick ascending loop of Henle and the distal tubule. In this case this activation of the calcium sensing receptor was triggered by amikacin. This phenomenon has been described with gentamicin though never with amikacin. Recovery of the tubular dysfunction took 15 days following cessation of the offending drug, Amikacin.

Effect of acute metabolic acid/base shifts on the human airway calibre.

NARCIS (Netherlands)

Brijker, F.; Elshout, F.J.J. van den; Heijdra, Y.F.; Bosch, F.H.; Folgering, H.T.M.

2001-01-01

Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined

Mild Hypokalemia and Supraventricular Ectopy Increases the Risk of Stroke in Community-Dwelling Subjects

DEFF Research Database (Denmark)

Mattsson, Nick; Kumarathurai, Preman; Larsen, Bjørn Strøier

2017-01-01

.0±6.94 versus 64.0±6.66 years; Pconfidence interval, 1.04-3.28) after...... covariate adjustments, as well as in a competing risk analysis with death (hazard ratio, 1.51; 95% confidence interval, 1.12-2.04). Excessive supraventricular ectopic activity was also associated with stroke (hazard ratio, 2.23; 95% confidence interval, 1.33-3.76). The combination of hypokalemia...

Experience of diagnosis and treatment of Gitelman syndrome

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Shuo TIAN

2017-12-01

Full Text Available Objective To analyze the clinical characteristics and provide the experiences in diagnosis and treatment of 3 cases of Gitelman syndrome (GitS. Methods Three patients diagnosed as GitS were selected as the objects in Tangshan gongren Hospital from Aug. 2010 to Jan. 2017. Their clinical data were retrospectively analyzed and combined with the related literatures, and the clinical characteristics and treatment experiences of the disease were discussed. Results Of the 3 patients, 2 were teenager onset and another one was adult onset. The blood pressure of the 3 patients was normal, and the clinical features were as paroxysmal weakness, tetany, polyuria and nocturia increased. Laboratory tests revealed low potassium, low sodium, low chlorine, hypomagnesemia, occasionally hypocalcemia, high urinary potassium, metabolic alkalosis, urine Ca/Cr ≤0.2, plasma rennin activity increased significantly and plasma aldosterone was normal. Being eliminated symptoms and phenomena were the potassium intake inadequate, loss of potassium in digestive tract, taking potassium excretion drugs, primary aldosteronism and Cushing syndrome. etc. Patients got symptoms relief and serum potassium level rose to near normal level after receiving the combined potassium and magnesium supplement. Conclusions The clinical characteristics of GitS manifest as fatigue, tetany, normal blood pressure, hypokalemia, hypomagnesemia, metabolic alkalosis, plasma rennin activity increases significantly and plasma aldosterone rises or normal. Treatment with combined potassium and magnesium supplement may lead to a good prognosis, but hypomagnesemia is harder to correct. Kidney damage can be avoided by early diagnosis and treatment. DOI: 10.11855/j.issn.0577-7402.2017.12.13

Type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea.

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Sakallı, Hale; Bucak, Hakan İbrahim

2012-01-01

Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. Sometimes a few status may be nested, as in our case presented here. An 8-month-old boy was referred to our hospital with of intractable diarrhea, polyuria, persistent hypokalemia, abdominal distension and failure to thrive. He was born in the 34 6/7 gestational week (GW) to consanguineous parents. In the 30(th) GW polyhydramnios was verified by ultrasonography. The laboratory results showed hypokalemic-hypochloremic metabolic alkalosis, hyponatremia, and increased urinary loss of chloride, potassium and calcium. An audiogram test revealed complete sensorineural deafness. Ultrasonography revealed medullary nephrocalcinosis in both kidneys. Elevated plasma renin activity and aldosterone were found and a provisional diagnosis of type-IV neonatal Bartter syndrome was made. Treatment with indomethacin, spironolactone and additional intake of NaCl/KCl was initiated. Despite these therapies, the child's diarrhea persisted but serum potassium concentration normalized, and hypercalciuria and urine output reduced. After determining the high fecal chloride concentration, there was an immediate decompensation of the disease on indomethacin withdrawal, thus a diagnosis of type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea was considered. Indomethacin, spironolactone and supplementary therapies with NaCl/KCl were continued, which resulted in the normalization of serum electrolytes as well as his physical development, but high contents of chloride in urine and faeces and nephrocalcinosis remains unchanged during 1-year follow-up. Because of the clinical and laboratory simulations between the various diseases that lead to hypokalemic-hypochloremic metabolic alkalosis, patients must be evaluated carefully.

A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs.

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Liu, Fan; Celi, Pietro; Chauhan, Surinder Singh; Cottrell, Jeremy James; Leury, Brian Joseph; Dunshea, Frank Rowland

2018-02-01

Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity) or HS (35°C, 35% to 45% humidity, 8 h daily) conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all prespiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

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Claudio Terzano

Full Text Available BACKGROUND: Hypercapnic Chronic Obstructive Pulmonary Disease (COPD exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV when treating hypercapnic respiratory failure. METHODS: Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2 and PaCO(2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. RESULTS: Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7% mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8% respiratory acidosis and 3/5 (60% mixed respiratory-metabolic acidosis patients (p = 0.026, with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016. The duration of ventilation was associated with higher blood lactate (p<0.001, lower pH (p = 0.016, lower serum sodium (p = 0.014 and lower chloride (p = 0.038. Hyponatremia without hypervolemic hypochloremia occurred in 11 respiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. CONCLUSIONS: Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

Apparent mineralocorticoid excess: time of manifestation and complications despite treatment.

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Knops, Noël B B; Monnens, Leo A; Lenders, Jacques W; Levtchenko, Elena N

2011-06-01

Here we describe the case of a patient followed from birth because of a positive family history for apparent mineralocorticoid excess (AME) in an older brother. The patient, a girl, had normal serum electrolyte and blood pressure measurements in the first months after birth. Not until the age of 11 months did she develop anorexia and failure to thrive in combination with hypertension, hypokalemia, and metabolic alkalosis, which are consistent with the diagnosis of AME. This diagnosis was confirmed by mutation analysis of the HSD11B2 gene (C1228T). Treatment with amiloride and furosemide electrolyte disturbances normalized her blood pressure. At the age of 19 years she unexpectedly suffered a stroke. Additional investigations revealed no accepted risk factor for stroke. We discuss the possible underlying mechanisms for the delayed manifestation of hypertension and electrolyte disturbances in AME, propose an additional explanation for the stroke in this patient, and advise treatment with a mineralocorticoid receptor antagonist to reduce stroke risk in patients with AME.

Type III Bartter-like syndrome in an infant boy with Gitelman syndrome and autosomal dominant familial neurohypophyseal diabetes insipidus.

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Brugnara, Milena; Gaudino, Rossella; Tedeschi, Silvana; Syrèn, Marie-Louise; Perrotta, Silverio; Maines, Evelina; Zaffanello, Marco

2014-09-01

We report the case of an infant boy with polyuria and a familial history of central diabetes insipidus. Laboratory blood tests disclosed hypokalemia, metabolic alkalosis, hyperreninemia, and hyperaldosteronism. Plasma magnesium concentration was slightly low. Urine analysis showed hypercalciuria, hyposthenuria, and high excretion of potassium. Such findings oriented toward type III Bartter syndrome (BSIII). Direct sequencing of the CLCNKB gene revealed no disease-causing mutations. The water deprivation test was positive. Magnetic resonance imaging showed a lack of posterior pituitary hyperintensity. Finally, direct sequencing of the AVP-NPII gene showed a point mutation (c.1884G>A) in a heterozygous state, confirming an autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI). This condition did not explain the patient's phenotype; thus, we investigated for Gitelman syndrome (GS). A direct sequencing of the SLC12A3 gene showed c.269A>C and c.1205C>A new mutations. In conclusion, the patient had a genetic combination of GS and adFNDI with a BSIII-like phenotype.

Protection against β adrenoceptor agonist reduction of plasma potassium in severe but not in moderate hypokalemia

DEFF Research Database (Denmark)

Tran, Cao Thach Tran; Kjeldsen, Keld

2011-01-01

K-depleted and control rats were anesthetized and infused with terbutalin. In controls, plasma K concentration (pK) decreased by 0.7 mm (P = 0.01). In moderate hypokalemia terbutalin-induced decrease in pK was reduced by 0.3 mm for each 1 mm decrease in pK (n = 8, R(2) = 0.82, P = 0.002) and by 0...

Dopamine enhances the phosphaturic effect of PTH during acute respiratory alkalosis.

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Berndt, T J; Tucker, R R; Kent, P D; Streiff, P C; Tyce, G M; Knox, F G

1999-12-01

The phosphaturic response to parathyroid hormone (PTH) is blunted during acute respiratory alkalosis. The objective of the present study was to determine the effect of dopamine on the blunted phosphaturic response to PTH during acute respiratory alkalosis. The phosphaturic response to PTH was determined in thyroparathyroidectomized (TPTX) normocapnic and respiratory alkalotic rats in the absence and presence of the infusion of exogenous dopamine (25 microg/kg/min) or of 3,4-dihydroxyphenylalanine (L-DOPA, 250 microg/kg/min) to increase endogenous dopamine synthesis. In normocapnic rats, PTH infusion (33 U/kg plus 1 U/kg/min) significantly increased the fractional excretion of phosphate (FE(Pi)), from 1.5%+/-0.5% to 28.4%+/-4.0%, (deltaFE(Pi) 26.9%+/-4.1%, n = 11, Prespiratory alkalotic rats, the increase was from 0.4%+/-0.1% to 11.4%+/-1.7% (deltaFE(Pi) 11.0%+/-1.8%, n = 13, Prespiratory alkalotic rats (deltaFE(Pi) 26.9%+/-4.1% vs 11.0%+/-1.9%, Prespiratory alkalotic rats, in the presence of dopamine infusion, PTH significantly increased the FE(Pi), from 0.6%+/-0.2% to 19.3%+/-3.3% (deltaFE(Pi) 18.7%+/-3.3%, n = 6); in the presence of L-DOPA infusion it increased from 1.0%+/-0.3% to 20.5%+/-2.8% (deltaFE(Pi) 19.5%+/-2.9%, n = 8, Prespiratory alkalotic rats was enhanced by stimulation of endogenous dopamine synthesis by the infusion of L-DOPA.

Microaggregates: Experimental and Clinical Aspects - Symposium on Microaggregates, Held at Letterman Army Institute of Research on 20-21 June 1977,

Science.gov (United States)

1980-06-01

clearing of lactic acidosis within 24 hr. By permission, Journal of Trauma, 1975. Respiratory alkalosis occurs secondary to hyperventillation...citrate moiety of liquid-preserved blood produces a metabolic alkalosis . The combination of respiratory and metabolic alkalosis , hypothermia, and...fThe Role of Microaggregates in the Respiratory 233 Distress Syndrome. Frank R. Lewis, M.D. Summary 247 Distribution List j 251 SESSION I June 20, 1977

Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus.

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Khositseth, Sookkasem; Uawithya, Panapat; Somparn, Poorichaya; Charngkaew, Komgrid; Thippamom, Nattakan; Hoffert, Jason D; Saeed, Fahad; Michael Payne, D; Chen, Shu-Hui; Fenton, Robert A; Pisitkun, Trairak

2015-12-17

Hypokalemia (low serum potassium level) is a common electrolyte imbalance that can cause a defect in urinary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown. We employed proteomic analysis of inner medullary collecting ducts (IMCD) from rats fed with a potassium-free diet for 1 day. IMCD protein quantification was performed by mass spectrometry using a label-free methodology. A total of 131 proteins, including the water channel AQP2, exhibited significant changes in abundance, most of which were decreased. Bioinformatic analysis revealed that many of the down-regulated proteins were associated with the biological processes of generation of precursor metabolites and energy, actin cytoskeleton organization, and cell-cell adhesion. Targeted LC-MS/MS and immunoblotting studies further confirmed the down regulation of 18 selected proteins. Electron microscopy showed autophagosomes/autophagolysosomes in the IMCD cells of rats deprived of potassium for only 1 day. An increased number of autophagosomes was also confirmed by immunofluorescence, demonstrating co-localization of LC3 and Lamp1 with AQP2 and several other down-regulated proteins in IMCD cells. AQP2 was also detected in autophagosomes in IMCD cells of potassium-deprived rats by immunogold electron microscopy. Thus, enhanced autophagic degradation of proteins, most notably including AQP2, is an early event in hypokalemia-induced NDI.

Chloride Test

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... metabolic acidosis ) or when a person hyperventilates (causing respiratory alkalosis ). A decreased level of blood chloride (called hypochloremia) ... disease , emphysema or other chronic lung diseases (causing respiratory ... metabolic alkalosis). An increased level of urine chloride can indicate ...

Refeeding and metabolic syndromes: two sides of the same coin

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Obeid, O A; Hachem, D H; Ayoub, J J

2014-01-01

Refeeding syndrome describes the metabolic and clinical changes attributed to aggressive rehabilitation of malnourished subjects. The metabolic changes of refeeding are related to hypophosphatemia, hypokalemia, hypomagnesemia, sodium retention and hyperglycemia, and these are believed to be mainly the result of increased insulin secretion following high carbohydrate intake. In the past few decades, increased consumption of processed food (refined cereals, oils, sugar and sweeteners, and so on) lowered the intake of several macrominerals (mainly phosphorus, potassium and magnesium). This seems to have compromised the postprandial status of these macrominerals, in a manner that mimics low grade refeeding syndrome status. At the pathophysiological level, this condition favored the development of the different components of the metabolic syndrome. Thus, it is reasonable to postulate that metabolic syndrome is the result of long term exposure to a mild refeeding syndrome. PMID:24979149

Profile of acid-base disturbances in an intensive care unit of Fortaleza, Ceará, Brazil.

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Renan Barbosa Rodrigues

2014-09-01

Full Text Available Introduction: Acid – base disturbances are entities caused by the deregulation of the concentration of bicarbonate ions, the concentration of hydrogen ions and the partial pressure of carbon dioxide in the blood. These disturbances modify most cell fuctions when present, jeopardizing the proper functioning of organs.Methods: Cross-sectional analytical study based upon data collected from medical files of patients in ICU as seen from August 1 to December 31, 2013 at the Dr. José Frota Institute in Fortaleza, Ceará. The variables studied were: age, sex, cause of ICU admission, pH, HCO3-, pO2, pCO2 , glomerular filtration rate ( GFR , serum potassium concentrarion, serum magnesium concentration, serum creatinine and hemoglobin levels.Results: The most frequent disorders were primary respiratory alkalosis with               33 ( 38,4 % cases, 30 ( 34,9 % of metabolic alkalosis, 13 ( 15.1% of metabolic acidosis,    7 ( 8,2% did not present acid-base disorders and respiratory acidosis           3 ( 3,5%. Patients admitted with TBI had respiratory alkalosis as the most common primary disorder, followed by metabolic alkalosis, 16 ( 47,0 % and 13 ( 38,2 % , respectively. The main disturbances were mixed respiratory alkalosis with metabolic alkalosis and respiratory alkalosis with metabolic alkalosis found in 15.12% of patients in each of these combinations. Conclusion:The importance  of a detailed evaluation of acid-base disturbances is necessary since these disorders lead to higher mortality rates, so it is necessary to establish the main types of disorders that are associated with a particular cause of hospitalization .

Pseudo-Bartter’s syndrome in patients with cystic fibrosis: A case series and review of the literature

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Vilotijević-Dautović Gordana

2015-01-01

Full Text Available Introduction. Pseudo-Bartter syndrome (PBS is characterized by hyponatremic, hypochloremic metabolic alkalosis that mimics Bartter syndrome but with no pathology in the renal tubules. We present five patients with cystic fibrosis (CF and PBS. Cases Outline. Four children aged between three and five-and-one-half months with previously diagnosed CF and one aged 17 months with previously undiagnosed disease, were hospitalized during the summer season, with severe dehydration, oliguria, apathy and adynamia. Additionally, one of them had an ileostomy due to meconium ileus after birth. All children were on a diet without additional salt intake. Laboratory analysis on admission showed hyponatremia (115-133 mmol/L, mean 122.4 mmol/L, high plasma renin activity (229-500 pg/ml, mean 324 pg/ml and metabolic alkalosis (pH 7.5-7.6, mean 7.56 in all the patients, and in four of them high blood level of aldosterone (74-560 pg/ml, mean 295.9 pg/ml, hypokalemia (2.3-2.8 mmol/L, mean 2.6 mmol/L, hypochloremia (59-71 mmol/L, mean 66 mmol/L and low urinary sodium (5-12 mmol/L, mean 9 mmol/L. After intravenous rehydration followed by additional use of sodium and chloride in mean dosis of 1.78 mmol/kg per day, all the patients made a complete recovery. With advice for additional use of salt in the mentioned amount, the patients were discharged from the hospital. Conclusion. PBS is one of CF complications, especially in infants and young children in situations accompanied by increased sweating and/or other causes of additional loss of sodium and chlorine. Sometimes, as was the case with one of our patients, PBS may be the initial presentation form of the disease.

Incidence of hypochloremic metabolic alkalosis in dogs and cats with and without nasogastric tubes over a period of up to 36 hours in the intensive care unit.

Science.gov (United States)

Chih, Annie; Rudloff, Elke; Waldner, Cheryl; Linklater, Andrew K J

2018-05-01

To evaluate the incidence of hypochloremic metabolic alkalosis (HCMA) in dogs and cats in the ICU that had intermittent nasogastric tube (NGT) aspiration for up to 36 hours. Prospective cohort study (December 2013 to October 2014). Privately owned emergency and referral teaching hospital. Forty-nine client-owned dogs and 16 client-owned cats. Patients wherein NGT placement was recommended and client consent was obtained were included in the interventional group. Those with an NGT placed (NGT group) had the NGT aspirated every 4 hours. Patients for whom placement of a NGT was declined by the owner served as a reference group (NoNGT). Venous blood gas and electrolyte values were obtained every 12 hours. Thirty-five dogs and cats had an NGT placed. Thirty dogs and cats did not have an NGT placed. The serum venous blood gas and electrolyte changes were compared over time within the NGT group and between the NGT and NoNGT groups. No cases developed HCMA. In the NGT group, blood pH increased over time. There was no significant difference between the NGT and the NoNGT group in the average value of pH, HCO 3 - , base excess, chloride, or corrected chloride. Serum venous blood gas, chloride, and corrected chloride changes were not associated with the volumes of gastric fluid aspirated over time. In this small population of dogs and cats, intermittent NGT aspiration was not associated with the development of HCMA over a period of up to 36 hours after NGT placement. © Veterinary Emergency and Critical Care Society 2018.

Respiratory acidosis prolongs, while alkalosis shortens, the duration and recovery time of vecuronium in humans.

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Yamauchi, Masanori; Takahashi, Hiromi; Iwasaki, Hiroshi; Namiki, Akiyoshi

2002-03-01

To determine the effects of respiratory acidosis and alkalosis by mechanical ventilation on the onset, duration, and recovery times of vecuronium. Randomized, prospective study. Operating rooms in the Sapporo Medical University Hospital and Kitami Red Cross Hospital. 90 ASA physical status I and II patients undergoing lower abdominal surgery. Patients were randomly allocated to one of three groups by arterial carbon dioxide tension level (PaCO2; mmHg) after induction: hyperventilation group (PaCO2 = 25-35), normoventilation group (PaCO2 = 35-45), and hypoventilation group (PaCO2 = 45-55). Anesthesia was maintained by spinal block with inhalation of 50% to 66% nitrous oxide in oxygen and intermittent intravenous administration of fentanyl and midazolam with tracheal intubation. After vecuronium 0.08 mg/kg was given, onset, duration, and recovery time were measured by mechanomyography (Biometer Myograph 2,000, Odense, Denmark). There were significant differences in the duration and recovery time of vecuronium among the normoventilation group (12.7 +/- 3.3 min and 11.8 +/- 2.8 min, respectively), the hyperventilation group (10.6 +/- 3.5 min and 9.2 +/- 2.7 min, respectively; p respiratory acidosis and shortened in respiratory alkalosis.

Acid-base disturbances in nephrotic syndrome: analysis using the CO2/HCO3 method (traditional Boston model) and the physicochemical method (Stewart model).

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Kasagi, Tomomichi; Imai, Hirokazu; Miura, Naoto; Suzuki, Keisuke; Yoshino, Masabumi; Nobata, Hironobu; Nagai, Takuhito; Banno, Shogo

2017-10-01

The Stewart model for analyzing acid-base disturbances emphasizes serum albumin levels, which are ignored in the traditional Boston model. We compared data derived using the Stewart model to those using the Boston model in patients with nephrotic syndrome. Twenty-nine patients with nephrotic syndrome and six patients without urinary protein or acid-base disturbances provided blood and urine samples for analysis that included routine biochemical and arterial blood gas tests, plasma renin activity, and aldosterone. The total concentration of non-volatile weak acids (A TOT ), apparent strong ion difference (SIDa), effective strong ion difference (SIDe), and strong ion gap (SIG) were calculated according to the formulas of Agrafiotis in the Stewart model. According to the Boston model, 25 of 29 patients (90%) had alkalemia. Eighteen patients had respiratory alkalosis, 11 had metabolic alkalosis, and 4 had both conditions. Only three patients had hyperreninemic hyperaldosteronism. The Stewart model demonstrated respiratory alkalosis based on decreased PaCO 2 , metabolic alkalosis based on decreased A TOT , and metabolic acidosis based on decreased SIDa. We could diagnose metabolic alkalosis or acidosis with a normal anion gap after comparing delta A TOT [(14.09 - measured A TOT ) or (11.77 - 2.64 × Alb (g/dL))] and delta SIDa [(42.7 - measured SIDa) or (42.7 - (Na + K - Cl)]). We could also identify metabolic acidosis with an increased anion gap using SIG > 7.0 (SIG = 0.9463 × corrected anion gap-8.1956). Patients with nephrotic syndrome had primary respiratory alkalosis, decreased A TOT due to hypoalbuminemia (power to metabolic alkalosis), and decreased levels of SIDa (power to metabolic acidosis). We could detect metabolic acidosis with an increased anion gap by calculating SIG. The Stewart model in combination with the Boston model facilitates the analysis of complex acid-base disturbances in nephrotic syndrome.

Favorable surgical outcomes of aldosterone-producing adenoma based on lateralization by CT imaging and hypokalemia: a non-AVS-based strategy.

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Li, Hai; Liu, Jianbin; Feng, Xiujuan; Liu, Liehua; Wei, Guohong; Cao, Xiaopei; Li, Yanbing

2017-12-01

To test the efficacy of a strategy based on CT imaging and clinical characteristics on lateralizing origin of excess aldosterone secretion in primary aldosteronism. Consecutive patients with diagnosed primary hyperaldosteronism from June 2006 to July 2012 in our center underwent adrenal surgeries without pre-operational adrenal venous sampling (AVS) if all the three criteria were met: (1) round- or oval-shaped occupational lesion of low density after contrast enhancement with diameter >1 cm on CT scan was located in one adrenal gland; (2) unequivocally normal contralateral adrenal gland; (3) serum potassium level lower than 3.5 mmol/L. Subjects who had received operation were taken into analysis and follow-ups. One hundred and twenty-five patients fulfilled the criteria and were recruited into our research. One hundred and twenty-two operated patients (97.6%) experienced complete resolution of hypokalemia as well as resolution or improvement in hypertension with reduction in antihypertensive medication, while 3 patients (2.4%) failed to obtain normal kalemia and continued on spironolactone therapy. At a median of 65-month (range 21-93) follow-up of these 122 subjects, 27 patients dropped out (22.1%). The 95 responding patients reported no episodes of paralysis or confirmed hypokalemia or any supplementation of potassium. Multivariate linear correlation analysis showed that plasma potassium level was correlated inversely with tumor diameter (r = -0.258, 95% CI -0.076, -0.514, p = 0.037) and basal plasma aldosterone level (r = -0.251, 95% CI -0.040, -0.464, p = 0.042). Most patients with typical unilateral adrenal macroadenomas, normal contralateral glands and hypokalemia could attain favorable surgical therapeutic outcomes without pre-operational AVS lateralization.

Adrenal Mass Causing Secondary Hypertension.

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Robinson, Darlene Y

2015-11-01

Most hypertensive patients have essential (primary) hypertension; only 5% to 10% have a secondary cause. Two clinical characteristics suggestive of secondary hypertension are early onset (hypertension (>180/110 mm Hg). When faced with these findings, clinicians should consider a secondary cause of hypertension. A 22-year-old woman being evaluated for asthma exacerbation in the emergency department was noted to have severe persistent hypertension. Additional evaluation revealed severe hypokalemia, metabolic alkalosis, and hypernatremia. The patient was admitted to the hospital for blood pressure management, electrolyte replacement, and further evaluation of presumed hyperaldosteronism. Diagnostic imaging revealed a large adrenal mass. Surgical resection was performed, leading to a diagnosis of hyperaldosteronism caused by adrenal carcinoma. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Secondary hypertension is far less common than essential hypertension; however, considering the large volume of patients seen in emergency departments, it is likely that some will have secondary hypertension. Emergency physicians should be aware of the clinical characteristics that suggest secondary hypertension so that the appropriate diagnostic and treatment pathways can be pursued. Copyright © 2015 Elsevier Inc. All rights reserved.

Liddle Syndrome: Review of the Literature and Description of a New Case

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Martina Tetti

2018-03-01

Full Text Available Liddle syndrome is an inherited form of low-renin hypertension, transmitted with an autosomal dominant pattern. The molecular basis of Liddle syndrome resides in germline mutations of the SCNN1A, SCNN1B and SCNN1G genes, encoding the α, β, and γ-subunits of the epithelial Na+ channel (ENaC, respectively. To date, 31 different causative mutations have been reported in 72 families from four continents. The majority of the substitutions cause an increased expression of the channel at the distal nephron apical membrane, with subsequent enhanced renal sodium reabsorption. The most common clinical presentation of the disease is early onset hypertension, hypokalemia, metabolic alkalosis, suppressed plasma renin activity and low plasma aldosterone. Consequently, treatment of Liddle syndrome is based on the administration of ENaC blockers, amiloride and triamterene. Herein, we discuss the genetic basis, clinical presentation, diagnosis and treatment of Liddle syndrome. Finally, we report a new case in an Italian family, caused by a SCNN1B p.Pro618Leu substitution.

Recurrent urinary tract infections in an infant with antenatal Bartter syndrome.

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Tasic, Velibor; Pota, Liljana; Gucev, Zoran

2011-02-01

antenatal variant of Bartter syndrome is characterized by a history of polyhydramnios, premature birth, metabolic alkalosis, hypokalemia, polyuria and renal salt wasting. In this report we present a premature female baby with antenatal Barter syndrome who had three episodes of urinary tract infection (UTI), without evidence for congenital anomaly of the kidneys or urinary tract. antenatal Bartter syndrome was diagnosed according to the standard criteria. Ultrasound scan and voiding cystourethrography were performed to exclude congenital anomaly of the kidneys and urinary tract. the baby presented with early hyperkalemia and acidosis. The typical biochemical features of the Bartter syndrome were observed in the second month. Despite appropriate treatment she had persistent hypercalciuria. The clinical course was complicated with recurrent episodes of febrile UTIs. Urinary tract system imaging did not demonstrate congenital anomalies. She finally died of severe dehydration, acidosis and renal failure. since no congenital anomaly of the kidneys or urinary tract was demonstrated in our patient, we believe that severe, persistent hypercalciuria is the most important risk factor for development of recurrent UTIs.

Antenatal Bartter Syndrome: A Review

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Y. Ramesh Bhat

2012-01-01

Full Text Available Antenatal Bartter syndrome (ABS is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS.

A novel mutation of CLCNKB in a Korean patient of mixed phenotype of Bartter-Gitelman syndrome.

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Cho, Hee-Won; Lee, Sang Taek; Cho, Heeyeon; Cheong, Hae Il

2016-11-01

Bartter syndrome (BS) is an inherited renal tubular disorder characterized by low or normal blood pressure, hypokalemic metabolic alkalosis, and hyperreninemic hyperaldosteronism. Type III BS is caused by loss-of-function mutations in CLCNKB encoding basolateral ClC-Kb. The clinical phenotype of patients with CLCNKB mutations has been known to be highly variable, and cases that are difficult to categorize as type III BS or other hereditary tubulopathies, such as Gitelman syndrome, have been rarely reported. We report a case of a 10-year-old Korean boy with atypical clinical findings caused by a novel CLCNKB mutation. The boy showed intermittent muscle cramps with laboratory findings of hypokalemia, severe hypomagnesemia, and nephrocalcinosis. These findings were not fully compatible with those observed in cases of BS or Gitelman syndrome. The CLCNKB mutation analysis revealed a heterozygous c.139G>A transition in exon 13 [p.Gly(GGG)465Glu(GAG)]. This change is not a known mutation; however, the clinical findings and in silico prediction results indicated that it is the underlying cause of his presentation.

Antenatal Bartter Syndrome: A Review

Science.gov (United States)

Bhat, Y. Ramesh; Vinayaka, G.; Sreelakshmi, K.

2012-01-01

Antenatal Bartter syndrome (ABS) is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS. PMID:22518185

[Case of distal renal tubular acidosis complicated with renal diabetes insipidus, showing aggravation of symptoms with occurrence of diabetes mellitus].

Science.gov (United States)

Liu, Hexing; Tomoda, Fumihiro; Koike, Tsutomu; Ohara, Maiko; Nakagawa, Taizo; Kagitani, Satoshi; Inoue, Hiroshi

2011-01-01

We report herein a 27-year-old male case of inherited distal renal tubular acidosis complicated with renal diabetes insipidus, the symptoms of which were aggravated by the occurrence of diabetes mellitus. At 2 months after birth, he was diagnosed as having inherited distal renal tubular acidosis and thereafter supplementation of both potassium and alkali was started to treat his hypokalemia and metabolic acidosis. At the age of 4 years, calcification of the bilateral renal medulla was detected by computed tomography. Subsequently his urinary volume gradually increased and polyuria of approximately 4 L/day persisted. At the age of 27 years, he became fond of sugar-sweetened drinks and also often forgot to take the medicine. He was admitted to our hospital due to polyuria of more than 10 L day, muscle weakness and gait disturbance. Laboratory tests disclosed worsening of both hypokalemia and metabolic acidosis in addition to severe hyperglycemia. It seemed likely that occurrence of diabetes mellitus and cessation of medications can induce osmotic diuresis and aggravate hypokalemia and metabolic acidosis. Consequently, severe dehydration, hypokalemia-induced damage of his urinary concentration ability and enhancement of the renin angiotensin system occurred and thereby possibly worsened his hypokalemia and metabolic acidosis. As normalization of hyperglycemia and metabolic acidosis might have exacerbated hypokalemia further, dehydration and hypokalemia were treated first. Following intensive treatment, these abnormalities were improved, but polyuria persisted. Elevated plasma antidiuretic hormone (12.0 pg/mL) and deficit of renal responses to antidiuretic hormone suggested that the polyuria was attributable to the preexisting renal diabetes insipidus possibly caused by bilateral renal medulla calcification. Thiazide diuretic or nonsteroidal anti-inflammatory drugs were not effective for the treatment of diabetes insipidus in the present case.

Een geval van hypochloremische alkalose bij een pasgeborene

NARCIS (Netherlands)

van de Bor, M.; Ruys, J. H.; Kenter, G.; Zoethout, H. E.

1984-01-01

A full term neonate in which by accident a metabolic alkalosis was found, is described. The origin of the metabolic alkalosis was excessive vomiting by the mother during the days prior to delivery. The simplified form of the Henderson Hasselbalch equation is used to describe the factors responsible

Renal scintigraphy by captopril in hypertension with hypokalemia

International Nuclear Information System (INIS)

Grandet, P.J.

1997-01-01

A study on 30 files of hypertensive patients with an associated hypokalemia was achieved from January 1996 to May 1997. The technique was that of a basic examination effected by MAG 3 (80 MBq), followed by oral intake of 25 to 50 mg of Captopril; one hour after, a new examination was done by MAG 3, with 130 MBq. The classical aspect of isotopic nephro-gram (IN) was not constantly found in case of renal artery stenosis. The reduction of the peak of the level approached might be the only sign, even without any delay of this summit; the lowering of the peak after Captopril of at least 50% should be taken into account. Thus, on the basis of these arguments, we have found 5 stenoses of renal artery. Twenty patients considered as normal have had not arteriography and are relatively well-equilibrated by medical treatment. Among the false negatives, one is explained by a renal insufficiency given an IE of bad quality, while the other is a dysplasia of renal arteries. The 3 false positives presented a discrete difference between the two examinations by MAG 3. Consequently, we considered that the discrete signs should not be retained. The slowing down of transit time, the net lowering of the peak or its delay (classically, 11 min) are good arguments

[Pseudo-Bartter syndrome--2 cases].

Science.gov (United States)

Jóźwiak, Lucyna; Jaroszyński, Andrzej; Baranowicz-Gaszczyk, Iwona; Borowicz, Ewa; Ksiazek, Andrzej

2010-01-01

Bartter syndrome represents the group of renal disturbances characterized by hypokaliemia and metabolic alkalosis. Some diseases could display hypokalemic metabolic alkalosis without primary tubular dysfunction. These disorders are called pseudo-Bartter syndrome. In this paper we present 2 cases of pseudo-Bartter syndrome related among to other things to overuse of diuretic drugs.

Bicarbonate Concentration, Acid-Base Status, and Mortality in the Health, Aging, and Body Composition Study.

Science.gov (United States)

Raphael, Kalani L; Murphy, Rachel A; Shlipak, Michael G; Satterfield, Suzanne; Huston, Hunter K; Sebastian, Anthony; Sellmeyer, Deborah E; Patel, Kushang V; Newman, Anne B; Sarnak, Mark J; Ix, Joachim H; Fried, Linda F

2016-02-05

Low serum bicarbonate associates with mortality in CKD. This study investigated the associations of bicarbonate and acid-base status with mortality in healthy older individuals. We analyzed data from the Health, Aging, and Body Composition Study, a prospective study of well functioning black and white adults ages 70-79 years old from 1997. Participants with arterialized venous blood gas measurements (n=2287) were grouped into respiratory alkalosis, and 1.35 (95% CI, 1.08 to 1.69) for metabolic alkalosis categories. Respiratory acidosis did not associate with mortality. In generally healthy older individuals, low serum bicarbonate associated with higher mortality independent of systemic pH and potential confounders. This association seemed to be present regardless of whether the cause of low bicarbonate was metabolic acidosis or respiratory alkalosis. Metabolic alkalosis also associated with higher mortality. Copyright © 2016 by the American Society of Nephrology.

TWIK-1 two-pore domain potassium channels change ion selectivity and conduct inward leak sodium currents in hypokalemia.

Science.gov (United States)

Ma, Liqun; Zhang, Xuexin; Chen, Haijun

2011-06-07

Background potassium (K+) channels, which are normally selectively permeable to K+, maintain the cardiac resting membrane potential at around -80 mV. In subphysiological extracellular K+ concentrations ([K+]o), which occur in pathological hypokalemia, the resting membrane potential of human cardiomyocytes can depolarize to around -50 mV, whereas rat and mouse cardiomyocytes become hyperpolarized, consistent with the Nernst equation for K+. This paradoxical depolarization of cardiomyocytes in subphysiological [K+]o, which may contribute to cardiac arrhythmias, is thought to involve an inward leak sodium (Na+) current. Here, we show that human cardiac TWIK-1 (also known as K2P1) two-pore domain K+ channels change ion selectivity, becoming permeable to external Na+, and conduct inward leak Na+ currents in subphysiological [K+]o. A specific threonine residue (Thr118) within the pore selectivity sequence TxGYG was required for this altered ion selectivity. Mouse cardiomyocyte-derived HL-1 cells exhibited paradoxical depolarization with ectopic expression of TWIK-1 channels, whereas TWIK-1 knockdown in human spherical primary cardiac myocytes eliminated paradoxical depolarization. These findings indicate that ion selectivity of TWIK-1 K+ channels changes during pathological hypokalemia, elucidate a molecular basis for inward leak Na+ currents that could trigger or contribute to cardiac paradoxical depolarization in lowered [K+]o, and identify a mechanism for regulating cardiac excitability.

[A man with a classic serious milk-alkali syndrome and a carcinoma of the stomach].

Science.gov (United States)

Verburg, F A J; van Zanten, R A A; Brouwer, R M L; Woittiez, A J J; Veneman, Th F

2006-07-22

A 42-year-old man was transferred to the Emergency Department after his friends had found him unresponsive and confused in his room. He had been experiencing upper abdominal complaints for a period of several months. He had taken large amounts of a calcium carbonate/magnesium subcarbonate preparation (Rennie) and had consumed at least 3 litres of dairy products per day. His behaviour was reported as being more and more abnormal during the previous few weeks. On admission he was confused and agitated and had involuntary movements of his limbs. Laboratory investigation indicated a triple acid base disorder, i.e. metabolic alkalosis, respiratory alkalosis and high anion gap metabolic acidosis, with severe dehydration. The metabolic alkalosis was caused by the intake of large amounts of dairy and antacids: milk-alkali syndrome. The metabolic acidosis was the result of hypovolaemia and pre-renal renal failure and the respiratory alkalosis was caused by hyperventilation due to the organic psychosyndrome. The patient was treated with volume expansion by isotonic saline and the administration of potassium and he was sedated with low-dose midazolam, which led to a full respiratory compensation of the metabolic alkalosis. A few days following admission, both the plasma calcium concentration and renal function returned to normal; the acid-base disorder completely normalized and the organic psychosyndrome disappeared. On gastroduodenoscopy a gastric ulcer was found; biopsies revealed a signet ring cell adenocarcinoma of the stomach.

A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs

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Fan Liu

2018-02-01

Full Text Available Objective Heat stress (HS triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. Methods A total of 24 pigs were given either a control diet (17 IU/kg VE or a high VE (200 IU/kg VE; HiVE diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity or HS (35°C, 35% to 45% humidity, 8 h daily conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Results Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all p<0.05 for diet×temperature the loss of blood CO2 partial pressure and bicarbonate, as well as the increase in blood pH in the heat-stressed pigs. The HS reduced (p = 0.003 plasma biological antioxidant potential (BAP and tended to increase (p = 0.067 advanced oxidized protein products (AOPP in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet× temperature. Conclusion A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

Electrolyte and Acid-Base Disturbances in End-Stage Liver Disease: A Physiopathological Approach.

Science.gov (United States)

Jiménez, José Víctor; Carrillo-Pérez, Diego Luis; Rosado-Canto, Rodrigo; García-Juárez, Ignacio; Torre, Aldo; Kershenobich, David; Carrillo-Maravilla, Eduardo

2017-08-01

Electrolyte and acid-base disturbances are frequent in patients with end-stage liver disease; the underlying physiopathological mechanisms are often complex and represent a diagnostic and therapeutic challenge to the physician. Usually, these disorders do not develop in compensated cirrhotic patients, but with the onset of the classic complications of cirrhosis such as ascites, renal failure, spontaneous bacterial peritonitis and variceal bleeding, multiple electrolyte, and acid-base disturbances emerge. Hyponatremia parallels ascites formation and is a well-known trigger of hepatic encephalopathy; its management in this particular population poses a risky challenge due to the high susceptibility of cirrhotic patients to osmotic demyelination. Hypokalemia is common in the setting of cirrhosis: multiple potassium wasting mechanisms both inherent to the disease and resulting from its management make these patients particularly susceptible to potassium depletion even in the setting of normokalemia. Acid-base disturbances range from classical respiratory alkalosis to high anion gap metabolic acidosis, almost comprising the full acid-base spectrum. Because most electrolyte and acid-base disturbances are managed in terms of their underlying trigger factors, a systematic physiopathological approach to their diagnosis and treatment is required.

Unusual Complication of Multidrug Resistant Tuberculosis

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Prerna Sharma

2017-01-01

Full Text Available Introduction. Capreomycin is a second-line drug often used for multidrug-resistant tuberculosis which can result in nephrotoxic effects similar to other aminoglycosides. We describe a case of capreomycin induced Bartter-like syndrome with hypocalcemic tetany. Case Report. 23-year-old female patient presented with carpopedal spasms and tingling sensations in hands. Patient was being treated with capreomycin for two months for tuberculosis. On further investigation, hypocalcemia, hyponatremia, hypomagnesemia, hypokalemia, and hypochloremic metabolic alkalosis were noted. Vitamin D and serum PTH levels were within normal limits. Hypercalciuria was confirmed by urine calcium/creatinine ratio. Calcium, potassium, and magnesium supplementation was given and capreomycin was discontinued. Electrolytes normalized in two days after cessation of capreomycin with no further abnormalities on repeat investigations. Discussion. Aminoglycosides can result in renal tubular dysfunction leading to Fanconi syndrome, Bartter syndrome, and distal tubular acidosis. Impaired mitochondrial function in the tubular cells has been hypothesized as the possible cause of these tubulopathies. Acquired Bartter-like syndrome phenotypically resembles autosomal dominant type 5 Bartter syndrome. Treatment consists of correction of electrolyte abnormalities, indomethacin, and potassium-sparing diuretics. Prompt diagnosis and treatment of severe dyselectrolytemia are warranted in patients on aminoglycoside therapy.

Update in diagnosis and management of primary aldosteronism.

Science.gov (United States)

Dick, Sofia M; Queiroz, Marina; Bernardi, Bárbara L; Dall'Agnol, Angélica; Brondani, Letícia A; Silveiro, Sandra P

2018-02-23

Primary aldosteronism (PA) is a group of disorders in which aldosterone is excessively produced. These disorders can lead to hypertension, hypokalemia, hypervolemia and metabolic alkalosis. The prevalence of PA ranges from 5% to 12% around the globe, and the most common causes are adrenal adenoma and adrenal hyperplasia. The importance of PA recognition arises from the fact that it can have a remarkably adverse cardiovascular and renal impact, which can even result in death. The aldosterone-to-renin ratio (ARR) is the election test for screening PA, and one of the confirmatory tests, such as oral sodium loading (OSL) or saline infusion test (SIT), is in general necessary to confirm the diagnosis. The distinction between adrenal hyperplasia (AH) or aldosterone-producing adenoma (APA) is essential to select the appropriate treatment. Therefore, in order to identify the subtype of PA, imaging exams such as computed tomography or magnetic ressonance imaging, and/or invasive investigation such as adrenal catheterization must be performed. According to the subtype of PA, optimal treatment - surgical for APA or pharmacological for AH, with drugs like spironolactone and amiloride - must be offered.

Teaching acid/base physiology in the laboratory

DEFF Research Database (Denmark)

Friis, Ulla G; Plovsing, Ronni; Hansen, Klaus

2010-01-01

exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical...... students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group...... failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied....

Effects of early administration of acetazolamide on the duration of mechanical ventilation in patients with chronic obstructive pulmonary disease or obesity-hypoventilation syndrome with metabolic alkalosis. A randomized trial.

Science.gov (United States)

Rialp Cervera, G; Raurich Puigdevall, J M; Morán Chorro, I; Martín Delgado, M C; Heras la Calle, G; Mas Serra, A; Vallverdú Perapoch, I

2017-06-01

Metabolic alkalosis (MA) inhibits respiratory drive and may delay weaning from mechanical ventilation (MV). MA is common in CO 2 -retainer patients that need MV. Acetazolamide (ACTZ) decreases serum bicarbonate concentration and stimulates respiratory drive. This study evaluated the effects of ACTZ on the duration of MV in patients with MA and COPD or obesity hypoventilation syndrome (OHS) intubated with acute respiratory failure. Multicenter, randomized, controlled, double-blind study, with COPD or OHS patients with MV 28 mmol/L and pH > 7.35. Test-treatment, ACTZ 500 mg or placebo, was daily administered if pH > 7.35 and bicarbonate >26 mmol/L. Clinical, respiratory and laboratory parameters were recorded. 47 patients (36 men) were randomized. There were no significant differences between groups in comorbidities, baseline characteristics or arterial blood gases at inclusion. The mean difference in the duration of MV between placebo and ACTZ group was 1.3 days (95%CI, -2.1-4.8; p = 0.44). Kaplan-Meier curves showed no differences in the duration of MV (Log-Rank p = 0.41). Between-group comparison of estimated marginal means (CI 95%) during MV were, respectively: PaCO 2 55 (51-59) vs 48 (47-50) mm Hg, p = 0.002; bicarbonate concentration 34 (32-35) vs 29 (28-30) mmol/L, p < 0.0001; and minute volume 9.7 (8.9-10.4) vs 10.6 (9.2-12.0) L/min, p = 0.26. There were no severe adverse effects with ACTZ administration. Among patients with MA and COPD or OHS, early treatment with ACTZ did not shorten significantly the duration of MV compared with placebo. clinical.trials.gov; NCT01499485; URL:.www.clinicaltrials.gov. Copyright © 2017 Elsevier Ltd. All rights reserved.

Respiratory alkalosis and primary hypocapnia in Labrador Retrievers participating in field trials in high-ambient-temperature conditions.

Science.gov (United States)

Steiss, Janet E; Wright, James C

2008-10-01

To determine whether Labrador Retrievers participating in field trials develop respiratory alkalosis and hypocapnia primarily in conditions of high ambient temperatures. 16 Labrador Retrievers. At each of 5 field trials, 5 to 10 dogs were monitored during a test (retrieval of birds over a variable distance on land [1,076 to 2,200 m]; 36 assessments); ambient temperatures ranged from 2.2 degrees to 29.4 degrees C. For each dog, rectal temperature was measured and a venous blood sample was collected in a heparinized syringe within 5 minutes of test completion. Blood samples were analyzed on site for Hct; pH; sodium, potassium, ionized calcium, glucose, lactate, bicarbonate, and total CO2 concentrations; and values of PvO2 and PvCO2. Scatterplots of each variable versus ambient temperature were reviewed. Regression analysis was used to evaluate the effect of ambient temperature ( 21 degrees C) on each variable. Compared with findings at ambient temperatures 21 degrees C; rectal temperature did not differ. Two dogs developed signs of heat stress in 1 test at an ambient temperature of 29 degrees C; their rectal temperatures were higher and PvCO2 values were lower than findings in other dogs. When running distances frequently encountered at field trials, healthy Labrador Retrievers developed hyperthermia regardless of ambient temperature. Dogs developed respiratory alkalosis and hypocapnia at ambient temperatures > 21 degrees C.

Out of Warburg effect: An effective cancer treatment targeting the tumor specific metabolism and dysregulated pH.

Science.gov (United States)

Schwartz, Laurent; Seyfried, Thomas; Alfarouk, Khalid O; Da Veiga Moreira, Jorgelindo; Fais, Stefano

2017-04-01

As stated by Otto Warburg nearly a century ago, cancer is a metabolic disease, a fermentation caused by malfunctioning mitochondria, resulting in increased anabolism and decreased catabolism. Treatment should, therefore, aim at restoring the energy yield. To decrease anabolism, glucose uptake should be reduced (ketogenic diet). To increase catabolism, the oxidative phosphorylation should be restored. Treatment with a combination of α-lipoic acid and hydroxycitrate has been shown to be effective in multiple animal models. This treatment, in combination with conventional chemotherapy, has yielded extremely encouraging results in glioblastoma, brain metastasis and lung cancer. Randomized trials are necessary to confirm these preliminary data. The major limitation is the fact that the combination of α-lipoic acid and hydroxycitrate can only be effective if the mitochondria are still present and/or functional. That may not be the case in the most aggressive tumors. The increased intracellular alkalosis is a strong mitogenic signal, which bypasses most inhibitory signals. Concomitant correction of this alkalosis may be a very effective treatment in case of mitochondrial failure. Copyright © 2017 Elsevier Ltd. All rights reserved.

Mineralocorticoid hypertension: clinical and laboratory studies with special reference to selective percutaneous venography combined with aldosterone assay in the adrenal venous blood

International Nuclear Information System (INIS)

Wajchenberg, B.L.; Liberman, B.; Novaes, M.

1977-01-01

With the purpose of demonstrating the presence of hypertension, hypokalemia and alkalosis were studied. The presence of daily aldosteronism was verified in five patients; the sixth one presented no daily aldosteronism but an increase of 18-OH-DOCA production, an ACTH dependente mineralocorticoid. The presence of tumor (less than 0.9cm) could not be shown in two patients by bilateral selective adrenal venography. The aldosterone assay during catherization of adrenal vein of those patients permitted to determine the tumoral side. Attention must be given to the fact that the blood collection of adrenal vein must always be made during adrenal venography to demonstrate the presence of short unilateral tumor or bilateral disease [pt

Adult presentation of Bartter syndrome type IV with erythrocytosis.

Science.gov (United States)

Heilberg, Ita Pfeferman; Tótoli, Cláudia; Calado, Joaquim Tomaz

2015-01-01

Bartter syndrome comprises a group of rare autosomal-recessive salt-losing disorders with distinct phenotypes, but one unifying pathophysiology consisting of severe reductions of sodium reabsorption caused by mutations in five genes expressed in the thick ascending limb of Henle, coupled with increased urinary excretion of potassium and hydrogen, which leads to hypokalemic alkalosis. Bartter syndrome type IV, caused by loss-of-function mutations in barttin, a subunit of chloride channel CLC-Kb expressed in the kidney and inner ear, usually occurs in the antenatal-neonatal period. We report an unusual case of late onset presentation of Bartter syndrome IV and mild phenotype in a 20 years-old man who had hypokalemia, deafness, secondary hyperparathyroidism and erythrocytosis.

Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion

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Mitch, William E.; Sands, Jeff M.

2015-01-01

Renal nitrogen metabolism primarily involves urea and ammonia metabolism, and is essential to normal health. Urea is the largest circulating pool of nitrogen, excluding nitrogen in circulating proteins, and its production changes in parallel to the degradation of dietary and endogenous proteins. In addition to serving as a way to excrete nitrogen, urea transport, mediated through specific urea transport proteins, mediates a central role in the urine concentrating mechanism. Renal ammonia excretion, although often considered only in the context of acid-base homeostasis, accounts for approximately 10% of total renal nitrogen excretion under basal conditions, but can increase substantially in a variety of clinical conditions. Because renal ammonia metabolism requires intrarenal ammoniagenesis from glutamine, changes in factors regulating renal ammonia metabolism can have important effects on glutamine in addition to nitrogen balance. This review covers aspects of protein metabolism and the control of the two major molecules involved in renal nitrogen excretion: urea and ammonia. Both urea and ammonia transport can be altered by glucocorticoids and hypokalemia, two conditions that also affect protein metabolism. Clinical conditions associated with altered urine concentrating ability or water homeostasis can result in changes in urea excretion and urea transporters. Clinical conditions associated with altered ammonia excretion can have important effects on nitrogen balance. PMID:25078422

Central lactic acidosis, hyperventilation, and respiratory alkalosis: leading clinical features in a 3-year-old boy with malignant meningeal melanoma.

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Blüher, Susann; Schulz, Manuela; Bierbach, Uta; Meixensberger, Jürgen; Tröbs, Ralf-Bodo; Hirsch, Wolfgang; Schober, Ralf; Kiess, Wieland; Siekmeyer, Werner

2008-04-01

Meningeal tumors are extremely rare in children and are diagnostically as well as therapeutically challenging. Among the least common types of malignancies in childhood is malignant melanoma, counting for less than 1% of pediatric tumors. Due to the rarity and the wide spectrum of appearance, initial clinical features may be misleading. A 3-year-old boy was referred to our hospital with symptoms of hyperventilation, dyspnoea, tachycardia, respiratory alkalosis, inarticulate speech, and fatigue. Measurement of pH in cerebrospinal fluid (CSF) yielded central lactic acidosis despite alkalosis in peripheral blood. Diagnostic imaging procedures as well as histology and immunohistochemistry revealed the diagnosis of a malignant meningeal melanoma. We hypothesize that central lactate production of the tumor nests might have induced central acidification, thus inducing hyperventilation by stimulation of central chemoreceptors. This case is a model example of the key role of central pH as an inducer/suppressor of ventilation in humans and illustrates the critical importance of central pH for regulating both ventilation and acid-base homeostasis. Thus, pH of CSF should be measured whenever a malignant brain tumor is suspected.

Bartter syndrome type 3 in an elderly complicated with adrenocorticotropin-deficiency.

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Tamagawa, Eri; Inaba, Hidefumi; Ota, Takayuki; Ariyasu, Hiroyuki; Kawashima, Hiromichi; Wakasaki, Hisao; Furuta, Hiroto; Nishi, Masahiro; Nakao, Taisei; Kaito, Hiroshi; Iijima, Kazumoto; Nakanishi, Koichi; Yoshikawa, Norishige; Akamizu, Takashi

2014-01-01

Bartter syndrome (BS) is a disorder with normotensive hypokalemic alkalosis and hyperreninemic hyperaldosteronemia. BS affects infants or early childhood. Patients with BS type 3 harbor mutation in CLCNKB, Cl channel Kb. Gitelman syndrome (GS) is a disorder in childhood, with mutation in SLC12A3. Isolated adrenocorticotropin deficiency (IAD) causes secondary adrenal insufficiency. Neither elderly cases, nor cases with IAD were previously reported in BS. A 72-year-old man was admitted with acute adrenal crisis. He had been treated for IAD for 19 years. He had no trouble during perinatal period, delivery, and growth. After the recovery from adrenal crisis, laboratory tests revealed hypokalemia; 3.0 mEq/L (normal: 3.5-4.5), impaired renal function: eGFR; 37.6 mL/min/1.73 m2, normomagnesemia; 2.1 mg/dL (1.7-2.3), hyperreninemia; 59.4 ng/mL/h (0.2-2.7), hyperaldosteronemia; 23.5 ng/dL (3.0-15.9), and normal urinary ratio of calcium/creatinine. In diuretic tests, he showed a fine response to furosemide, and a mild response to thiazide. In genetic tests, no mutation of SLC12A3 was found and homozygous mutation: c.1830 G > A in CLCNKB was shown. Thus he was diagnosed as BS type 3. Current case presented with unusual features as BS type 3, 1) his late and mild clinical manifestation suggested GS rather than BS, 2) laboratory data and diuretics tests did not show typical features as BS, and 3) IAD and chronic renal failure altered electrolyte metabolism. In conclusion, current case implies that BS type 3 should be considered even in elderly cases with normotensive hypokalemia, and highlights importance of endocrinological and genetic examinations.

Homespun remedy, homespun toxicity: baking soda ingestion for dyspepsia.

Science.gov (United States)

Ajbani, Keyur; Chansky, Michael E; Baumann, Brigitte M

2011-04-01

A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities. Copyright © 2011 Elsevier Inc. All rights reserved.

Bartter Syndrome with Normal Aldosterone Level: An Unusual Presentation.

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Huque, S S; Rahman, M H; Khatun, S

2016-04-01

Bartter syndrome (BS) is a hereditary disease, with an autosomal recessive or autosomal dominant mode of transmission. It is characterized by salt wasting hypochloraemic, hypokalaemic metabolic alkalosis and hyperreninaemia with normal blood pressure. The primary defect is in the thick ascending limb of loop of Henle (TAL). Herein, we report a case that had typical features of BS like severe dehydration, severe hypokalaemia, metabolic alkalosis and failure to thrive but had normal aldosterone level which is very uncommon.

Mixed Bartter-Gitelman syndrome: an inbred family with a heterogeneous phenotype expression of a novel variant in the CLCNKB gene.

Science.gov (United States)

Al-Shibli, Amar; Yusuf, Madinah; Abounajab, Issam; Willems, Patrick J

2014-01-01

Patients with renal diseases associated with salt-losing tubulopathies categorized as Gitelman and classic form of Bartter syndrome have undergone genetic screening for possible mutation capture in two different genes: SLC12A3 and CLCNKB. Clinical symptoms of these two diseases may overlap. Bartter syndrome and Gitelman syndrome are autosomal recessive salt-losing tubulopathies with hypokalemia, metabolic alkalosis, hyperreninemia, hyperplasia of the juxtaglomerular apparatus, hyperaldosteronism, and, in some patients, hypomagnesemia. Here we describe four patients from an inbred family with a novel missense variant in the CLCNKB gene. All of patients are asymptomatic; yet they have the typical metabolic abnormality of salt losing tubulopathies. One of those patients had hypomagnesaemia while others not. Clinical and laboratory data of all patients was described. All 4 patients have a homozygous c.490G > T missense variant in exon 5 of the CLCNKB gene. This variant alters a glycine into a cysteine on amino acid position 164 of the resulting protein (p.Gly164Cys). The c.490G > T variant is a novel variant not previously described in other patients nor controls. Polyphen analysis predicts the variation to be possibly damaging. Analysis of SLC12A3 was normal. Here in we are describing a novel homozygous c.490G > T missense variation was identified in exon 5 of the CLCNKB gene was identified in an Emirati patients with a mild manifestation of Bartter - Gitelman syndrome.

Maternal Pseudo-Bartter Syndrome Associated with Severe Perinatal Brain Injury.

Science.gov (United States)

Vora, Shrenik; Ibrahim, Thowfique; Rajadurai, Victor Samuel

2017-09-15

Maternal electrolyte imbalance is rarely reported as causative factor of severe perinatal brain injury. This case outlines a unique maternal and neonatal pseudo-Bartter syndrome presented with metabolic alkalosis and hypochloremia due to maternal severe vomiting. Neonatal MRI brain revealed extensive brain hemorrhages with porencephalic cysts. Subsequent investigation workup points towards maternal severe metabolic alkalosis as its cause. Careful medical attention should be paid to pregnant women with excessive vomiting to ensure a healthy outcome for both the mother and the baby.

Bartter syndrome presenting as poor weight gain and abdominal mass in an infant.

Science.gov (United States)

Heffernan, Annie; Steffensen, Thora S; Gilbert-Barness, Enid; Perlman, Sharon

2008-01-01

Bartter syndrome, a group of disorders that encompasses multiple genetic defects with similar clinical presentation, has been divided into six different genotypes, according to different genetic defects, and into three main clinical variants (or phenotypes). Classic laboratory findings in all variants include hypochloremia, hypokalemia, and metabolic alkalosis with excessive excretion of chloride and potassium. Classic Bartter syndrome, neonatal Bartter syndrome, and Gitelman syndrome are the three main clinical variants. Classic Bartter syndrome and neonatal Bartter syndrome have defects in genes that affect transport channels in the ascending loop of Henle, where as in Gitleman syndrome the defect occurs in the transport channels of the distal convoluted tubule. Classic Bartter syndrome and neonatal Bartter syndrome have similar presenting symptoms, potential outcomes, and treatment, but different ages at presentation. Gitelman syndrome, a more benign condition than the other clinical variants, has the classic hallmark finding of hypomagnesemia and low to normal excretion of calcium. This differentiates it from the classic and neonatal variants of the disease. With early diagnosis and proper treatment, Bartter syndrome has a good prognosis. But failure to identify it can lead to tubulointerstitial nephritis and renal failure. We present a case of a 6-month-old boy with Bartter syndrome who presented with poor weight gain and an abdominal mass.

ClC-K chloride channels: emerging pathophysiology of Bartter syndrome type 3.

Science.gov (United States)

Andrini, Olga; Keck, Mathilde; Briones, Rodolfo; Lourdel, Stéphane; Vargas-Poussou, Rosa; Teulon, Jacques

2015-06-15

The mutations in the CLCNKB gene encoding the ClC-Kb chloride channel are responsible for Bartter syndrome type 3, one of the four variants of Bartter syndrome in the genetically based nomenclature. All forms of Bartter syndrome are characterized by hypokalemia, metabolic alkalosis, and secondary hyperaldosteronism, but Bartter syndrome type 3 has the most heterogeneous presentation, extending from severe to very mild. A relatively large number of CLCNKB mutations have been reported, including gene deletions and nonsense or missense mutations. However, only 20 CLCNKB mutations have been functionally analyzed, due to technical difficulties regarding ClC-Kb functional expression in heterologous systems. This review provides an overview of recent progress in the functional consequences of CLCNKB mutations on ClC-Kb chloride channel activity. It has been observed that 1) all ClC-Kb mutants have an impaired expression at the membrane; and 2) a minority of the mutants combines reduced membrane expression with altered pH-dependent channel gating. Although further investigation is needed to fully characterize disease pathogenesis, Bartter syndrome type 3 probably belongs to the large family of conformational diseases, in which the mutations destabilize channel structure, inducing ClC-Kb retention in the endoplasmic reticulum and accelerated channel degradation. Copyright © 2015 the American Physiological Society.

Acetazolamide: a second wind for a respiratory stimulant in the intensive care unit?

Science.gov (United States)

Heming, Nicholas; Urien, Saïk; Faisy, Christophe

2012-08-07

Patients with chronic obstructive pulmonary disease (COPD) are affected by episodes of respiratory exacerbations, some of which can be severe and may necessitate respiratory support. Prolonged invasive mechanical ventilation is associated with increased mortality rates. Persistent failure to discontinue invasive mechanical ventilation is a major issue in patients with COPD. Pure or mixed metabolic alkalosis is a common finding in the intensive care unit (ICU) and is associated with a worse outcome. In patients with COPD, the condition is called post-hypercapnic alkalosis and is a complication of mechanical ventilation. Reversal of metabolic alkalosis may facilitate weaning from mechanical ventilation of patients with COPD. Acetazolamide, a non-specific carbonic anhydrase inhibitor, is one of the drugs employed in the ICU to reverse metabolic alkalosis. The drug is relatively safe, undesirable effects being rare. The compartmentalization of the different isoforms of the carbonic anhydrase enzyme may, in part, explain the lack of evidence of the efficacy of acetazolamide as a respiratory stimulant. Recent findings suggest that the usually employed doses of acetazolamide in the ICU may be insufficient to significantly improve respiratory parameters in mechanically ventilated patients with COPD. Randomized controlled trials using adequate doses of acetazolamide are required to address this issue.

BMP (Basic Metabolic Panel)

Science.gov (United States)

... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... as kidney failure, insulin shock or diabetic coma, respiratory distress, or heart rhythm changes. What does the ...

Milk alkali syndrome induced by calcitriol and calcium bicarbonate in a patient with hypoparathyroidism

Directory of Open Access Journals (Sweden)

Eda Altun

2013-01-01

Full Text Available The milk-alkali syndrome (MAS was a common cause of hypercalcemia, metabolic alkalosis, and renal failure in the early 20 th century. This syndrome was first recognized secondary to treatment of peptic ulcer disease with milk and absorbable alkali. Its incidence fell after the introduction of H2-blocker and proton pump inhibitor. Persistent ingestion of calcium carbonate and vitamin D caused MAS. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis and renal failure secondary to treatment of idiopathic hypoparathyroidism.

Acid-base status after whole-body irradiation in dairy cows

International Nuclear Information System (INIS)

Schaefer, M.; Koch, F.; Dyrba, W.; Kirbach, M.

1989-01-01

Whole-body irradiation using 9 MeV X-rays of a linear accelerator of 10 clinically healthy lactating cows aged between 3.5 and 8 years produced an acute radiation syndrome in the LD 100/30 range. Blood analysis 1 day after irradiation showed a compensated metabolic acidosis with a low renal net acid-base excretion and hyerphosphaturia. Later the acid-base status indicated a differently marked metabolic alkalosis. In the main reaction period acidotic disturbances occurred, which partially were camouflaged by respiratory alkalosis. (author)

Acute encephalopathy with concurrent respiratory and metabolic disturbances in first known parenteral human administration of flunixin meglumine and acepromazine maleate.

Science.gov (United States)

Kamali, Michael F; Wilson, Anwar C; Acquisto, Nicole M; Spillane, Linda; Schneider, Sandra M

2013-08-01

Flunexin is a nonsteroidal anti-inflammatory drug approved for veterinary use in horses and cattle. Acepromazine is a phenothiazine derivative used in horses, dogs, and cats. Human exposure to these substances is rare. We report a case of a human injection of two equine medications, flunixin and acepromazine, which resulted in altered mental status, respiratory alkalosis, gastrointestinal bleeding, and elevation of liver transaminases in a 43-year-old woman who worked as a horse trainer. The patient intentionally self-injected these medications and subsequently presented to the Emergency Department with altered mental status and lethargy. The patient required hospitalization for metabolic abnormalities, including respiratory alkalosis, and suffered a gastrointestinal bleed requiring blood transfusion. The patient ultimately recovered with supportive measures. We believe this to be the first case of concomitant injection of flunixin and acepromazine in a human. This report explains a case of parenteral administration of two equine medications and the subsequent complications in a patient that presented to the Emergency Department. Human exposure to veterinary medications cannot be predicted by their effect in animals due to variations in absorption, distribution, and metabolism. Physicians should be aware that individuals who work with animals may have access to large quantities of veterinary medicine. This case also exemplifies the challenges that Emergency Physicians face on a daily basis, and generates additional consideration for overdoses and intoxications from medications that are not considered commonplace in humans. Copyright © 2013 Elsevier Inc. All rights reserved.

Construction and validation of a decision tree for treating metabolic acidosis in calves with neonatal diarrhea

Directory of Open Access Journals (Sweden)

Trefz Florian M

2012-12-01

Full Text Available Abstract Background The aim of the present prospective study was to investigate whether a decision tree based on basic clinical signs could be used to determine the treatment of metabolic acidosis in calves successfully without expensive laboratory equipment. A total of 121 calves with a diagnosis of neonatal diarrhea admitted to a veterinary teaching hospital were included in the study. The dosages of sodium bicarbonate administered followed simple guidelines based on the results of a previous retrospective analysis. Calves that were neither dehydrated nor assumed to be acidemic received an oral electrolyte solution. In cases in which intravenous correction of acidosis and/or dehydration was deemed necessary, the provided amount of sodium bicarbonate ranged from 250 to 750 mmol (depending on alterations in posture and infusion volumes from 1 to 6.25 liters (depending on the degree of dehydration. Individual body weights of calves were disregarded. During the 24 hour study period the investigator was blinded to all laboratory findings. Results After being lifted, many calves were able to stand despite base excess levels below −20 mmol/l. Especially in those calves, metabolic acidosis was undercorrected with the provided amount of 500 mmol sodium bicarbonate, which was intended for calves standing insecurely. In 13 calves metabolic acidosis was not treated successfully as defined by an expected treatment failure or a measured base excess value below −5 mmol/l. By contrast, 24 hours after the initiation of therapy, a metabolic alkalosis was present in 55 calves (base excess levels above +5 mmol/l. However, the clinical status was not affected significantly by the metabolic alkalosis. Conclusions Assuming re-evaluation of the calf after 24 hours, the tested decision tree can be recommended for the use in field practice with minor modifications. Calves that stand insecurely and are not able to correct their position if pushed

Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report

Directory of Open Access Journals (Sweden)

Raza Farhan

2012-10-01

Full Text Available Abstract Introduction Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty. Case presentation A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours. Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake

Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report.

Science.gov (United States)

Raza, Farhan; Sultan, Mubashar; Qamar, Khola; Jawad, Ali; Jawa, Ali

2012-10-02

Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty. A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL) with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours). Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake. Diagnosis of Gitelman syndrome is usually made incidentally

Relationship of metabolic alkalosis, azotemia and morbidity in patients with chronic obstructive pulmonary disease and hypercapnia.

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Ucgun, Irfan; Oztuna, Funda; Dagli, Canan Eren; Yildirim, Huseyin; Bal, Cengiz

2008-01-01

Exacerbation of chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality, but the effect of metabolic compensation of respiratory acidosis (RA) on mortality is not fully understood. To investigate the relationship between metabolic compensation and mortality in COPD patients with RA. We prospectively investigated all COPD patients with RA admitted to the respiratory intensive care unit between February 2001 and March 2007. Two hundred and thirteen patients (159 male, 54 female; mean age 65 +/- 10.8 years) were divided into three groups (71 patients each) according to base excess (BE) levels: (1) low BE, (2) medium BE, and (3) high BE. H(+) concentration was calculated according to their standard formula and BE was calculated according to the Van Slyke equation. The overall mortality rate was 24.9%. The group mortality rates were 32, 17 and 25% in the low, medium and high BE groups, respectively (p = 0.001). When patients were divided into three groups according to the HCO(3)(-) levels, the group mortality rate was 59.1% in the low HCO(3)(-) group and 19.8% in the high HCO(3)(-) group. Based on univariate analysis, six factors affecting mortality were identified. However, multivariate analysis showed that the levels of serum HCO(3)(-) (p = 0.013; OR: 0.552; CI: 0.345-0.882) and creatinine (p = 0.019; OR: 2.114; CI: 1.132-3.949) had an independent effect. In patients with COPD exacerbation and hypercapnia, the development of sufficient metabolic compensation and adequate renal function significantly decreases mortality. Copyright 2008 S. Karger AG, Basel.

Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosis

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Chin, Lisa M. K.; Heigenhauser, George J. F.; Paterson, Donald H.

2010-01-01

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (V̇o2p) and leg femoral conduit artery (“bulk”) blood flow (LBF) during moderate-intensity exercise (Mod) was examined in eight young male adults. Subjects completed four to six repetitions of alternate-leg knee-extension exercise during normal breathing [Con; end-tidal partial pressure of CO2 (PetCO2) ∼40 mmHg] and sustained hyperventilation (Hypo; PetCO2 ∼20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold). V̇o2p was measured breath by breath by mass spectrometry and volume turbine, and LBF (calculated from mean femoral artery blood velocity and femoral artery diameter) was measured simultaneously by Doppler ultrasound. Concentration changes of deoxy (Δ[HHb])-, oxy (Δ[O2Hb])-, and total hemoglobin-myoglobin (Δ[HbTot]) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). The kinetics of V̇o2p, LBF, and Δ[HHb] were modeled using a monoexponential equation by nonlinear regression. The time constants for the phase 2 V̇o2p (Hypo, 49 ± 26 s; Con, 28 ± 8 s) and LBF (Hypo, 46 ± 16 s; Con, 23 ± 6 s) were greater (P alkalosis is associated with slower convective (i.e., slowed femoral artery and microvascular blood flow) and diffusive (i.e., greater fractional O2 extraction for a given ΔV̇o2p) O2 delivery, which may contribute to the hyperventilation-induced slowing of V̇o2p (and muscle O2 utilization) kinetics. PMID:20339012

Journal of Special Operations Medicine. Volume 9, Edition 4, Fall 2009

Science.gov (United States)

2009-01-01

place in the evaluation, without full blood gas analysis, the body’s compensation mechanisms such as a respiratory alkalosis may maintain a normal or...sam- pling and relatively simple handheld diagnostic tools. Arterial pH has long been used to assess pa- tients for presence of respiratory /metabolic...acido- sis/ alkalosis . There is only a narrow physiologic range of intracellular pH which allows for normal function, typically 7.35-7.45. Acidosis

Hjertestopbehandling. Nyere aspekter af kardiopulmonal genoplivning

DEFF Research Database (Denmark)

Herlevsen, Per Ove; Andersen, H H; Jepsen, S

1989-01-01

compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis...

Gymnocypris przewalskii decreases cytosolic carbonic anhydrase expression to compensate for respiratory alkalosis and osmoregulation in the saline-alkaline lake Qinghai.

Science.gov (United States)

Yao, Zongli; Guo, Wenfei; Lai, Qifang; Shi, Jianquan; Zhou, Kai; Qi, Hongfang; Lin, Tingting; Li, Ziniu; Wang, Hui

2016-01-01

Naked carp (Gymnocypris przewalskii), endemic to the saline-alkaline Lake Qinghai, have the capacity to tolerate combined high salinity and alkalinity, but migrate to spawn in freshwater rivers each year. In this study, the full-length cDNA of the cytosolic carbonic anhydrase c isoform of G. przewalskii (GpCAc) was amplified and sequenced; mRNA levels and enzyme activity of GpCAc and blood chemistry were evaluated to understand the compensatory responses as the naked carp returned to the saline-alkaline lake after spawning. We found that GpCAc had a total length of 1400 bp and encodes a peptide of 260 amino acids. Comparison of the deduced amino acid sequences and phylogenetic analysis showed that GpCAc was a member of the cytosolic carbonic anhydrase II-like c family. Cytosolic-carbonic-anhydrase-c-specific primers were used to analyze the tissue distribution of GpCAc mRNA expression. Expression of GpCAc mRNA was found in brain, gill, liver, kidney, gut, and muscle tissues, but primarily in the gill and posterior kidney; however, none was evident in red blood cells. Transferring fish from river water to lake water resulted in a respiratory alkalosis, osmolality, and ion rise in the blood, as well as significant decreases in the expression and enzyme activity of GpCAc in both the gill and kidney within 96 h. These results indicate that GpCAc may play an important role in the acclimation to both high salinity and carbonate alkalinity. Specifically, G. przewalskii decreases cytosolic carbonic anhydrase c expression to compensate for a respiratory alkalosis and to aid in osmoregulation during the transition from river to saline-alkaline lake.

Incidence of Postoperative Acid-Base Disturbances in Abdominal Surgery

Directory of Open Access Journals (Sweden)

Taghavi Gilani M

2014-04-01

Full Text Available Introduction: Respiratory and blood pressure changes as well as fluid administration alter the acid-base balance during the perioperative period which may cause consciousness disturbance and additional hemodynamic disorders. The aim of this study was to identify frequent postoperative acid-base disturbances in order to control postoperative complications. Materials and Methods:This prospective, observational study design was used on patients who underwent abdominal surgery during a six-month period. Gasometry was performed immediately after the patients’ admittion to ICU and six and 12 hours postoperatively. SPSS v13 software was used, and PResults: 213 patients (123 male and 90 female aged 14-85 years (51.7± 22.4 were evaluated. During admission, PH and PaCO2 were (7.29±0.13 and (38.3±11.9, respectively; however, although PH increased gradually (P=0.001, PaCO2 was reduced (P=0.03. Bicarbonate and base excess had opposite effects; bicarbonate initially decreased but increased after 12 hours (P=0.001, whereas base excess initially increased (-6.3±11.6 and then decreased gradually (P=0.003. The arterial oxygen pressure was reduced for 22.5% of the patients throughout the admission period, and this did not significantly change (P=0.57. Conclusion: According to the results, in admission, 65.7% had metabolic acidosis, but metabolic alkalosis was the least. Gradually, metabolic acidosis was modified, but metabolic alkalosis increased. Intraoperative hypotension and fluid infusion may be the main factors of early metabolic acidosis and control of hypotension, or correction of acidosis may increase metabolic alkalosis.

Respiratory Adaptations in Acid-base Disturbances: Role of Cerebral Fluids,

Science.gov (United States)

1979-06-19

The respiratory and metabolic components of acid-base homeostasis are defined. A quantitative empirical description of the (incomplete) mutual...literature. Respiratory adaptations in steady acid-base disturbances of metabolic origin (hyperventilation with hypocapnia in primary metabolic acidosis, and...hypoventilation with hypercapnia in metabolic alkalosis ) are analyzed as a function of the acidity of the cerebral fluids (cerebrospinal and cerebral interstitial fluid). (Author)

Gitelman's syndrome: a rare presentation mimicking cauda equina syndrome.

LENUS (Irish Health Repository)

Quinlan, C S

2012-02-01

We describe a case of bilateral weakness of the lower limbs, sensory disturbance and intermittent urinary incontinence, secondary to untreated Gitelman\\'s syndrome, in a 42-year-old female who was referred with presumed cauda equina syndrome. On examination, the power of both legs was uniformly reduced, and the perianal and lower-limb sensation was altered. However, MRI of the lumbar spine was normal. Measurements of serum and urinary potassium were low and blood gas analysis revealed metabolic alkalosis. Her symptoms resolved following potassium replacement. We emphasise the importance of measurement of the plasma and urinary levels of electrolytes in the investigation of patients with paralysis of the lower limbs and suggest that they, together with blood gas analysis, allow the exclusion of unusual causes of muscle weakness resulting from metabolic disorders such as metabolic alkalosis.

Cerebral vascular control and metabolism in heat stress

DEFF Research Database (Denmark)

Bain, Anthony R; Nybo, Lars; Ainslie, Philip N

2015-01-01

implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced...

Mineralocorticoid hypertension

Directory of Open Access Journals (Sweden)

Vishal Gupta

2011-01-01

Full Text Available Hypertension affects about 10 - 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta, aldosterone-producing pathologies (primary aldosteronism - Conns syndrome, familial hyperaldosteronism 1, 2, and 3, non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH syndrome, congenitalvadrenal hyperplasia, and drugs with mineraocorticoid activity (locorice, carbenoxole therapy to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics. Direct aldosterone synthetase antagonists represent a promising future therapy.

Novel Compound Heterozygous CLCNKB Gene Mutations (c.1755A>G/ c.848_850delTCT) Cause Classic Bartter Syndrome.

Science.gov (United States)

Wang, Chunli; Chen, Ying; Zheng, Bixia; Zhu, Mengshu; Fan, Jia; Wang, Juejin; Jia, Zhanjun; Huang, Songming; Zhang, Aihua

2018-02-14

Inactivated variants in CLCNKB gene encoding the basolateral chloride channel ClC-Kb cause classic Bartter syndrome characterized by hypokalemic metabolic alkalosis and hyperreninemic hyperaldosteronism. Here we identified two cBS siblings presenting hypokalemia in a Chinese family due to novel compound heterozygous CLCNKB mutations (c.848_850delTCT/c.1755A>G). Compound heterozygosity was confirmed by amplifying and sequencing the patient's genomic DNA. The synonymous mutation c.1755A>G (Thr585Thr) was located at +2bp from the 5' splice donor site in exon 15, further transcript analysis demonstrated that this single nucleotide mutation causes exclusion of exon 15 in the cDNA from the proband and his mother. Furthermore, we investigated the expression and protein trafficking change of c.848_850delTCT (TCT) and exon 15 deletion（E15）mutation in vitro. The E15 mutation markedly decreased the expression of ClC-Kb and resulted in a low-molecular-weight band (~55kD) trapping in the endoplasmic reticulum, while the TCT mutant only decreased the total and plasma membrane ClC-Kb protein expression but did not affect the subcellular localization. Finally, we studied the physiological functions of mutations by using whole-cell patch clamp and found that E15 or TCT mutation decreased the current of ClC-Kb/barttin channel. These results suggested that the compound defective mutations of CLCNKB gene are the molecular mechanism of the two cBS siblings.

Chloride test - blood

Science.gov (United States)

Serum chloride test ... A greater-than-normal level of chloride is called hyperchloremia. It may be due to: Carbonic anhydrase inhibitors (used to treat glaucoma) Diarrhea Metabolic acidosis Respiratory alkalosis (compensated) Renal ...

Acid-base status determines the renal expression of Ca2+ and Mg2+ transport proteins.

NARCIS (Netherlands)

Nijenhuis, T.; Renkema, K.Y.; Hoenderop, J.G.J.; Bindels, R.J.M.

2006-01-01

Chronic metabolic acidosis results in renal Ca2+ and Mg2+ wasting, whereas chronic metabolic alkalosis is known to exert the reverse effects. It was hypothesized that these adaptations are mediated at least in part by the renal Ca2+ and Mg2+ transport proteins. The aim of this study, therefore, was

[A clinical and hereditary analysis of novel complex heterozygous KCNJ1 mutation in a Bartter syndrome type Ⅱ patient].

Science.gov (United States)

Li, X Y; Jiang, Y; Xu, L J; Duan, L; Peng, X Y; Chen, L M; Xia, W B; Xing, X P

2017-10-01

Bartter syndrome (BS) is a hereditary condition transmitted as an autosomal recessive (Bartter type 1 to 4) or dominant trait (Bartter type 5). The disease associates hypokalemic alkalosis with varying degrees of hypercalciuria. Here we presented a case (BS type Ⅱ) of a 17 years old female presented with polyhydramnios, polyuria, nephrocalcinosis and hypokalemia, which was alleviated after treatment with celecoxib and vitamin D(3). DNA sequencing identified compound heterozygous KCNJ 1 gene mutations, c. 931C >T (p.R311W) and c. 445-446insCCTGAACAC (p.V149Afs, 150X), with the latter a novel mutation. Her father and mother were heterozygous carriers of c. 931C >T (p.R311W) and c. 445-446insCCTGAACAC (p.V149Afs, 150X), respectively. In conclusion, this case of BS type Ⅱ is caused by a novel compound heterozygous KCNJ 1 mutation. Further studies are needed to verify the effect of celecoxib in BS patients.

Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay.

Science.gov (United States)

Banga, Amit; Khilnani, G C

2009-12-01

Posthypercapnic alkalosis (PHA) is frequently overlooked as a complication of mechanical ventilation in patients with exacerbation of chronic obstructive pulmonary disease (COPD). The current study was conducted to determine the incidence, risk factors for development and effect on outcome of PHA. Eighty-four patients (62 +/- 11 years, range 42-78 years, M:F 58: 26) with exacerbation of COPD with underlying chronic hypercapnic respiratory failure requiring mechanical ventilation were included in a retrospective fashion. PHA was defined as static or rising serum bicarbonate levels, 72 hours or more after return of PaCO2 to baseline, with concurrent pH > 7.44. Development of PHA was noted in 17 patients (20.2%). Corticosteroid use >or=10 days during the hospital stay was an independent risk factor for development of PHA (Adjusted OR, 95% CI: 9.4, 1.6-55.3; P = 0.013). Development of PHA was associated with an increased incidence of ventilator dependence (64.7% vs. 37.3%, OR, 95% CI: 3.1, 1.1-9.4, P = 0.04) and duration of ICU stay (14.7 +/- 6.7 vs. 9.5 +/- 5.9, P = 0.01) but no increase in hospital mortality (43.3% vs. 41.2%, P = NS). It is concluded that PHA is a common complication in patients with exacerbation of COPD requiring mechanical ventilation and is associated with increased incidence of ventilator dependence and ICU stay.

Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations

Science.gov (United States)

Al Shibli, Amar; Narchi, Hassib

2015-01-01

Bartter and Gitelman syndromes (BS and GS) are inherited disorders resulting in defects in renal tubular handling of sodium, potassium and chloride. Previously considered as genotypic and phenotypic heterogeneous diseases, recent evidence suggests that they constitute a spectrum of disease caused by different genetic mutations with the molecular defects of chloride reabsorption originating at different sites of the nephron in each condition. Although they share some characteristic metabolic abnormalities such as hypokalemia, metabolic alkalosis, hyperplasia of the juxtaglomerular apparatus with hyperreninemia, hyperaldosteronism, the clinical and laboratory manifestations may not always allow distinction between them. Diuretics tests, measuring the changes in urinary fractional excretion of chloride from baseline after administration of either hydrochlorothiazide or furosemide show very little change (< 2.3%) in the fractional excretion of chloride from baseline in GS when compared with BS, except when BS is associated with KCNJ1 mutations where a good response to both diuretics exists. The diuretic test is not recommended for infants or young children with suspected BS because of a higher risk of volume depletion in such children. Clinical symptoms and biochemical markers of GS and classic form of BS (type III) may overlap and thus genetic analysis may specify the real cause of symptoms. However, although genetic analysis is available, its use remains limited because of limited availability, large gene dimensions, lack of hot-spot mutations, heavy workup time and costs involved. Furthermore, considerable overlap exists between the different genotypes and phenotypes. Although BS and GS usually have distinct presentations and are associated with specific gene mutations, there remains considerable overlap between their phenotypes and genotypes. Thus, they are better described as a spectrum of clinical manifestations caused by different gene mutations. PMID:26140272

Prioritization of the Oral (Ingestive) Hazard of Industrial Chemicals

Science.gov (United States)

2011-10-28

or Respiration - respiratory obstruction VCVN1* "Vrednie chemichescie veshestva. Neorganicheskie soedinenia elementov I-IV groopp" (Hazardous...section Lungs, Thorax, or Respiration - respiratory depression Gastrointestinal - changes in structure or function of esophagus MJAUAJ Medical Journal...impaired Nutritional and Gross Metabolic - metabolic alkalosis JTCTDW Journal of Toxicology, Clinical Toxicology. 33 Sodium chloride #(T3) 7647-14-5 LD50

Respiratory alkalosis may impair the production of vitamin D and lead to significant morbidity, including the fibromyalgia syndrome.

Science.gov (United States)

Lewis, John M; Fontrier, Toinette H; Coley, J Lynn

2017-05-01

Hyperventilation caused by physical and/or psychological stress may lead to significant respiratory alkalosis and an elevated systemic pH. The alkalotic pH may in turn suppress the normal renal release of phosphate into the urine, thereby interrupting the endogenous production of 1,25-dihydroxyvitamin D (calcitriol). This could cause a shortfall in its normal production, leading to a variety of adverse consequences. It might partially explain the pathogenesis of acute mountain sickness, a treatable disease characterized by severe hyperventilation secondary to the hypoxia of high altitude exposure. Milder degrees of hyperventilation due to different forms of stress may produce other conditions which share characteristics with acute mountain sickness. One of these may be the fibromyalgia syndrome, a chronic painful disorder for which no satisfactory treatment exists. Should fibromyalgia and acute mountain sickness have a common etiology, may they also share a common form of treatment? Evidence is presented to support this hypothesis. Copyright © 2017 Elsevier Ltd. All rights reserved.

Newborn ventilatory response to maternal chronic hypercapnia.

Science.gov (United States)

DeLuca, L; Holzman, I; Gibbs, K

2012-10-01

This is a case of a neonate born with a respiratory acidosis with a compensatory metabolic alkalosis. This case demonstrates placental physiology of gas exchange as well as the blunted ventilatory response in the neonate from chronic hypercapnia.

Generaliserede kramper som debutsymptom ved Gitelmans syndrom

DEFF Research Database (Denmark)

Hvelplund, Carolina; Jeppesen, Eva Mosfeldt; Mortensen, Henrik B

2009-01-01

Gitelman's syndrome is a rare autosomal recessive syndrome presenting with hypocalciuria, hypomagnesiemia and hypokalemic metabolic alkalosis. This case reports a patient admitted with generalized seizures with the above-mentioned biochemical abnormalities, thus representing a rare onset of Gitel...

The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron.

Science.gov (United States)

Hennings, J Christopher; Andrini, Olga; Picard, Nicolas; Paulais, Marc; Huebner, Antje K; Cayuqueo, Irma Karen Lopez; Bignon, Yohan; Keck, Mathilde; Cornière, Nicolas; Böhm, David; Jentsch, Thomas J; Chambrey, Régine; Teulon, Jacques; Hübner, Christian A; Eladari, Dominique

2017-01-01

Chloride transport by the renal tubule is critical for blood pressure (BP), acid-base, and potassium homeostasis. Chloride uptake from the urinary fluid is mediated by various apical transporters, whereas basolateral chloride exit is thought to be mediated by ClC-Ka/K1 and ClC-Kb/K2, two chloride channels from the ClC family, or by KCl cotransporters from the SLC12 gene family. Nevertheless, the localization and role of ClC-K channels is not fully resolved. Because inactivating mutations in ClC-Kb/K2 cause Bartter syndrome, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a critical role in salt handling by the thick ascending limb. To dissect the role of this channel in detail, we generated a mouse model with a targeted disruption of the murine ortholog ClC-K2. Mutant mice developed a Bartter syndrome phenotype, characterized by renal salt loss, marked hypokalemia, and metabolic alkalosis. Patch-clamp analysis of tubules isolated from knockout (KO) mice suggested that ClC-K2 is the main basolateral chloride channel in the thick ascending limb and in the aldosterone-sensitive distal nephron. Accordingly, ClC-K2 KO mice did not exhibit the natriuretic response to furosemide and exhibited a severely blunted response to thiazide. We conclude that ClC-Kb/K2 is critical for salt absorption not only by the thick ascending limb, but also by the distal convoluted tubule. Copyright © 2016 by the American Society of Nephrology.

JPRS Report, Science & Technology, USSR: Space Biology & Aerospace Medicine, Vol. 21, No. 6, November-December 1987.

Science.gov (United States)

1988-03-11

that regulation of blood clotting under hypoxic conditions is consistent with tissular metabolism. Thus, tissue hypoxia and respiratory alkalosis ...79 Effect of Oxygen Inhalation on Respiratory Function During Exercise and Exposure to Added Resistance to Respiration 86 Polar Work Adaptability...cardiovascular, respiratory , digestive, ner- vous and endocrine systems, system of immune defense and metabolic processes. The first phase of the

Gitelman syndrome : consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

NARCIS (Netherlands)

Blanchard, Anne; Bockenhauer, Detlef; Bolignano, Davide; Calò, Lorenzo A; Cosyns, Etienne; Devuyst, Olivier; Ellison, David H; Karet Frankl, Fiona E; Knoers, Nine V A M; Konrad, Martin; Lin, Shih-Hua; Vargas-Poussou, Rosa

Gitelman syndrome (GS) is a rare, salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. The disease is recessively inherited, caused by inactivating mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium-chloride

Influence of bicarbonate on ventilatory drive in healthy subjects

NARCIS (Netherlands)

Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Peter; Heunks, Leo M.A.

2016-01-01

Background Acute hypoventilation results in CO2 retention and respiratory acidosis. Bicarbonate retention aims to restore pH level. However, after institution of mechanical ventilation metabolic alkalosis may develop, which could impair respiratory drive. Aim To investigate whether increased plasma

Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD.

NARCIS (Netherlands)

Ven, M.J.T. van de; Colier, W.N.J.M.; Sluijs, M.C. van der; Oeseburg, B.; Vis, P.; Folgering, H.T.M.

2002-01-01

STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and

Refeeding syndrome: clinical and nutritional relevance.

Science.gov (United States)

Viana, Larissa de Andrade; Burgos, Maria Goretti Pessoa de Araújo; Silva, Rafaella de Andrade

2012-01-01

Feedback syndrome is characterized clinically by neurological alterations, respiratory symptoms, arrhythmias and heart failure few days after refeeding. It happens due to severe electrolyte changes, such as hypophosphatemia, hypomagnesemia and hypokalemia associated with metabolic abnormalities that may occur as a result of nutritional support (oral, enteral or parenteral) in severely malnourished patients. To evaluate its causes and the preventive dietary measures aiming to reduce the morbimortality. Was conducted literature review in SciELO, LILACS, Medline / PUBMED, Cochrane Library and government websites in Portuguese, English and Spanish. The survey was about the last 15 years, selecting the headings: refeeding syndrome, malnutrition, hypophosphatemia, hypokalemia, hypomagnesemia. The monitoring of metabolic parameters and electrolyte levels before starting nutritional support and periodically during feeding should be based on protocols and the duration of therapy. Patients at high risk and other metabolic complications should be followed closely, and depletion of minerals and electrolytes should be replaced before starting the diet. A multidisciplinary team of nutrition therapy can guide and educate other health professionals in prevention, diagnosis and treatment of the syndrome.

[Acid-base equilibrium and the brain].

Science.gov (United States)

Rabary, O; Boussofara, M; Grimaud, D

1994-01-01

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation.

Science.gov (United States)

Leithäuser, Renate M; Böning, Dieter; Hütler, Matthias; Beneke, Ralph

2016-07-01

Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. Compared with the control condition, hyperventilation reduced (all P respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Antenatal Bartter's syndrome with sensorineural deafness

OpenAIRE

Bhamkar, R. P.; Gajendragadkar, A.

2009-01-01

Bartter's syndrome is a group of inherited, salt-losing tubulopathies presenting as metabolic alkalosis with normotensive hyperreninemia and hyperaldosteronism. We report here the first case of a neonate with bilateral, sensorineural deafness, a variant of antenatal Bartter's syndrome from an Indian community.

Classic Bartter syndrome: a rare cause of failure to thrive in a child.

Science.gov (United States)

Vieira, Helena; Mendes, Leonor; Mendes, Patricia; da Silva, José Esteves

2012-06-28

Bartter syndrome is a group of rare autosomal-recessive disorders caused by a defect in distal tubule transport of sodium and chloride. Blood gases and plasma electrolytes raise suspicion of this diagnosis and the definitive diagnosis is made by genetic study. Early treatment improves prognosis. The authors present the case of an 11-month-old child with early failure to thrive and severe regurgitation. Blood gases revealed hypochloraemic metabolic alkalosis, hyponatraemia and hypokalaemia. Blood pressure was normal and polyuria was documented. She began therapy with potassium chloride supplementation and indomethacin. There was clinical improvement and plasma potassium and bicarbonate normalised. The molecular study confirmed it was the classic form of Bartter syndrome. Despite being rare in clinical practice, which may lead to unnecessary medical investigation and diagnosis delay, in a child with failure to thrive, hypochloraemic metabolic alkalosis and hypokalaemia, this diagnosis must be considered.

A Clinical Approach to the Diagnosis of Acid-Base Disorders

OpenAIRE

Bear, Robert A.

1986-01-01

The ability to diagnose and manage acid-base disorders rapidly and effectively is essential to the care of critically ill patients. This article presents an approach to the diagnosis of pure and mixed acid-base disorders, metabolic or respiratory. The approach taken is based on using the law of mass-action equation as it applies to the bicarbonate buffer system (Henderson equation), using sub-classifications for diagnostic purposes of causes of metabolic acidosis and metabolic alkalosis, and ...

Point-of-care testing on admission to the intensive care unit: lactate and glucose independently predict mortality.

Science.gov (United States)

Martin, Jan; Blobner, Manfred; Busch, Raymonde; Moser, Norman; Kochs, Eberhard; Luppa, Peter B

2013-02-01

The aim of the study was to retrospectively investigate whether parameters of routine point-of-care testing (POCT) predict hospital mortality in critically ill surgical patients on admission to the intensive care unit (ICU). Arterial blood analyses of 1551 patients on admission to the adult surgical ICU of the Technical University Munich were reviewed. POCT was performed on a blood gas analyser. The association between acid-base status and mortality was evaluated. Metabolic acidosis was defined by base excess (BE) lactate >50% of BE, anion gap (AG)-acidosis by AG >16 mmol/L, hyperchloraemic acidosis by chloride >115 mmol/L. Metabolic alkalosis was defined by BE ≥3 mmol/L. Logistic regression analysis identified variables independently associated with mortality. Overall mortality was 8.8%. Mortality was greater in male patients (p=0.012). Mean age was greater in non-survivors (p55 mm Hg (mortality 23.1%). Three hundred and seventy-seven patients presented with acidosis (mortality 11.4%), thereof 163 patients with lactic acidosis (mortality 19%). Mortality for alkalosis (174 patients) was 12.1%. Mean blood glucose level for non-survivors was higher compared to survivors (plactate, glucose, age, male gender as independent predictors of mortality. Lactate and glucose on ICU admission independently predict mortality. BE and AG failed as prognostic markers. Lactic acidosis showed a high mortality rate implying that lactate levels should be obtained on ICU admission. Prevalence of hyperchloraemic acidosis was low. Metabolic alkalosis was associated with an increased mortality. Further studies on this disturbance and its attendant high mortality are warranted.

The effect of glutamine administration on urinary ammonium excretion in normal subjects and patients with renal disease.

Science.gov (United States)

Welbourne, T; Weber, M; Bank, N

1972-07-01

The effect of acute changes in the delivery rate of glutamine to the kidney on urinary ammonium excretion was studied in man. Healthy subjects and patients with intrinsic renal disease were studied under three different acid-base conditions: unaltered acid-base balance; NH(4)Cl-induced acidosis; and NaHCO(3)-induced alkalosis. Anhydrous L-glutamine was administered orally in a single dose of 260 mmoles during each of these three acid-base states. We found that endogenous venous plasma glutamine concentration fell during acidosis and rose during alkalosis in both healthy subjects and patients with renal disease. In healthy subjects, orally administered glutamine raised plasma glutamine concentration markedly over a 2-3 hr period. This was accompanied by an increase in urinary ammonium excretion and a rise in urine pH under normal acid-base conditions and during metabolic acidosis. No increase in ammonium excretion occurred when glutamine was administered during metabolic alkalosis in spite of an equivalent rise in plasma glutamine concentration. In patients with renal disease, endogenous venous plasma glutamine concentration was lower than in healthy subjects, perhaps as a result of mild metabolic acidosis. Acute oral glutamine loading failed to increase urinary ammonium excretion significantly during either unaltered acid-base conditions or after NH(4)Cl-induced acidosis, even though plasma glutamine rose as high as in healthy subjects. We conclude from these observations that glutamine delivery to the kidney is a rate-limiting factor for ammonium excretion in healthy subjects, both before and after cellular enzyme adaptation induced by metabolic acidosis. In contrast, in patients with renal disease, glutamine delivery is not rate-limiting for ammonium excretion. Presumably other factors, such as surviving renal mass and the activity of intracellular enzymes necessary for ammonia synthesis limit ammonium excretion in these patients.

Diffuse Lymphomatous Infiltration of Kidney Presenting as Renal Tubular Acidosis and Hypokalemic Paralysis: Case Report

Science.gov (United States)

Jhamb, Rajat; Gupta, Naresh; Garg, Sandeep; Kumar, Sachin; Gulati, Sameer; Mishra, Deepak; Beniwal, Pankaj

2007-01-01

We report the case of a 22-year-old woman who presented with acute onset flaccid quadriparesis. Physical examination showed mild pallor with cervical and axillary lymphadenopathy, hepatomegaly, and bilateral smooth enlarged kidneys. Neurological examination revealed lower motor neuron muscle weakness in all the four limbs with hyporeflexia and normal sensory examination. Laboratory investigations showed anemia, severe hypokalemia, and metabolic acidosis. Urinalysis showed a specific gravity of 1.010, pH of 7.0, with a positive urine anion gap. Ultrasound revealed hepatosplenomegaly with bilateral enlarged smooth kidneys. Renal biopsy was consistent with the diagnosis of non-Hodgkin lymphoma (B cell type). Metabolic acidosis, alkaline urine, and severe hypokalemia due to excessive urinary loss in our patient were suggestive of distal renal tubular acidosis. Renal involvement in lymphoma is usually subclinical and clinically overt renal disease is rare. Diffuse lymphomatous infiltration of the kidneys may cause tubular dysfunction and present with hypokalemic paralysis. PMID:18074421

[Development and basics of metabolic monitoring in dairy cows. Focus on research in Eastern Germany and at the University of Leipzig, Germany].

Science.gov (United States)

Fürll, M

2016-01-01

Systematic metabolic monitoring began in German-speaking countries in the late 1960s, early 1970s, due to an increase in metabolic disorders as a cause of infertility and mastitis and aimed at their prevention through early diagnosis. Development of a unified monitoring standard: Initiated by Rossow, Gürtler, Ehrentraut, Seidel and Furcht a standard "metabolic monitoring in cattle production" was developed in the 1970s. It included farm analysis, clinical and biochemical controls, prophylaxis and follow-up controls. Key points were: periodic screenings of heavily loaded, healthy indicator animals 2-4 days post partum (p.  p.), 2-8 weeks p.  p. and 1-2 weeks ante partum, maximal 10 animals/group, pooled samples are useful, optimal are individual samples, use of informative sample substrate and parameters, precise handling of specimens, expert assessment and follow-up. Metabolic controls during 1982-1989 in approximately 242  000 cows revealed means of 32.9% ketoses, 20.0% metabolic acidosis, 21.9% metabolic alkalosis, 34.2% nitrogen-metabolism disorders, 17.3% sodium deficiency and 23.7% liver disorders. Development of a metabolic profile after 1989: Reference values at higher milk yield, early diagnosis of diseases of the fat mobilization syndrome and improved early diagnosis by new indicators, including creatine kinase (CK), alkaline phosphatase (AP) with isoenzymes, acute phase proteins, cytokines, antioxidants, carnitine and lipoprotein fractions, were established. Optimized blood and urine screenings have important advantages over milk analysis. They are an important method of health and performance stabilization by exact analysis of causes and derived prevention. The fertility related parameters free fatty acids, β-hydroxybutyrate, urea, inorganic phosphate, CK, AP, sodium, potassium, selenium, copper, β-carotene and net acid-base excretion proved to be a standard spectrum for screenings. These should be tested once a year/herd, if necessary as

Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis

OpenAIRE

Mata-Gómez, Javier; Guerrero-Domínguez, Rosana; García-Santigosa, Marta; Ontanilla, Antonio

2015-01-01

BACKGROUND AND OBJECTIVES: Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH ...

Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit – the role of renal replacement therapy

OpenAIRE

Naka, Toshio; Bellomo, Rinaldo

2004-01-01

Acid–base disorders are common in critically ill patients. Metabolic acid–base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base status using the Stewart–Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accu...

[What you should know of the arterial blood gases during the watch].

Science.gov (United States)

Márquez-González, Horacio; Pámanes-González, Jesús; Márquez-Flores, Horacio; Gómez-Negrete, Alonso; Muñoz-Ramírez, Mireya C; Villa-Romero, Antonio Rafael

2012-01-01

Gasometry is the measurement of dissolved gases in the blood, by measuring pH, carbon dioxide pressure (pCO(2)), serum bicarbonate (HCO(3-)), and lactate and serum electrolytes: sodium, potassium and chlorine you can make a diagnosis, etiology and treatment in the critically ill patient. The aim is to provide five steps for the interpretation of blood gases by: 1. The definition of acidemia or acidosis, or alkalemia or alkalosis. 2. Defining the metabolic component or respiratory. 3. To determine the anion gap; levels above 15 ± 2 determine other likely causes of excess anions (methanol, uremia, diabetic ketoacidosis, paraldehyde, ionized, lactic acidosis, ethylene glycol and salicylates. 4. Compensation, using the Winter formula. 5. The delta gap, with the formula for determining intrinsic and metabolic alkalosis. When anion gap is normal, is calculated urinary anion gap; the value is negative if the loss is extrarenal, contrary to the positive result is renal etiology.

Neonatal Bartter Syndrome in association with congenital adrenal hyperplasia in a neonate - a rare combination.

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Hussain, Shabbir

2016-05-01

Neonatal Bartter syndrome (NBS) is an autosomal recessive renal tubulopathy characterized by hypokalaemic, hypochloraemic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. There is hyperreninaemia and hyperaldosteronaemia but normotension. Congenital adrenal hyperplasia (CAH), another autosomal recessive condition, may present in the neonatal period with vomiting, hypovolaemia, failure to gain weight or ambiguous genitalia. We report a case of NBS and CAH combination in a neonate. A male neonate born at term was admitted with history of recurrent vomiting and dehydration episodes. Investigations revealed electrolytes imbalance, metabolic alkalosis, raised aldosterone and renin levels suggestive of NBS. He was treated successfully and discharged. He was re-admitted with the same symptoms. Further evaluation confirmed the presence of CAH as well. We report this case because of the rarity of this combination (NBS plus CAH) and to the best of our knowledge this is the first such case report from Pakistan.

A Rare Disorder with Common Clinical Presentation: Neonatal Bartter Syndrome.

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Hussain, Shabbir; Tarar, Saba Haider; Al-Muhaizae, Muhammad

2015-04-01

Bartter syndrome is an autosomal recessive renal tubulopathy that presents with hypokalemic, hypochloremic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. There is hyperreninemia and hyperaldosteronemia but normotension. A full term male neonate was referred at 20-day of age with features of sepsis and respiratory distress. He was evaluated and managed as case of septicemia with all supportive paraphernalia including mechanical ventilation. Investigations revealed electrolytes imbalance and metabolic alkalosis suggestive of Neonatal Bartter Syndrome (NBS). Raised aldosterone and renin levels confirmed the diagnosis. Electrolyte imbalance was corrected with fluids and indomethacin, treated successfully, discharged and parents counseled. He was thriving well at 9 months of age. Another 2 months old male baby presented with recurrent episodes of lethargy with dehydration and failure to gain weight. Investigations confirmed the diagnosis of NBS. He was also successfully treated with same medication. We report these 2 cases because of the rarity of NBS, presentation of which may mimic common illnesses like sepsis and gastroenteritis.

Respiratory alkalosis and associated electrolytes in long-term ventilator dependent persons with tetraplegia.

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Watt, J W; Silva, P

2001-11-01

A pilot case control study of the acid-base and electrolyte status in 30 long-term ventilator-dependent (LTVD) and 30 self ventilating persons with tetraplegia. To assess the extent of respiratory alkalosis and screen for associated hypokalaemia, hypomagnesaemia and/or hypophosphataemia. Medically stable persons with tetraplegia under the long-term care of the Southport Spinal Injuries Centre, England. Blood gases and electrolytes were sampled from 30 control patients with tetraplegia and from 30 patients having been LTVD for more than 12 months. All the blood gas measurements in the LTVD group lay outside both the reference range and the 95% confidence intervals (CI) of the control group: pH 7.46 (0.06); PCO(2) 3.46 (1.1) kPa; bicarbonate 18.3 (3.8) and base excess -3.2 (2.8) mmol/l; PO(2) 13.8 (2.8) kPa (means and standard deviations). The serum potassium, magnesium, phosphate, and sodium means lay within the reference ranges but the potassium, phosphate and calcium were at or below the 95% CI of the control values. One patient on part-time ventilatory support having less bicarbonate compensation had low serum electrolytes during ventilation. There was no evidence of biochemical jeopardy from long-term mechanical hyperventilation although acutely administered hyperventilation has the potential to cause falls in serum potassium, magnesium and phosphate and so caution should be exercised in part-time ventilated persons. The full range of electrolytes should be assayed during stabilisation in LTVD and periodically thereafter. Hyperventilation helps to maintain good oxygenation in LTVD persons with paralysis and normal lungs. None.

[Disorders of the acid-base balance and the anion gap].

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Kimmel, Martin; Alscher, Mark Dominik

2016-10-01

The regulation of the acid-base balance and pH is critical for the organism. The most important buffer system is CO 2 / HCO 3 - . The kidney controls systemic bicarbonate and therefore the metabolic regulation and the lung is relevant for respiratory regulation by an effective CO 2 elimination. There are four acid-base disorders with two metabolic and two respiratory disorders (acidosis and alkalosis). The anion gap enables a further workup of metabolic acidosis. © Georg Thieme Verlag KG Stuttgart · New York.

A New Therapeutic Strategy for Autosomal Dominant Polycystic Kidney Disease: Activation of AMP Kinase by Metformin

Science.gov (United States)

2012-07-01

role for CHOP during inhibition of the mitochondrial respiratory chain. J. Biochem. 146, 123–132. Joly, D., Ishibe, S., Nickel, C., Yu, Z., Somlo, S...urinary HCO3 excretion in response to an initial alkali load, resulting in compensated metabolic alkalosis . Therefore, it appears that the IRR may play a

[Dynamics of bioelectric activity of the brain and erythrocyte ultrastructure after intravenous infusion of sodium bicarbonate to oncologic patients].

Science.gov (United States)

Davydova, I G; Kassil', V L; Raĭkhlin, N T; Filippova, N A

1992-04-01

23 patients with malignant tumors of different location and histogenesis were investigated. There were no metastases in 9 cases. 10 patients had metastases in regional areas and 4--distant. The results were compared with those obtained in 4 patients with nonmalignant diseases. EEG, blood gases, plasma acid--base balance and ultrastructure of erythrocytes were explored before and after intravenous infusion of 4.2% sodium bicarbonate solution. The metabolic alkalosis induced amelioration of EEG, which was changed basically, the condense of pre-membrane layer disappeared or decreased in erythrocytes, and disaggregation of erythrocytes took place in cancer patients vs those with nonmalignant tumors. The results confirm the suggestion of generalized intracellular acidosis in malignant tumor patients. This acidosis can be temporarily avoided or diminished artificially by blood alkalosis.

Association of Smoking, Sleep Apnea, and Plasma Alkalosis With Nocturnal Ventricular Arrhythmias in Men With Systolic Heart Failure

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Shukla, Rakesh; Wexler, Laura

2012-01-01

Background: Excess sudden death due to ventricular tachyarrhythmias remains a major mode of mortality in patients with systolic heart failure. The aim of this study was to determine the association of nocturnal ventricular arrhythmias in patients with low ejection fraction heart failure. We incorporated a large number of known pathophysiologic triggers to identify potential targets for therapy to reduce the persistently high incidence of sudden death in this population despite contemporary treatment. Methods: Eighty-six ambulatory male patients with stable low (≤ 45%) ejection fraction heart failure underwent full-night attendant polysomnography and simultaneous Holter recordings. Patients were divided into groups according to the presence or absence of couplets (paired premature ventricular excitations) and ventricular tachycardia (VT) (at least three consecutive premature ventricular excitations) during sleep. Results: In multiple regression analysis, four variables (current smoking status, increased number of arousals, plasma alkalinity, and old age) were associated with VT and two variables (apnea-hypopnea index and low right ventricular ejection fraction) were associated with couplets during sleep. Conclusions: We speculate that cessation of smoking, effective treatment of sleep apnea, and plasma alkalosis could collectively decrease the incidence of nocturnal ventricular tachyarrhythmias and the consequent risk of sudden death, which remains high despite the use of β blockades. PMID:22172636

Gastro-oesophageal reflux: An overview of the cost-effectiveness of ...

African Journals Online (AJOL)

with normal acid-base balance and cause metabolic alkalosis, or ... be dependent on the diagnosis, side-effects and cost-effectiveness of the .... care, e.g. time lost from work due to illness.5 When different ... negative impact on a patient's psychological well-being, than ... as well as the effects on the patient's quality of life.

Fires. A Joint Publication for U.S. Artillery Professionals. November - December 2009

Science.gov (United States)

2009-11-01

called respiratory alkalosis . If the pH is low, the blood is more acidic. Respiratory alkalosis . Respiratory alkalosis helps offset hypo- baric... Respiratory alkalosis allows more oxygen to be carried to working tissue such as muscle to fuel work. However, respiratory alkalosis also makes unload...ing oxygen to working muscle more difficult. Eventually, the hypoxic drive (the need for oxygen) overrides respiratory alkalosis due to the

Expanding the spectrum of genetic mutations in antenatal Bartter syndrome type II.

Science.gov (United States)

Fretzayas, Andreas; Gole, Evangelia; Attilakos, Achilleas; Daskalaki, Anna; Nicolaidou, Polyxeni; Papadopoulou, Anna

2013-06-01

Bartter syndrome (BS) is a group of genetic disorders characterized by hypokalemic metabolic alkalosis, hyponatremia and elevated renin and aldosterone plasma concentrations. BS type II is caused by mutations in the KCNJ1 gene and usually presents with transient hyperkalemia. We report here a novel KCNJ1 mutation in a male neonate, prematurely born after a pregnancy complicated by polyhydramnios. The infant presented with typical clinical and laboratory findings of BS type II, such as hyponatremia, hypochloremic metabolic alkalosis, severe weight loss, elevated renin and aldosterone levels and transient hyperkalemia in the early postnatal period, which were later normalized. Molecular analysis revealed a compound heterozygous mutation in the KCNJ1 gene, consisting of a novel K76E and an already described V315G mutation, both affecting functional domains of the channel protein. Typical manifestations of antenatal BS in combination with hyperkalemia should prompt the clinician to search for mutations in the KCNJ1 gene first. © 2013 The Authors. Pediatrics International © 2013 Japan Pediatric Society.

Gitelman syndrome combined with complete growth hormone deficiency

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Se Ra Min

2013-03-01

Full Text Available Gitelman syndrome is a rare autosomal recessive hereditary salt-losing tubulopathy, that manifests as hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutations in the solute carrier family 12(sodium/chloride transporters, member 3 (SLC12A3 gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT in the distal convoluted tubule of the kidney. It is associated with muscle weakness, cramps, tetany, vomiting, diarrhea, abdominal pain, and growth retardation. The incidence of growth retardation, the exact cause of which is unknown, is lower than that of Bartter syndrome. Herein, we discuss the case of an overweight 12.9-year-old girl of short stature presenting with hypokalemic metabolic alkalosis. The patient, on the basis of detection of a heterozygous mutation in the SLC12A3 gene and poor growth hormone (GH responses in two provocative tests, was diagnosed with Gitelman syndrome combined with complete GH deficiency. GH treatment accompanied by magnesium oxide and potassium replacement was associated with a good clinical response.

Reverse ventilation--perfusion mismatch

International Nuclear Information System (INIS)

Palmaz, J.C.; Barnett, C.A.; Reich, S.B.; Krumpe, P.E.; Farrer, P.A.

1984-01-01

Patients having lobar airway obstruction or consolidation usually have decreases of both ventilation and perfusion on lung scans. We report three patients in whom hypoxic vasoconstriction was apparently incomplete, resulting in a ''reversed'' ventilation-perfusion mismatch. Perfusion of the hypoxic lobe on the radionuclide scan was associated with metabolic alkalosis, pulmonary venous and pulmonary arterial hypertension in these patients

Chronic mesenteric volvulus in a dog

Science.gov (United States)

Spevakow, Andrea B.; Nibblett, Belle Marie D.; Carr, Anthony P.; Linn, Kathleen A.

2010-01-01

A chronic, partial mesenteric volvulus was found on laparotomy of an adult Bernese mountain dog with a 4-month history of intermittent vomiting, diarrhea, and weight loss. The dog had elevated cholestatic and hepatocellular leakage enzymes, increased bile acids, azotemia, isosthenuria, and a hypokalemic, hypochloremic, metabolic alkalosis. The dog recovered fully following reduction of the volvulus. PMID:20357947

The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions

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Aibek E. Mirrakhimov

2017-01-01

Full Text Available Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions.

Science.gov (United States)

Mirrakhimov, Aibek E; Ayach, Taha; Barbaryan, Aram; Talari, Goutham; Chadha, Romil; Gray, Adam

2017-01-01

Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

Suicide by Fire Extinguisher Powder Ingestion: A Case Report

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Hamid Mohammadi Kojidi

2017-07-01

Full Text Available A 51-year-old man committed suicide by swallowing the contents of a fire extinguisher. A few hours after his suicide attempt, he was referred to the medical center for poisoning. At the time of admission, the patient was conscious with stable vital signs. The patient complained of burning lips and mouth, mentioning diarrhea. Initial treatments included gastric lavage with activated charcoal, while paraclinical measures were requested. The patient had undergone hypernatremia (Na: 152 mEq/l and metabolic alkalosis. Treatment focused on the adjustment of sodium level and alkalosis. On the first day of hospitalization, the patient experienced recurrent episodes of tonic-clonic seizure along with the loss of consciousness. On the third day of hospitalization, the patient developed respiratory arrest followed by cardiac arrest and death.

Cerebral circulation, metabolism, and blood-brain barrier of rats in hypocapnic hypoxia

International Nuclear Information System (INIS)

Beck, T.; Krieglstein, J.

1987-01-01

The effects of hypoxic hypoxia on physiological variables, cerebral circulation, cerebral metabolism, and blood-brain barrier were investigated in conscious, spontaneously breathing rats by exposing them to an atmosphere containing 7% O 2 . Hypoxia affected a marked hypotension, hypocapnia and alkalosis. Cortical tissue high-energy phosphates and glucose content were not affected by hypoxia, glucose 6-phosphate lactate, and pyruvate levels were significantly increased. Blood-brain barrier permeability, regional brain glucose content and lumped constant were not changed by hypoxia. Local cerebral glucose utilization (LCGU) rose by 40-70% of control values in gray matter and by 80-90% in white matter. Under hypoxia, columns of increased and decreased LCGU and were detectable in cortical gray matter. Color-coded [ 14 C]2-deoxy-D-glucose autoradiograms of rat brain are shown. Local cerebral blood flow (LCBF) increased by 50-90% in gray matter and by up to 180% in white matter. Coupling between LCGU and LCBF in hypoxia remained unchanged. The data suggests a stimulation of glycolysis, increased glucose transport into the cell, and increased hexokinase activity. The physiological response of gray and white matter to hypoxia obviously differs. Uncoupling of the relation between LCGU and LCBF does not occur

Laxative-induced rhabdomyolysis

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Alfonso Merante

2010-03-01

Full Text Available Alfonso Merante1, Pietro Gareri2,3, Norma Maria Marigliano2, Salvatore De Fazio2, Elvira Bonacci1, Carlo Torchia1, Gaetano Russo1, Pasquale Lacroce1, Roberto Lacava3, Alberto Castagna3, Giovambattista De Sarro2, Giovanni Ruotolo11Geriatrist, Geriatric Unit “Pugliese-Ciaccio” Hospital, Catanzaro, Italy; 2Department of Experimental and Clinical Medicine, Faculty of Medicine and Surgery, University Magna Graecia of Catanzaro, Clinical Pharmacology and Pharmacovigilance Unit, Mater Domini University Hospital, Catanzaro, Italy; 3Geriatrist, Operative Unit Elderly Health Care, Catanzaro, ItalyAbstract: The present study describes a case of laxative-induced rhabdomyolysis in an elderly patient. An 87-year-old woman was hospitalized for the onset of confusion, tremors, an inability to walk, and a fever that she had been experiencing for 36 hours. She often took high dosages of lactulose and sorbitol syrup as a laxative (about 70 g/day. During her physical examination, the patient was confused, drowsy, and she presented hyposthenia in her upper and lower limbs, symmetric and diffuse moderate hyporeflexia, and her temperature was 37.8°C. Laboratory tests revealed severe hyponatremia with hypokalemia, hypocalcemia, hypochloremia, and metabolic alkalosis. Moreover, rhabdomyolysis markers were found. The correction of hydroelectrolytic imbalances with saline, potassium and sodium chlorure, calcium gluconate was the first treatment. During her hospitalization the patient presented acute delirium, treated with haloperidol and prometazine chloridrate intramuscularly. She was discharged 12 days later, after resolution of symptoms, and normalized laboratory tests. Over-the-counter drugs such as laxatives are usually not considered dangerous; on the other hand, they may cause serum electrolytic imbalance and rhabdomyolysis. A careful monitoring of all the drugs taken by the elderly is one of the most important duties of a physician since drug interactions and

Poor phenotype-genotype association in a large series of patients with Type III Bartter syndrome.

Science.gov (United States)

García Castaño, Alejandro; Pérez de Nanclares, Gustavo; Madariaga, Leire; Aguirre, Mireia; Madrid, Álvaro; Chocrón, Sara; Nadal, Inmaculada; Navarro, Mercedes; Lucas, Elena; Fijo, Julia; Espino, Mar; Espitaletta, Zilac; García Nieto, Víctor; Barajas de Frutos, David; Loza, Reyner; Pintos, Guillem; Castaño, Luis; Ariceta, Gema

2017-01-01

Type III Bartter syndrome (BS) is an autosomal recessive renal tubule disorder caused by loss-of-function mutations in the CLCNKB gene, which encodes the chloride channel protein ClC-Kb. In this study, we carried out a complete clinical and genetic characterization in a cohort of 30 patients, one of the largest series described. By comparing with other published populations, and considering that 80% of our patients presented the p.Ala204Thr Spanish founder mutation presumably associated with a common phenotype, we aimed to test the hypothesis that allelic differences could explain the wide phenotypic variability observed in patients with type III BS. Clinical data were retrieved from the referral centers. The exon regions and flanking intronic sequences of the CLCNKB gene were screened for mutations by polymerase chain reaction (PCR) followed by direct Sanger sequencing. Presence of gross deletions or duplications in the region was checked for by MLPA and QMPSF analyses. Polyuria, polydipsia and dehydration were the main common symptoms. Metabolic alkalosis and hypokalemia of renal origin were detected in all patients at diagnosis. Calciuria levels were variable: hypercalciuria was detected in 31% of patients, while 23% had hypocalciuria. Nephrocalcinosis was diagnosed in 20% of the cohort. Two novel CLCNKB mutations were identified: a small homozygous deletion (c.753delG) in one patient and a small deletion (c.1026delC) in another. The latter was present in compound heterozygosis with the already previously described p.Glu442Gly mutation. No phenotypic association was obtained regarding the genotype. A poor correlation was found between a specific type of mutation in the CLCNKB gene and type III BS phenotype. Importantly, two CLCNKB mutations not previously described were found in our cohort.

Poor phenotype-genotype association in a large series of patients with Type III Bartter syndrome.

Directory of Open Access Journals (Sweden)

Alejandro García Castaño

Full Text Available Type III Bartter syndrome (BS is an autosomal recessive renal tubule disorder caused by loss-of-function mutations in the CLCNKB gene, which encodes the chloride channel protein ClC-Kb. In this study, we carried out a complete clinical and genetic characterization in a cohort of 30 patients, one of the largest series described. By comparing with other published populations, and considering that 80% of our patients presented the p.Ala204Thr Spanish founder mutation presumably associated with a common phenotype, we aimed to test the hypothesis that allelic differences could explain the wide phenotypic variability observed in patients with type III BS.Clinical data were retrieved from the referral centers. The exon regions and flanking intronic sequences of the CLCNKB gene were screened for mutations by polymerase chain reaction (PCR followed by direct Sanger sequencing. Presence of gross deletions or duplications in the region was checked for by MLPA and QMPSF analyses.Polyuria, polydipsia and dehydration were the main common symptoms. Metabolic alkalosis and hypokalemia of renal origin were detected in all patients at diagnosis. Calciuria levels were variable: hypercalciuria was detected in 31% of patients, while 23% had hypocalciuria. Nephrocalcinosis was diagnosed in 20% of the cohort. Two novel CLCNKB mutations were identified: a small homozygous deletion (c.753delG in one patient and a small deletion (c.1026delC in another. The latter was present in compound heterozygosis with the already previously described p.Glu442Gly mutation. No phenotypic association was obtained regarding the genotype.A poor correlation was found between a specific type of mutation in the CLCNKB gene and type III BS phenotype. Importantly, two CLCNKB mutations not previously described were found in our cohort.

Mixed acid-base disorder secondary to topiramate use in traumatic brain injury

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S Golla

2016-01-01

Full Text Available We report a case of a man with traumatic brain injury. He was started on to prophylactic topiramate which led to a mixed acid-base disorder. He had severe metabolic acidosis secondary to renal tubular acidification defect and respiratory alkalosis secondary to hyperventilation. Withdrawal of the offending drug led to the prompt resolution of the acid-base disturbance.

Multiple Electrolyte and Metabolic Emergencies in a Single Patient

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Caprice Cadacio

2017-01-01

Full Text Available While some electrolyte disturbances are immediately life-threatening and must be emergently treated, others may be delayed without immediate adverse consequences. We discuss a patient with alcoholism and diabetes mellitus type 2 who presented with volume depletion and multiple life-threatening electrolyte and metabolic derangements including severe hyponatremia (serum sodium concentration [SNa] 107 mEq/L, hypophosphatemia (“undetectable,” <1.0 mg/dL, and hypokalemia (2.2 mEq/L, moderate diabetic ketoacidosis ([DKA], pH 7.21, serum anion gap [SAG] 37 and hypocalcemia (ionized calcium 4.0 mg/dL, mild hypomagnesemia (1.6 mg/dL, and electrocardiogram with prolonged QTc. Following two liters of normal saline and associated increase in SNa by 4 mEq/L and serum osmolality by 2.4 mosm/Kg, renal service was consulted. We were challenged with minimizing the correction of SNa (or effective serum osmolality to avoid the osmotic demyelinating syndrome while replacing volume, potassium, phosphorus, calcium, and magnesium and concurrently treating DKA. Our management plan was further complicated by an episode of significant aquaresis. A stepwise approach was strategized to prioritize and correct all disturbances with considerations that the treatment of one condition could affect or directly worsen another. The current case demonstrates that a thorough understanding of electrolyte physiology is required in managing complex electrolyte disturbances to avoid disastrous outcomes.

The venous-arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers.

Science.gov (United States)

Morel, Jerome; Gergelé, Laurent; Dominé, Alexandre; Molliex, Serge; Perrot, Jean-Luc; Labeille, Bruno; Costes, Frederic

2017-08-01

The venous-arterial difference in CO 2 (ΔCO 2 ) has been proposed as an index of the adequacy of tissue perfusion in shock states. We hypothesized that the variation in PaCO 2 (hyper- or hypocapnia) could impact ΔCO 2 , partly through microcirculation adaptations. Fifteen healthy males volunteered to participate. For hypocapnia condition (hCO 2 ), the subjects were asked to hyperventilate, while they were asked to breathe a gas mixture containing 8 % CO 2 for hypercapnia condition (HCO 2 ). The 2 conditions were randomly assigned. Blood gases were measured at baseline before each condition, and after 5-7 min of either hCO 2 or HCO 2 condition. Microcirculation was assessed by the muscle reoxygenation slope measured with near infrared spectroscopy following a vascular occlusion test and by skin circulation with in vivo reflectance confocal microscopy. ΔCO 2 was significantly increased with hCO 2 while it tended to decrease with HCO 2 (non-significant). HCO 2 induced a moderate increase of the resaturation slope of NIRS oxygenation. Skin microcirculatory blood flow significantly dropped with hCO 2 , while it remained unchanged with hypercapnia. Our results warrant cautious interpretation of ΔCO 2 as an indicator of tissue perfusion during respiratory alkalosis.

Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain.

Science.gov (United States)

Djerad, A; Monier, C; Houzé, P; Borron, S W; Lefauconnier, J M; Baud, F J

2001-06-01

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.

Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis

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Javier Mata-Gómez

2015-08-01

Full Text Available BACKGROUND AND OBJECTIVES: Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH normalization, cerebrospinal fluid can keep a state of metabolic alkalosis. This circumstance, in addition to the residual effect of neuromuscular blocking agents, inhalant anesthetics and opioids could increase the risk of postoperative apnea after a general anesthesia.CASE REPORT: We present the successful management in 3 neonates in those a pyloromyotomy was carried out because they had presented congenital hypertrophic pyloric stenosis. This procedure was done under general anesthesia with orotracheal intubation and rapid sequence induction. Then, ultrasound-guided paravertebral block was performed as analgesic method without the need for administrating opioids within intraoperative period and keeping an appropriate analgesic level.CONCLUSIONS: Local anesthesia has demonstrated to be safe and effective in pediatric practice. We consider the ultrasound-guided paravertebral block with one dose as a possible alternative for other local techniques described, avoiding the use of opioids and neuromuscular blocking agents during general anesthesia, and reducing the risk of central apnea within postoperative period.

Clinical Management of Heat-Related Illnesses

Science.gov (United States)

2012-01-01

from CNS impairment.18,41,102 Hyperventilation and elevation of Tco primarily lead to respiratory alkalosis , which in EHS may be masked by metabolic...acute phase.69,102,116 Other common disturbances during the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dys...acidosis as a result of increased glycolysis and hyperlacticacidemia.26,74 Hypoxemia may be present in patients with respiratory complica- tions

USSR and Eastern Europe Scientific Abstracts, Biomedical and Behavioral Sciences, Number 84

Science.gov (United States)

1977-12-28

disease is attributable to the constantly stressed compensa- tory forces, respiratory alkalosis and metabolic acidosis, low arterial pressure, and...34 cells decreases as compared with the "bottom" cells. The higher respiratory indices of the "top" cells indicate predominance of anaerobic energy...Russian, 10 Western. 48 USSR UDC 591.1+12 INFLUENCE OF VAGUS AFFERENTATION UPON THE RESPIRATORY CENTER DURING HYPERVENTILATION Moscow

Effect of airway acidosis and alkalosis on airway vascular smooth muscle responsiveness to albuterol.

Science.gov (United States)

Cancado, Jose E; Mendes, Eliana S; Arana, Johana; Horvath, Gabor; Monzon, Maria E; Salathe, Matthias; Wanner, Adam

2015-04-02

In vitro and animal experiments have shown that the transport and signaling of β2-adrenergic agonists are pH-sensitive. Inhaled albuterol, a hydrophilic β2-adrenergic agonist, is widely used for the treatment of obstructive airway diseases. Acute exacerbations of obstructive airway diseases can be associated with changes in ventilation leading to either respiratory acidosis or alkalosis thereby affecting albuterol responsiveness in the airway. The purpose of this study was to determine if airway pH has an effect on albuterol-induced vasodilation in the airway. Ten healthy volunteers performed the following respiratory maneuvers: quiet breathing, hypocapnic hyperventilation, hypercapnic hyperventilation, and eucapnic hyperventilation (to dissociate the effect of pH from the effect of ventilation). During these breathing maneuvers, exhaled breath condensate (EBC) pH and airway blood flow response to inhaled albuterol (ΔQ̇aw) were assessed. Mean ± SE EBC pH (units) and ΔQ̇aw (μl.min(-1).mL(-1)) were 6.4 ± 0.1 and 16.8 ± 1.9 during quiet breathing, 6.3 ± 0.1 and 14.5 ± 2.4 during eucapnic hyperventilation, 6.6 ± 0.2 and -0.2 ± 1.8 during hypocapnic hyperventilation (p = 0.02 and <0.01 vs. quiet breathing), and 5.9 ± 0.1 and 2.0 ± 1.5 during hypercapnic hyperventilation (p = 0.02 and <0.02 vs quiet breathing). Albuterol responsiveness in the airway as assessed by ΔQ̇aw is pH sensitive. The breathing maneuver associated with decreased and increased EBC pH both resulted in a decreased responsiveness independent of the level of ventilation. These findings suggest an attenuated response to hydrophilic β2-adrenergic agonists during airway disease exacerbations associated with changes in pH. Registered at clinicaltrials.gov: NCT01216748 .

Renal abnormalities in congenital chloride diarrhea

International Nuclear Information System (INIS)

Al-Hamad, Nadia M.; Al-Eisa, Amal A.

2004-01-01

Congenital chloride diarrhea CLD is a rare autosomal recessive disorder caused by a defect in the chloride/ bicarbonate exchange in the ileum and colon. It is characterized by watery diarrhea, abdominal distension, hypochloremic hypokalemic metabolic alkalosis with high fecal content of chloride >90 mmol/l. We report 3 patients with CLD associated with various renal abnormalities including chronic renal failure secondary to renal hypoplasia, nephrocalcinosis and congenital nephrotic syndrome. (author)

Training Supplement Winter 2010 Journal of Special Operations Medicine. A Peer Reviewed Journal for SOF Medical Professionals

Science.gov (United States)

2010-01-01

Alkalinization agent for specific toxins (salicylates, phenobarbital) Dose: o 1mEq/kg IV Contraindications: o Metabolic or respiratory alkalosis o...cause of death from altitude illness. 2. Usually occurs above 8,000ft. Respiratory distress at high altitude is HAPE until proven otherwise. 3...HAPE since this will exacerbate symptoms. 5. Treat per Pain Management Protocol, but avoid the use of narcotics since they may depress respiratory

Military Nutrition Research.

Science.gov (United States)

1983-10-01

Hypophosphatemia was exaggerated, possibly because of respiratory alkalosis . Phosphate losses in urine and sweat were minimal, preventing appreciable loss... respiratory gases, the newer modifications for simplification of the measurements, and the total errors that are anticipated in its use. Data are presented... respiratory requirements at the altitude of the V icecap (7,000 feet) with that of sea level (actually 165 feet). (3) Energy metabolism was measured for

Effects of a Taser: Conducted Energy Weapon on the Circulating Red-Blood-Cell Population and Other Factors in Sus scrofa

Science.gov (United States)

2013-03-30

changes had not been used in previous CEW studies. In the present studies, in addition to standard measurements (including heart and respiratory rates...our study favoring either young or old RBCs being released from the spleen is unknown. Since alkalosis (rather than acidosis) tends to result in...cardiovascular, respiratory , and metabolic effects of a long duration electronic control device exposure in human volunteers. Forensic Sci Med Pathol. 2010;6

Nephrocalcinosis as adult presentation of Bartter syndrome type II.

Science.gov (United States)

Huang, L; Luiken, G P M; van Riemsdijk, I C; Petrij, F; Zandbergen, A A M; Dees, A

2014-02-01

Bartter syndrome consists a group of rare autosomal-recessive renal tubulopathies characterised by renal salt wasting, hypokalaemic metabolic alkalosis, hypercalciuria and hyperreninaemic hyperaldosteronism. It is classified into five types. Mutations in the KCNJ1 gene (classified as type II) usually cause the neonatal form of Bartter syndrome. We describe an adult patient with a homozygous KCNJ1 mutation resulting in a remarkably mild phenotype of neonatal type Bartter syndrome.

Effect of Acetazolamide vs Placebo on Duration of Invasive Mechanical Ventilation Among Patients With Chronic Obstructive Pulmonary Disease: A Randomized Clinical Trial.

Science.gov (United States)

Faisy, Christophe; Meziani, Ferhat; Planquette, Benjamin; Clavel, Marc; Gacouin, Arnaud; Bornstain, Caroline; Schneider, Francis; Duguet, Alexandre; Gibot, Sébastien; Lerolle, Nicolas; Ricard, Jean-Damien; Sanchez, Olivier; Djibre, Michel; Ricome, Jean-Louis; Rabbat, Antoine; Heming, Nicholas; Urien, Saïk; Esvan, Maxime; Katsahian, Sandrine

2016-02-02

Acetazolamide has been used for decades as a respiratory stimulant for patients with chronic obstructive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled trial is available to confirm this approach. To determine whether acetazolamide reduces mechanical ventilation duration in critically ill patients with COPD and metabolic alkalosis. The DIABOLO study, a randomized, double-blind, multicenter trial, was conducted from October 2011 through July 2014 in 15 intensive care units (ICUs) in France. A total of 382 patients with COPD who were expected to receive mechanical ventilation for more 24 hours were randomized to the acetazolamide or placebo group and 380 were included in an intention-to treat analysis. Acetazolamide (500-1000 mg, twice daily) vs placebo administered intravenously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission and continued during the ICU stay for a maximum of 28 days. The primary outcome was the duration of invasive mechanical ventilation via endotracheal intubation or tracheotomy. Secondary outcomes included changes in arterial blood gas and respiratory parameters, weaning duration, adverse events, use of noninvasive ventilation after extubation, successful weaning, the duration of ICU stay, and in-ICU mortality. Among 382 randomized patients, 380 (mean age, 69 years; 272 men [71.6%]; 379 [99.7%] with endotracheal intubation) completed the study. For the acetazolamide group (n = 187), compared with the placebo group (n = 193), no significant between-group differences were found for median duration of mechanical ventilation (-16.0 hours; 95% CI, -36.5 to 4.0 hours; P = .17), duration of weaning off mechanical ventilation (-0.9 hours; 95% CI, -4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/min; P = .72), or partial carbon-dioxide pressure in arterial blood (-0.3 mm Hg; 95% CI, -0.8 to 0.2 mm

Intestinal Ileus as a Possible Cause of Hypobicarbonatemia

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Andres Serrano

2007-01-01

Full Text Available The possible occurrence of metabolic acidosis in patients with intestinal ileus is not well recognized. We describe a patient with acute alcohol-induced pancreatitis and a large transverse colon ileus in which plasma bicarbonate dropped rapidly in the absence of an increase in the plasma anion gap. The urinary anion gap and ammonium excretion were consistent with an appropriate renal response to metabolic acidosis and against the possibility of respiratory alkalosis. The cause of the falling plasma bicarbonate was ascribed to intestinal bicarbonate sequestration owing to the enhancement of chloride-bicarbonate exchange in a dilated paralyzed colon.

Population pharmacodynamic modeling and simulation of the respiratory effect of acetazolamide in decompensated COPD patients.

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Nicholas Heming

Full Text Available Chronic obstructive pulmonary disease (COPD patients may develop metabolic alkalosis during weaning from mechanical ventilation. Acetazolamide is one of the treatments used to reverse metabolic alkalosis.619 time-respiratory (minute ventilation, tidal volume and respiratory rate and 207 time-PaCO2 observations were obtained from 68 invasively ventilated COPD patients. We modeled respiratory responses to acetazolamide in mechanically ventilated COPD patients and then simulated the effect of increased amounts of the drug.The effect of acetazolamide on minute ventilation and PaCO2 levels was analyzed using a nonlinear mixed effect model. The effect of different ventilatory modes was assessed on the model. Only slightly increased minute ventilation without decreased PaCO2 levels were observed in response to 250 to 500 mg of acetazolamide administered twice daily. Simulations indicated that higher acetazolamide dosage (>1000 mg daily was required to significantly increase minute ventilation (P0.75 L min(-1 in 60% of the population. The model also predicts that 45% of patients would have a decrease of PaCO2>5 mmHg with doses of 1000 mg per day.Simulations suggest that COPD patients might benefit from the respiratory stimulant effect after the administration of higher doses of acetazolamide.

A novel CLCN5 mutation in a boy with Bartter-like syndrome and partial growth hormone deficiency.

Science.gov (United States)

Bogdanović, Radovan; Draaken, Markus; Toromanović, Alma; Dordević, Maja; Stajić, Natasa; Ludwig, Michael

2010-11-01

Dent disease is an X-linked recessive disorder affecting the proximal tubule and is characterized by low-molecular-weight proteinuria (LMWP), hypercalciuria, nephrocalcinosis/nephrolithiasis with a variable number of features of Fanconi syndrome. It is most often associated with mutations in CLCN5, which encodes the endosomal electrogenic chloride/proton exchanger ClC-5. Renal acidification abnormalities are only rarely seen in Dent disease, whereas the hypokalemic metabolic alkalosis associated with hyperreninemic hyperaldosteronism (Bartter-like syndrome) has been reported in only one patient so far. We report on a 5-year-old boy with Dent disease caused by mutation in CLCN5 gene, c.1073G>A, who presented with hypokalemic metabolic alkalosis and hyperreninemic hyperaldosteronism persisting over the entire follow-up. No mutations were found in NKCC2, ROMK, NCCT, or ClC-Kb genes. In addition, the patient exhibited growth failure associated with partial growth hormone (GH) deficiency. Coexistence of Bartter-like syndrome features with LMWP should prompt a clinician to search for Dent disease. The Bartter syndrome phenotype seen in Dent disease patients may represent a distinct form of Bartter syndrome, the exact mechanism of which has yet to be fully elucidated. Growth delay that persists in spite of appropriate therapy should raise suspicion of other causes, such as GH deficiency.

Simulation Crisis Team Training Effect on Rural Hospital Safety Climate (SIMCRITTER)

Science.gov (United States)

2008-09-01

showed sinus tachycardia. ABG showed a mild respiratory and metabolic alkalosis , with adequate oxygenation on 6 liters nasal cannula. The chest x-ray is...Total Attending / Staff Physician 5 1.37% Physician In Training 0 0.00% Pharmacist 0 0.00% Respiratory Therapist 9 2.47% PT / OT / Speech 12 3.29...groups (e.g., nurses, physicians, and respiratory therapists). The unique aspects of the proposed project included the application of high-fidelity

Quantified pH imaging with hyperpolarized 13C‐bicarbonate

DEFF Research Database (Denmark)

Scholz, David Johannes; Janich, Martin A.; Köllisch, Ulrich

2015-01-01

for various flip angles for bicarbonate (BiC) and CO2 with spectral‐spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction...... and interpreted within inflammation and acute metabolic alkalosis models. Magn Reson Med 73:2274–2282, 2015. © 2014 Wiley Periodicals, Inc....

Classic Bartter syndrome: a rare cause of failure to thrive in a child

OpenAIRE

Vieira, Helena; Mendes, Leonor; Mendes, Patricia; da Silva, José Esteves

2012-01-01

Bartter syndrome is a group of rare autosomal-recessive disorders caused by a defect in distal tubule transport of sodium and chloride. Blood gases and plasma electrolytes raise suspicion of this diagnosis and the definitive diagnosis is made by genetic study. Early treatment improves prognosis. The authors present the case of an 11-month-old child with early failure to thrive and severe regurgitation. Blood gases revealed hypochloraemic metabolic alkalosis, hyponatraemia and hypokalaemia. Bl...

[Acid-base status in patients treated with peritoneal dialysis].

Science.gov (United States)

Katalinić, Lea; Blaslov, Kristina; Pasini, Eva; Kes, Petar; Bašić-Jukić, Nikolina

2014-04-01

When compared to hemodialysis, peritoneal dialysis is very simple yet low cost method of renal replacement therapy. Series of studies have shown its superiority in preserving residual renal function, postponing uremic complications, maintaining the acid-base balance and achieving better post-transplant outcome in patients treated with this method. Despite obvious advantages, its role in the treatment of chronic kidney disease is still not as important as it should be. Metabolic acidosis is an inevitable complication associated with progressive loss of kidney function. Its impact on mineral and muscle metabolism, residual renal function, allograft function and anemia is very complex but can be successfully managed. The aim of our study was to evaluate the efficiency in preserving the acid-base balance in patients undergoing peritoneal dialysis at Zagreb University Hospital Center. Twenty-eight patients were enrolled in the study. The mean time spent on the treatment was 32.39 ± 43.43 months. Only lactate-buffered peritoneal dialysis fluids were used in the treatment. Acid-base balance was completely maintained in 73.07% of patients; 11.54% of patients were found in the state of mild metabolic acidosis, and the same percentage of patients were in the state of mild metabolic alkalosis. In one patient, mixed alkalosis with respiratory and metabolic component was present. The results of this study showed that acid-base balance could be maintained successfully in patients undergoing peritoneal dialysis, even only with lactate-buffered solutions included in the treatment, although they were continuously proclaimed as inferior in comparison with bicarbonate-buffered ones. In well educated and informed patients who carefully use this method, accompanied by the attentive and thorough care of their physicians, this method can provide quality continuous replacement of lost renal function as well as better quality of life.

Is Bicarbonate Therapy Useful?

Science.gov (United States)

Hopper, Kate

2017-03-01

Despite concerns about the negative effects of metabolic acidosis, there is minimal evidence that sodium bicarbonate administration is an effective treatment. In addition, sodium bicarbonate therapy is associated with many adverse effects, including paradoxic intracellular acidosis, hypokalemia, hypocalcemia, hypernatremia, and hyperosmolality. Definitive recommendations regarding bicarbonate therapy are challenging as there is little high-quality evidence available. In most clinical scenarios of metabolic acidosis, treatment efforts should focus on resolution of the underlying cause, and sodium bicarbonate therapy should be used with caution, if at all. An exception to this is kidney disease, wherein sodium bicarbonate therapy may have a valuable role. Published by Elsevier Inc.

Distal renal tubular acidosis and amelogenesis imperfecta: A rare association

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P Ravi

2013-01-01

Full Text Available Renal tubular acidosis (RTA is characterized by a normal anion gap with hyperchloremic metabolic acidosis. Primary distal RTA (type I is the most common RTA in children. Childhood presentation of distal RTA includes vomiting, failure to thrive, metabolic acidosis, and hypokalemia. Amelogenesis imperfecta (AI represents a condition where the dental enamel and oral tissues are affected in an equal manner resulting in the hypoplastic or hypopigmented teeth. We report a 10-year-old girl, previously asymptomatic presented with the hypokalemic paralysis and on work-up found out to have type I RTA. The discoloration of teeth and enamel was diagnosed as AI.

Acid-Base and Electrolyte Disorders in Patients with and without Chronic Kidney Disease: An Update.

Science.gov (United States)

Dhondup, Tsering; Qian, Qi

2017-12-01

Kidneys play a pivotal role in the maintenance and regulation of acid-base and electrolyte homeostasis, which is the prerequisite for numerous metabolic processes and organ functions in the human body. Chronic kidney diseases compromise the regulatory functions, resulting in alterations in electrolyte and acid-base balance that can be life-threatening. In this review, we discuss the renal regulations of electrolyte and acid-base balance and several common disorders including metabolic acidosis, alkalosis, dysnatremia, dyskalemia, and dysmagnesemia. Common disorders in chronic kidney disease are also discussed. The most recent and relevant advances on pathophysiology, clinical characteristics, diagnosis, and management of these conditions have been incorporated.

Diospyros rhodocalyx (Tako-Na), a Thai folk medicine, associated with hypokalemia and generalized muscle weakness: a case series.

Science.gov (United States)

Othong, Rittirak; Trakulsrichai, Satariya; Wananukul, Winai

2017-11-01

Diospyros rhodocalyx (Tako-Na) is a Thai folk medicine purported to promote longevity, treat impotence, etc. We present patients with hypokalemia, weakness and hypertension after consuming Tako-Na tea. Case 1: A 61-year-old man was brought in nine hours after drinking 400-500 mL of Tako-Na tea. One handful of Tako-Na bark was boiled in water to make tea. He had vomiting and watery diarrhea six hours after drinking it. He took no medications and had no history of hypertension. The only remarkable vital sign was BP 167/90 mmHg. Physical examination revealed generalized muscle weakness. Laboratory findings were potassium 2.7 mmol/L, bicarbonate 24 mmol/L, and transtubular potassium gradient (TTKG) 5.6. He was discharged the next day with a BP 140/90 mmHg and potassium 4.2 mmol/L. Case 2: A 78-year-old man, a friend of case 1, also drank Tako-Na tea from the same pot at the same time as case 1. He also had vomiting and diarrhea six hours later. He took no medications despite past history of hypertension (baseline SBP 140-160). Initial BP was 230/70 mmHg. He also had muscle weakness. Laboratory findings were potassium 3.3 mmol/L, bicarbonate 24 mmol/L, TTKG 7.37 and normal thyroid function. He was also discharged the next day with a BP 148/70 mmHg and potassium 4.2 mmol/L. Case 3-7: These were patients reported to a poison center and their potassium concentrations were 1.4, 1.4, 3.3, 1.3 and 1.2 mmol/L, respectively. Three of them were intubated and case 3 died. Tako-Na contains betulin, betulinic acid, taraxerone, lupeol, and lupenone. Their structures are similar to glycyrrhetic acid, the active metabolite of glycyrrhizic acid found in licorice which is well known to cause pseudoaldosteronism. Glycyrrhetic acid is potent in inhibiting 11-beta-hydroxysteroid dehydrogenase, and causes pseudoaldosteronism. We hypothesize that the compounds in Tako-Na act in the same way as glycyrrhetic acid in producing pseudoaldosteronism.

Unusual case of failure to thrive: Type III Bartter syndrome.

Science.gov (United States)

Agrawal, S; Subedi, K; Ray, P; Rayamajhi, A

2016-09-01

Bartter syndrome Type III is a rare autosomal recessive disorder resulting from an inherited defect in the thick ascending limb of the loop of henle of the nephrons in kidney. The typical clinical manifestations in childhood are failure to thrive and recurrent episodes of vomiting. Typical laboratory findings which help in the diagnosis are hypokalemic metabolic alkalosis, hypomagnesemia and hypercalciuria. We report a case of Type III Bartter syndrome not responding to repeated conventional treatment of failure to thrive.

Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Chronic Alcoholism: A Case Report.

Science.gov (United States)

Tsai, Ming-Hsien; Lin, Shih-Hua; Leu, Jyh-Gang; Fang, Yu-Wei

2015-09-01

Thyrotoxic periodic paralysis (TPP) is characterized by the presence of muscle paralysis, hypokalemia, and hyperthyroidism. We report the case of a young man with paralysis of the lower extremities, severe hypokalemia, and concurrent hyperthyroidism. TPP was suspected; therefore, treatment consisting of judicious potassium (K+) repletion and β-blocker administration was initiated. However, urinary K+ excretion rate, as well as refractoriness to treatment, was inconsistent with TPP. Chronic alcoholism was considered as an alternative cause of hypokalemia, and serum K+ was restored through vigorous K repletion and the addition of K+ -sparing diuretics. The presence of thyrotoxicosis and hypokalemia does not always indicate a diagnosis of TPP. Exclusion of TPP can be accomplished by immediate evaluation of urinary K+ excretion, acid-base status, and the amount of potassium chloride required to correct hypokalemia at presentation.

Control of rectal gland secretion by blood acid-base status in the intact dogfish shark (Squalus acanthias).

Science.gov (United States)

Wood, Chris M; Munger, R Stephen; Thompson, Jill; Shuttleworth, Trevor J

2007-05-14

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa type

Directory of Open Access Journals (Sweden)

Berend K

2013-12-01

Full Text Available Kenrick BerendSt Elisabeth Hospital, Willemstad, CuraçaoImashuku et al1 describe a 77-year-old male patient with multiple myeloma who was admitted to the hospital after suffering a pelvic bone fracture due to a road traffic accident. Several days after admission the arterial blood gas showed a pH of 7.481; arterial carbon dioxide tension (PaCO2 of 28.2 mmHg; arterial oxygen tension (PaO2 of 84.0 mmHg; HCO3- of 20.8 mmol/L (normal; 23–31 mmol/L; and an anion gap of 8.9 mmol/L (normal;12 mmol/L. These data, as the authors concluded, were suggestive of metabolic acidosis. First, this is not true because a high pH and low PaCO2 confirm a respiratory alkalosis. Since the test was conducted days later we may expect a chronic respiratory alkalosis to be present, perhaps because of pain or a secondary pulmonary problem, as may be expected with a relatively low PaO2. In chronic respiratory alkalosis one would expect the HCO3- to decrease about 4 mmol/L with every 10 mmHg decrease of PaCO2.2 If the initial HCO3- had been about 25 mmol/L, the expected PaCO2 would be about 20.28 mmol/L, almost identical with the patient’s HCO3-.View original paper by Imashuku and colleagues.

Quantified pH imaging with hyperpolarized (13) C-bicarbonate.

Science.gov (United States)

Scholz, David Johannes; Janich, Martin A; Köllisch, Ulrich; Schulte, Rolf F; Ardenkjaer-Larsen, Jan H; Frank, Annette; Haase, Axel; Schwaiger, Markus; Menzel, Marion I

2015-06-01

Because pH plays a crucial role in several diseases, it is desirable to measure pH in vivo noninvasively and in a spatially localized manner. Spatial maps of pH were quantified in vitro, with a focus on method-based errors, and applied in vivo. In vitro and in vivo (13) C mapping were performed for various flip angles for bicarbonate (BiC) and CO2 with spectral-spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction. After optimizing the signal to noise ratio of the hyperpolarized (13) C-bicarbonate, error estimation of the spectral-spatial excited spectrum reveals that the method covers the biologically relevant pH range of 6 to 8 with low pH error (< 0.2). Quantification of pH maps shows negligible impact of the residual bicarbonate signal. pH maps reflect the induction of acute metabolic alkalosis. Inflamed, infected regions exhibit lower pH. Hyperpolarized (13) C-bicarbonate pH mapping was shown to be sensitive in the biologically relevant pH range. The mapping of pH was applied to healthy in vivo organs and interpreted within inflammation and acute metabolic alkalosis models. © 2014 Wiley Periodicals, Inc.

(/sup 11/C )-DMO for evaluation of regional tissue pH in patients with hemispheric infarction using positron emission tomography

Energy Technology Data Exchange (ETDEWEB)

Castaing, M; Syrota, A; Rougemont, D; Berridge, M; Chretien, L; Baron, J C; Bousser, M G

1983-06-01

Changes in brain intracellular pH resulting from cerebral infarction were evaluated using the /sup 11/C-DMO (dimethyloxazolidine-dione) method, in 9 patients. A /sup 15/O/sub 2/-C/sup 15/O/sub 2/ study was performed the day following the DMO examination in order to obtain the values of cerebral blood flow, oxygen extraction and oxygen metabolic rate in the same regions-of-interest. The results emphasized the relationship between tissue alkalosis and luxury perfusion during recent infarction.

CHANGES ELECTROLYTES AND BLOOD GASES IN ARABIAN HORSES DURING TO 60 KM ENDURANCE RACE ALTERAÇÕES HEMOGASOMÉTRICAS E ELETROLÍTICAS DE CAVALOS DA RAÇA ÁRABE DURANTE PROVA DE ENDURO DE 60 KM

Directory of Open Access Journals (Sweden)

José Corrêa de Lacerda Neto

2009-09-01

Full Text Available Changes in venous blood pH, pCO2, pO2, HCO-3 and cBase, and in serum concentrations of sodium, potassium, ionized calcium and chloride were studied in eight Arabian horses during endurance ride of 60km, with controlled speed of 12km/h-. The blood samples were collected prior to the beginning (M0 of the exercise, immediately after the ride (M1 and one hour after the ride (M2, with the animals resting. Immediately after the end of the exercise (M1 the animals presented higher values for pH which, added to the increase of cHCO3- and cBase, characterized the metabolic alkalosis, probably due to losses of chloride ions in the sweat. The metabolic changes observed in M1 were quickly corrected by respiratory changes, characterized by increased pCO2 or hypoventilation. Additionally, the horses presented dehydration, hypocalcemia and hypokalemia. The metabolic disturbances observed were not associated with clinical changes.

KEY WORDS: Acid-base, electrolytes, endurance, equine
Avaliaram-se as alterações do pH, pCO2, pO2, HCO-3 e da cBase do sangue venoso e das concentrações séricas de sódio, potássio, cálcio ionizado e cloreto de oito cavalos adultos da raça Árabe, durante prova de enduro de 60 km de extensão, com velocidade média de 12km h-1. As amostras de sangue foram coletadas antes do início da prova (M0, imediatamente após o seu término (M1 e sessenta minutos após a realização da prova (M2, com os animais já em repouso. Imediatamente após o término do exercício (M1, os animais apresentaram aumento nos valores do pH o qual, associado ao aumento da cHCO3- e da cBase, caracterizou a alcalose metabólica, que teve como provável origem a perda de cloro no suor. As alterações metabólicas observadas no M1 foram rapidamente corrigidas por modificações respiratórias, caracterizadas pelo aumento da pCO2 ou hipoventilação. Adicionalmente, apresentaram desidratação, hipocalemia e hipocalcemia. Não se

Hypercapnea and Acidemia despite Hyperventilation following Endotracheal Intubation in a Case of Unknown Severe Salicylate Poisoning

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Shannon M. Fernando

2017-01-01

Full Text Available Salicylates are common substances for deliberate self-harm. Acute salicylate toxicity is classically associated with an initial respiratory alkalosis, followed by an anion gap metabolic acidosis. The respiratory alkalosis is achieved through hyperventilation, driven by direct stimulation on the respiratory centers in the medulla and considered as a compensatory mechanism to avoid acidemia. However, in later stages of severe salicylate toxicity, patients become increasingly obtunded, with subsequent loss of airway reflexes, and therefore intubation may be necessary. Mechanical ventilation has been recommended against in acute salicylate poisoning, as it is believed to take away the compensatory hyperpnea and tachypnea. Despite the intuitive physiological basis for this recommendation, there is a paucity of evidence to support it. We describe a case of a 59-year-old male presenting with decreased level of consciousness and no known history of ingestion. He was intubated and experienced profound hypercarbia and acidemia despite mechanical ventilation with high minute ventilation and tidal volumes. This case illustrates the deleterious effects of intubation in severe salicylate toxicity.

Interaction of Stress and Anxiogenic Drugs on Behaviors of Rats and Antagonism with Indomethacin

Science.gov (United States)

2001-10-19

also produces panic attacks. Hyperventilation produces respi ratory alkalosis and hypocapnea 22 (reduced CO2 tension in arterial blood) . and...minute stressor hyperventilated, a result would be hypocapnia and alkalosis (Guyton & Hall, 1996). Alkalosis is known to increase the binding of...neuroanatomical hypothesis for panic disorder. American Journal of Psychology, 146, 148-161 . Gorman, J.M., & Papp, LA (1990). Respiratory

Antenatal Bartter syndrome.

Science.gov (United States)

Afzal, Muhammad; Khan, Ejaz A; Khan, Wisal A; Anwar, Viqas; Yaqoob, Asma; Rafiq, Shahid; Azam, Shaheena

2014-05-01

Antenatal Bartter syndrome is characterized by severe polyhydramnios in mother leading to premature delivery. Antenatal treatment has proven effective to prevent these problems. Postnatally newborns suffer from recurrent episodes of severe dehydration and electrolyte imbalance which can lead to fatal outcome. These manifestations are likely to be overlooked and missed under the umbrella of diagnosis of prematurity. This premature newborn with antenatal polyhydramnios had severe manifestations of polyuria, recurrent dehydration, electrolyte derangements and metabolic alkalosis. She was managed accordingly but unfortunately could not survive beyond 4 weeks.

Acute Infectious Disease,

Science.gov (United States)

1984-03-23

accelerated respiration. This tachypnia causes an exaggerated loss of carbon dioxide.3 The respiratory alkalosis that ensues is typically seen during all...with respiratory alkalosis . During periods of heat-induced tachypnia, U’. inorganic phosphates may virtually disappear for a time from urine and sweat...urine and sweat during the period when respiratory alkalosis and hyperventilation are taking place. On the other hand, losses of phosphate may be

The influence of sodium bicarbonate on maximal force and rates of force development in the triceps surae and brachii during fatiguing exercise.

Science.gov (United States)

Siegler, Jason C; Mudie, Kurt; Marshall, Paul

2016-11-01

What is the central question of this study? Does metabolic alkalosis in humans, induced by sodium bicarbonate, affect rates of skeletal muscle fatigue differentially in muscle groups composed predominately of slow- and fast-twitch fibres? What is the main finding and its importance? Sodium bicarbonate exhibited no effect on the fatigue profile observed between triceps surae and brachii muscle groups during and after 2 min of tetanic stimulation. For the first time in exercising humans, we have profiled the effect of sodium bicarbonate on the voluntary and involuntary contractile characteristics of muscle groups representative of predominately slow- and fast-twitch fibres. The effect of metabolic alkalosis on fibre-specific maximal force production and rates of force development (RFD) has been investigated previously in animal models, with evidence suggesting an improved capacity to develop force rapidly in fast- compared with slow-twitch muscle. We have attempted to model in vivo the fatigue profile of voluntary and involuntary maximal force and RFD in the triceps surae and brachii after sodium bicarbonate (NaHCO 3 ) ingestion. In a double-blind, three-way repeated-measures design, participants (n = 10) ingested either 0.3 g kg -1 NaHCO 3 (ALK) or equivalent calcium carbonate (PLA) prior to 2 min of continuous (1 Hz) supramaximal stimulation (300 ms at 40 Hz) of the triceps surae or brachii, with maximal voluntary efforts (maximal voluntary torque) coupled with direct muscle stimulation also measured at baseline, 1 and 2 min. Metabolic alkalosis was achieved in both ALK trials but was not different between muscle groups. Regardless of the conditions, involuntary torque declined nearly 60% in the triceps brachii (P < 0.001) and ∼30% in the triceps surae (P < 0.001). In all trials, there was a significant decline in normalized involuntary RFD (P < 0.05). Maximal voluntary torque declined nearly 28% but was not different between conditions (P < 0

Using omeprazole to link the components of the post-prandial alkaline tide in the spiny dogfish, Squalus acanthias.

Science.gov (United States)

Wood, Chris M; Schultz, Aaron G; Munger, R Stephen; Walsh, Patrick J

2009-03-01

After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H(+), K(+)-ATPase pump inhibitor omeprazole to determine whether these post-prandial alkaline tide events were linked to secretion of H(+) (accompanied by Cl(-)) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5 mg omeprazole per kilogram over 48 h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pre-treatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in Cl(-) concentration of the chyme and altered the patterns of other ions, indicating inhibition of H(+) and accompanying Cl(-) secretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48 h. Arterial blood CO(2) pressure (Pa(CO(2))) and plasma ions were not substantially altered. These results indicate that elevated gastric H(+) secretion (as HCl) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the alkaline tide in the dogfish.

Population pharmacodynamic model of bicarbonate response to acetazolamide in mechanically ventilated chronic obstructive pulmonary disease patients

Science.gov (United States)

2011-01-01

Introduction Acetazolamide is commonly given to chronic obstructive pulmonary disease (COPD) patients with metabolic alkalosis. Little is known of the pharmacodynamics of acetazolamide in the critically ill. We undertook the pharmacodynamic modeling of bicarbonate response to acetazolamide in COPD patients under mechanical ventilation. Methods This observational, retrospective study included 68 invasively ventilated COPD patients who received one or multiple doses of 250 or 500 mg of acetazolamide during the weaning period. Among the 68 investigated patients, 207 time-serum bicarbonate observations were available for analysis. Population pharmacodynamics was modeled using a nonlinear mixedeffect model. The main covariates of interest were baseline demographic data, Simplified Acute Physiology Score II (SAPS II) at ICU admission, cause of respiratory failure, co-prescription of drugs interfering with the acid-base equilibrium, and serum concentrations of protein, creatinin, potassium and chloride. The effect of acetazolamide on serum bicarbonate levels at different doses and in different clinical conditions was subsequently simulated in silico. Results The main covariates interacting with acetazolamide pharmacodynamics were SAPS II at ICU admission (P = 0.01), serum chloride (P 500 mg twice daily is required to reduce serum bicarbonate concentrations > 5 mmol/L in the presence of high serum chloride levels or coadministration of systemic corticosteroids or furosemide. Conclusions This study identified several covariates that influenced acetazolamide pharmacodynamics and could allow a better individualization of acetazolamide dosing when treating COPD patients with metabolic alkalosis. PMID:21917139

Baking soda pica associated with rhabdomyolysis and cardiomyopathy in pregnancy.

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Scolari Childress, Katherine M; Myles, Thomas

2013-08-01

Pica is a commonly underappreciated disorder in pregnancy that can lead to several complications, including severe metabolic derangements and other adverse outcomes. We report a case of baking soda pica in pregnancy associated with both rhabdomyolysis and cardiomyopathy. A multigravid woman at 37 weeks of gestation presented with weakness and severe hypokalemia. She subsequently had development of rhabdomyolysis and presumed peripartum cardiomyopathy. After delivery, it was discovered that the patient had a long history of consumption of large quantities of baking soda. Her condition improved with cessation of the pica. Clinicians must have a high index of suspicion for pica in pregnancy because it can lead to complex diagnostic challenges and pregnancy complications. The diagnosis should be considered in a patient with unexplained metabolic abnormalities.

Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism

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Parvaiz Ahmad Koul

2011-01-01

Full Text Available A 43- year- old woman on treatment for primary hypothyroidism presented with 1- day progressive weakness of all her limbs and history of similar episodes in the past. Clinical examination revealed grade 2 hyporeflexive weakness. Investigations revealed features of hypokalemia, metabolic acidosis, alkaline urine, and a fractional bicarbonate excretion of 3.5%, consistent with distal renal tubular acidosis. Antithyroid peroxidase and antithroglobulin antibodies were positive, suggesting an autoimmune basis for the pathogenesis of the functional tubular defect. Bicarbonate therapy resulted in a sustained clinical recovery.

Nephropathic Cystinosis Mimicking Bartter Syndrome: a Novel Mutation.

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Bastug, Funda; Nalcacioglu, Hulya; Ozaltin, Fatih; Korkmaz, Emine; Yel, Sibel

2018-01-01

Cystinosis is a rare autosomal recessive disorder resulting from defective lysosomal transport of cystine due to mutations in the cystinosin lysosomal cystine transporter (CTNS) gene. The clinical phenotype of nephropathic cystinosis is characterized by renal tubular Fanconi syndrome and development of end-stage renal disease during the first decade. Although metabolic acidosis is the classically prominent finding of the disease, a few cases may present with hypokalemic metabolic alkalosis mimicking Bartter syndrome. Bartter-like presentation may lead to delay in diagnosis and initiation of specific treatment for cystinosis. We report a case of a 6-year-old girl initially presenting with the features of Bartter syndrome that was diagnosed 2 years later with nephropathic cystinosis and a novel CTNS mutation.

Is glycyrrhizin sensitivity increased in anorexia nervosa and should licorice be avoided? Case report and review of the literature

DEFF Research Database (Denmark)

Støving, René K; Lingqvist, Linnéa E; Bonde, Rasmus K

2011-01-01

OBJECTIVE: Hypokalemia is a potentially life-threatening electrolyte disturbance in anorexia nervosa and is most frequently caused by purging behavior. We report a case of severe hypokalemia in anorexia nervosa induced by daily ingestion of approximately 20 g of licorice. METHODS: To confirm...... low daily dose of licorice suggests high glycyrrhizin sensitivity. CONCLUSION: Patients with anorexia nervosa not only have decreased food intake but also selective and sometimes bizarre eating habits that, in association with increased sensitivity to glycyrrhizin, may cause severe hypokalemia....

On the Mechanism of Polyuria in Potassium Depletion

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Berl, Tomas; Linas, Stuart L.; Aisenbrey, Gary A.; Anderson, Robert J.

1977-01-01

The association of potassium (K) depletion with polyuria and a concentrating defect is established, but the extent to which these defects could be secondary to an effect of low K on water intake has not been systematically investigated. To determine whether hypokalemia has a primary effect to increase thirst and whether any resultant polyuria and polydipsia contribute to the concentrating defect, we studied three groups of rats kept in metabolic cages for 15 days. The groups were set up as follows: group 1, normal diets and ad lib. fluids (n = 12); group 2, K-deficient diet on ad lib. fluids (n = 12); and group 3, K-deficient diet and fluid intake matched to group 1 (n = 14). Daily urine flow and urinary osmolality of groups 1 and 3 were not significantly different throughout the study. In contrast, as of day 6, group 2 rats consistently had a higher fluid intake (P polyuria. After 15 days of a K-deficient diet, the impaired maximal urinary concentration in hypokalemia, however, was not related to increased water intake, since fluid restriction did not abolish the renal concentrating defect. PMID:893666

Correlation between arterial blood gas analysis and peripheral blood gas analysis in acid-base unbalance state

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Hyun Lee Kim

2012-06-01

Full Text Available Acid-base unbalance is most common problem in severe ill patient, especially in condition of abnormal renal function state. Acid-base unbalances are respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Metabolic acidosis is frequently appeared in clinical state. Arterial blood gas analysis is considered as a basic test to the intensive care unit patient and emergency state. Recently some researches were done, comparing with arterial blood gas analysis and venous blood gas analysis. Because of venous blood sampling is safer than arterial blood gas analysis, and beside not so different among them for detecting pH, pCO2, HCO3, except pO2 measuring. This research was done in emergency room, and for explaining no different between arterial blood gas analysis and peripheral blood gas analysis result in acid-base unbalance state patient. Especially in kidney functions decreased state. : The study was done from March, 2010 to January, 2011. The object was 89 peoples who came to emergency room for treating internal medicine problem. (Women 53, average age: 66.7±12.1 Then compare between arterial blood gas analysis and peripheral blood gas analysis. Result: The mean arterial minus venous difference for pH, pCO2, and bicarbonate was −0.0170, 2.6528, and 0.6124. Bland-Altman plot was done for predicting agreement of two groups, and the scale was pH −2.95 to 4.17, pCO2 −4.45 to 9.76, bicarbonate −2.95 to 4.16, in 95% relative. Conclusion: The peripheral blood gas pH, pCO2, bicarbonate level is almost same as arterial blood gas analysis results. And enough to measuring acid-base unbalance state, in absent of arterial blood testing.

Strong ion and weak acid analysis in severe preeclampsia: potential clinical significance.

Science.gov (United States)

Ortner, C M; Combrinck, B; Allie, S; Story, D; Landau, R; Cain, K; Dyer, R A

2015-08-01

The influence of common disturbances seen in preeclampsia, such as changes in strong ions and weak acids (particularly albumin) on acid-base status, has not been fully elucidated. The aims of this study were to provide a comprehensive acid-base analysis in severe preeclampsia and to identify potential new biological predictors of disease severity. Fifty women with severe preeclampsia, 25 healthy non-pregnant- and 46 healthy pregnant controls (26-40 weeks' gestation), were enrolled in this prospective case-control study. Acid-base analysis was performed by applying the physicochemical approach of Stewart and Gilfix. Mean [sd] base excess was similar in preeclamptic- and healthy pregnant women (-3.3 [2.3], and -2.8 [1.5] mEq/L respectively). In preeclampsia, there were greater offsetting contributions to the base excess, in the form of hyperchloraemia (BE(Cl) -2 [2.3] vs -0.4 [2.3] mEq/L, Palkalosis was associated with a non-reassuring/abnormal fetal heart tracing (Prespiratory and hypoalbuminaemic alkalosis that was metabolically offset by acidosis, secondary to unmeasured anions and dilution. While the overall base excess in severe preeclampsia is similar to that in healthy pregnancy, preeclampsia is associated with a greater imbalance offsetting hypoalbuminaemic alkalosis and hyperchloraemic acidosis. Rather than the absolute value of base excess, the magnitude of these opposing contributors may be a better indicator of the severity of this disease. Hypoalbuminaemic alkalosis may also be a predictor of fetal compromise. clinicaltrials.gov: NCT 02164370. © The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Blood Gases Test

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... pulmonary disease (COPD) , and over-sedation from narcotics. Respiratory alkalosis, characterized by a raised pH and a decreased ... myasthenia gravis Greater than 7.45 Low Low Respiratory alkalosis Hyperventilation, pain, anxiety, brain trauma, pneumonia, certain drugs ( ...

[Celiac crisis with quadriplegia due to potassium depletion as presenting feature of celiac disease].

Science.gov (United States)

Atikou, A; Rabhi, M; Hidani, H; El Alaoui Faris, M; Toloune, F

2009-06-01

Adult coeliac disease revealed by coeliac crisis and quadriplegia due to potassium depletion is an extremely rare situation. A 26-year-old woman presented with a suddenly developed weakness of all four limbs and a severe diarrhea. Authors emphasize coeliac crisis, which is a presenting feature of coeliac disease, characterized by acute diarrhea with life-threatening acid base and electrolyte abnormalities. The patient improved with correction of hypokalemia and gluten-free diet. A severe acute diarrhea with metabolic and systemic complications, the so-called coeliac crisis, is a possible presenting clinical feature of a previously undiagnosed adult celiac disease.

Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

LENUS (Irish Health Repository)

Hayes, N E

2011-04-01

We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

LENUS (Irish Health Repository)

Hayes, N E

2012-02-01

We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

in Critically Ill Patients: Success and Limits

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Filippo Mariano

2011-01-01

Full Text Available Citrate anticoagulation has risen in interest so it is now a real alternative to heparin in the ICUs practice. Citrate provides a regional anticoagulation virtually restricted to extracorporeal circuit, where it acts by chelating ionized calcium. This issue is particularly true in patients ongoing CRRT, when the “continuous” systemic anticoagulation treatment is per se a relevant risk of bleeding. When compared with heparin most of studies with citrate reported a longer circuit survival, a lower rate of bleeding complications, and transfused packed red cell requirements. As anticoagulant for CRRT, the infusion of citrate is prolonged and it could potentially have some adverse effects. When citrate is metabolized to bicarbonate, metabolic alkalosis may occur, or for impaired metabolism citrate accumulation leads to acidosis. However, large studies with dedicated machines have indeed demonstrated that citrate anticoagulation is well tolerated, safe, and an easy to handle even in septic shock critically ill patients.

Plant metabolic modeling: achieving new insight into metabolism and metabolic engineering.

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Baghalian, Kambiz; Hajirezaei, Mohammad-Reza; Schreiber, Falk

2014-10-01

Models are used to represent aspects of the real world for specific purposes, and mathematical models have opened up new approaches in studying the behavior and complexity of biological systems. However, modeling is often time-consuming and requires significant computational resources for data development, data analysis, and simulation. Computational modeling has been successfully applied as an aid for metabolic engineering in microorganisms. But such model-based approaches have only recently been extended to plant metabolic engineering, mainly due to greater pathway complexity in plants and their highly compartmentalized cellular structure. Recent progress in plant systems biology and bioinformatics has begun to disentangle this complexity and facilitate the creation of efficient plant metabolic models. This review highlights several aspects of plant metabolic modeling in the context of understanding, predicting and modifying complex plant metabolism. We discuss opportunities for engineering photosynthetic carbon metabolism, sucrose synthesis, and the tricarboxylic acid cycle in leaves and oil synthesis in seeds and the application of metabolic modeling to the study of plant acclimation to the environment. The aim of the review is to offer a current perspective for plant biologists without requiring specialized knowledge of bioinformatics or systems biology. © 2014 American Society of Plant Biologists. All rights reserved.

Treatment of heartwater : potential adverse effects of furosemide administration on certain homeostatic parameters in normal sheep

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A.S. Shakespeare

1998-07-01

Full Text Available Diuretics, in particular furosemide, are generally recommended as a supportive treatment in the advanced stages of heartwater in ruminants. However, after what appeared to be possible adverse effects accompanying its use in field cases of heartwater, the effects of this drug on certain blood and urine parameters were investigated in normal sheep at the same dose rates. Diuresis with concomitant natriuresis was significant after furosemide administration, as was the expected plasma volume decrease. Other significant changes included metabolic alkalosis, hypokalaemia and reduced blood ionised calcium. The difference in duration of the diuretic effect and the duration of the changes in blood parameters from c. 3 h and c. 6 h respectively make it difficult to determine a time interval between successive treatments with furosemide. It appears that the probable cause of death of sheep with heartwater is a drastic reduction in blood volume and decreased cardiac output that leads to general circulatory failure. A therapeutic approach that involves further loss of plasma volume due to diuresis appears contradictory. The added effects of potentiating respiratory alkalosis and the terminal drop in blood ionised calcium seen in heartwater-affected animals indicate that the use of furosemide in supportive treatment of this disease is not warranted.

Exogenous sphingosine-1-phosphate boosts acclimatization in rats exposed to acute hypobaric hypoxia: assessment of haematological and metabolic effects.

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Sonam Chawla

Full Text Available The physiological challenges posed by hypobaric hypoxia warrant exploration of pharmacological entities to improve acclimatization to hypoxia. The present study investigates the preclinical efficacy of sphingosine-1-phosphate (S1P to improve acclimatization to simulated hypobaric hypoxia.Efficacy of intravenously administered S1P in improving haematological and metabolic acclimatization was evaluated in rats exposed to simulated acute hypobaric hypoxia (7620 m for 6 hours following S1P pre-treatment for three days.Altitude exposure of the control rats caused systemic hypoxia, hypocapnia (plausible sign of hyperventilation and respiratory alkalosis due to suboptimal renal compensation indicated by an overt alkaline pH of the mixed venous blood. This was associated with pronounced energy deficit in the hepatic tissue along with systemic oxidative stress and inflammation. S1P pre-treatment improved blood oxygen-carrying-capacity by increasing haemoglobin, haematocrit, and RBC count, probably as an outcome of hypoxia inducible factor-1α mediated erythropoiesis and renal S1P receptor 1 mediated haemoconcentation. The improved partial pressure of oxygen in the blood could further restore aerobic respiration and increase ATP content in the hepatic tissue of S1P treated animals. S1P could also protect the animals from hypoxia mediated oxidative stress and inflammation.The study findings highlight S1P's merits as a preconditioning agent for improving acclimatization to acute hypobaric hypoxia exposure. The results may have long term clinical application for improving physiological acclimatization of subjects venturing into high altitude for occupational or recreational purposes.

Complicated pregnancies in inherited distal renal tubular acidosis: importance of acid-base balance.

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Seeger, Harald; Salfeld, Peter; Eisel, Rüdiger; Wagner, Carsten A; Mohebbi, Nilufar

2017-06-01

Inherited distal renal tubular acidosis (dRTA) is caused by impaired urinary acid excretion resulting in hyperchloremic metabolic acidosis. Although the glomerular filtration rate (GFR) is usually preserved, and hypertension and overt proteinuria are absent, it has to be considered that patients with dRTA also suffer from chronic kidney disease (CKD) with an increased risk for adverse pregnancy-related outcomes. Typical complications of dRTA include severe hypokalemia leading to cardiac arrhythmias and paralysis, nephrolithiasis and nephrocalcinosis. Several physiologic changes occur in normal pregnancy including alterations in acid-base and electrolyte homeostasis as well as in GFR. However, data on pregnancy in women with inherited dRTA are scarce. We report the course of pregnancy in three women with hereditary dRTA. Complications observed were severe metabolic acidosis, profound hypokalemia aggravated by hyperemesis gravidarum, recurrent urinary tract infection (UTI) and ureteric obstruction leading to renal failure. However, the outcome of all five pregnancies (1 pregnancy each for mothers n. 1 and 2; 3 pregnancies for mother n. 3) was excellent due to timely interventions. Our findings highlight the importance of close nephrologic monitoring of women with inherited dRTA during pregnancy. In addition to routine assessment of creatinine and proteinuria, caregivers should especially focus on acid-base status, plasma potassium and urinary tract infections. Patients should be screened for renal obstruction in the case of typical symptoms, UTI or renal failure. Furthermore, genetic identification of the underlying mutation may (a) support early nephrologic referral during pregnancy and a better management of the affected woman, and (b) help to avoid delayed diagnosis and reduce complications in affected newborns.

Mujer joven con diarrea crónica

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María Vares González

2013-12-01

Chronic diarrhea is frequent. The causes are multiple, so reaching the definitive diagnosis can be complex. The diagnostic delay can be deadly. We describe the case of a young woman who developed severe hypokalemia secondary to VIPoma, neuroendocrine tumor secreting vasoactive intestinal peptide, a hormone responsible for the clinical: watery diarrhea, hypokalemia and achlorhydria

Hyperchloremia – Why and how

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Glenn T. Nagami

2016-07-01

Full Text Available Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.

A case of Pseudo-Bartter syndrome

International Nuclear Information System (INIS)

Yang, Ik; Choi, Bo Whan; Lee, Yul; Chung, Soo Young

1994-01-01

Pseudo-Bartter Syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patients with clinically proved Pseudo-Bartter syndrome. The patient was a 37 year old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. T1-weighted MRI revealed indistinct corticomedullary differentiation

A case of Pseudo-Bartter syndrome

Energy Technology Data Exchange (ETDEWEB)

Yang, Ik; Choi, Bo Whan; Lee, Yul; Chung, Soo Young [College of Medicine, Hallym University, Seoul (Korea, Republic of)

1994-10-15

Pseudo-Bartter Syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patients with clinically proved Pseudo-Bartter syndrome. The patient was a 37 year old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. T1-weighted MRI revealed indistinct corticomedullary differentiation.

[Clinical case of the month. Renovascular arterial hypertension complicated by diabetes insipidus: report of a case and review of the literature].

Science.gov (United States)

Feloni, S; Radermacher, L; Remy, C; Jousten, J; Corman, V

2013-01-01

Mrs. A, a 62 year old patient with a history of hypertension, polyuria and polydipsia is hospitalized after a malaise. A severe hypokalemia, which is the cause of the polyuria and polydipsia, is discovered. The presence of hypertension and hypokalemia arises suspicion of a primary hyperaldosteronism and the plasma levels of renin and aldosterone are measured. Elevated aldosterone levels are combined with high plasma renin concentrations which permits to rule out primary hyperaldosteronism. Further explorations reveal a subocclusive ostial stenosis of the right renal artery. A treatment by sartan is instaured, which allows arterial pressure control and kalemia normalization. Chronic hypokalemia can be the cause of tubular nephropathy manifested by nephrogenic diabetes insipidus.

Variability of Acid-Base Status in Acetate-Free Biofiltration 84% versus Bicarbonate Dialysis

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Harzallah Kais

2008-01-01

Full Text Available The ultimate goal of hemodialysis (HD treatment is to achieve the highest level of efficacy in the presence of maximal clinical tolerance. With an aim to offer good hemodynamic stability, as observed during the acetate-free biofiltration 14% (AFB 14% to patients who are intolerant to bicarbonate dialysis (BD and with less cost, we have developed since June 1994, a new HD technique, namely AFB 84%. This study was carried out to analyze acid-base variations during the AFB 84% in comparison to BD in hemodynamically stable patients on regular HD. This was a prospective randomized crossover study carried out on 12 patients (6 males and 6 females for a total of 144 HD sessions (72 BD and 72 AFB 84%. Patients with decompensated cardiomyopathy, respiratory diseases or uncontrolled hypertension were not included in the trial. All the patients were treated with BD or AFB 84%; the latter is characterized by the absence of acetate in the dialysate and a complete correction of buffer balance by post-dilutional infusion of bicarbonate-based replacement solution. The comparison of pre-dialysis arterial acid-base and blood-gas parameters revealed no significant differences of pH, HCO 3 - and paCO 2 levels between the two techniques. Analysis of post-dialysis parameters showed that, among patients dialyzed with BD, there was over correction of metabolic acidosis with a tendency towards metabolic alkalosis. In contrast, in patients dialyzed with AFB 84%, we observed a significant improvement in pH and HCO 3 - levels but the increase in paCO2 level was not significant. A comparison of these parameters between the two techniques showed statistically significant difference in pH, HCO3 - and paCO2 levels, but not for paO2 level. AFB 84% can offer some important advantages with the complete absence of acetate from the substitution fluids, and permits a better correction of metabolic acidosis than BD, without causing alkalosis.

Pattern of acid base abnormalities in critically ill patinets

International Nuclear Information System (INIS)

Ahmad, T.M.; Mehmood, A.; Malik, T.M.

2015-01-01

To find out the pattern of acid base abnormalities in critically ill patients in a tertiary care health facility. Study Design: A descriptive study. Place and Duration of Study: The study was carried out in the department of pathology, Combined Military Hospital Kharian from January 2013 to June 2013. Patients and Methods: Two hundred and fifty patients suffering from various diseases and presenting with exacerbation of their clinical conditions were studied. These patients were hospitalized and managed in acute care units of the hospital. Arterial blood gases were analysed to detect acid base status and their correlation with their clinical condition. Concomitant analysis of electrolytes was carried out. Tests related to concurrent illnesses e.g. renal and liver function tests, cardiac enzymes and plasma glucose were assayed by routine end point and kinetic methods. Standard reference materials were used to ensure internal quantify control of analyses. Results: Two hundred and fifteen patients out of 250 studied suffered from acid base disorders. Gender distribution showed a higher percentage of male patients and the mean age was 70.5 ± 17.4 years. Double acid base disorders were the commonest disorders (34%) followed by metabolic acidosis (30%). Anion gap was calculated to further stratify metabolic acidosis and cases of diabetic ketoacidosis were the commonest in this category (47%). Other simple acid base disorders were relatively less frequent. Delta bicarbonate was calculated to unmask the superimposition of respiratory alkalosis or acidosis with metabolic acidosis and metabolic alkalosis. Though triple acid base disorders were noted in a small percentage of cases (05%), but were found to be the most complicated and challenging. Mixed acid base disorders were associated with high mortality. Conclusion: A large number of critically ill patients manifested acid base abnormalities over the full spectrum of these disorders. Mixed acid base disorders were

Metabolic cartography: experimental quantification of metabolic fluxes from isotopic labelling studies.

Science.gov (United States)

O'Grady, John; Schwender, Jörg; Shachar-Hill, Yair; Morgan, John A

2012-03-01

For the past decade, flux maps have provided researchers with an in-depth perspective on plant metabolism. As a rapidly developing field, significant headway has been made recently in computation, experimentation, and overall understanding of metabolic flux analysis. These advances are particularly applicable to the study of plant metabolism. New dynamic computational methods such as non-stationary metabolic flux analysis are finding their place in the toolbox of metabolic engineering, allowing more organisms to be studied and decreasing the time necessary for experimentation, thereby opening new avenues by which to explore the vast diversity of plant metabolism. Also, improved methods of metabolite detection and measurement have been developed, enabling increasingly greater resolution of flux measurements and the analysis of a greater number of the multitude of plant metabolic pathways. Methods to deconvolute organelle-specific metabolism are employed with increasing effectiveness, elucidating the compartmental specificity inherent in plant metabolism. Advances in metabolite measurements have also enabled new types of experiments, such as the calculation of metabolic fluxes based on (13)CO(2) dynamic labelling data, and will continue to direct plant metabolic engineering. Newly calculated metabolic flux maps reveal surprising and useful information about plant metabolism, guiding future genetic engineering of crops to higher yields. Due to the significant level of complexity in plants, these methods in combination with other systems biology measurements are necessary to guide plant metabolic engineering in the future.

Life-Threatening Hypokalemic Paralysis in a Young Bodybuilder

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Kitty K. T. Cheung

2014-01-01

Full Text Available We report a case of life-threatening hypokalemia in a 28-year-old bodybuilder who presented with sudden onset bilateral lower limbs paralysis few days after his bodybuilding competition. His electrocardiogram (ECG showed typical u-waves due to severe hypokalemia (serum potassium 1.6 mmol/L, reference range (RR 3.5–5.0 mmol/L. He was admitted to the intensive care unit (ICU and was treated with potassium replacement. The patient later admitted that he had exposed himself to weight loss agents of unknown nature, purchased online, and large carbohydrate loads in preparation for the competition. He made a full recovery after a few days and discharged himself from the hospital against medical advice. The severe hypokalemia was thought to be caused by several mechanisms to be discussed in this report. With the ever rising number of new fitness centers recently, the ease of online purchasing of almost any drug, and the increasing numbers of youngsters getting into the bodybuilding arena, clinicians should be able to recognize the possible causes of sudden severe hypokalemia in these patients in order to revert the pathophysiology.

Life-threatening hypokalemic paralysis in a young bodybuilder.

Science.gov (United States)

Cheung, Kitty K T; So, Wing-Yee; Kong, Alice P S; Ma, Ronald C W; Chow, Francis C C

2014-01-01

We report a case of life-threatening hypokalemia in a 28-year-old bodybuilder who presented with sudden onset bilateral lower limbs paralysis few days after his bodybuilding competition. His electrocardiogram (ECG) showed typical u-waves due to severe hypokalemia (serum potassium 1.6 mmol/L, reference range (RR) 3.5-5.0 mmol/L). He was admitted to the intensive care unit (ICU) and was treated with potassium replacement. The patient later admitted that he had exposed himself to weight loss agents of unknown nature, purchased online, and large carbohydrate loads in preparation for the competition. He made a full recovery after a few days and discharged himself from the hospital against medical advice. The severe hypokalemia was thought to be caused by several mechanisms to be discussed in this report. With the ever rising number of new fitness centers recently, the ease of online purchasing of almost any drug, and the increasing numbers of youngsters getting into the bodybuilding arena, clinicians should be able to recognize the possible causes of sudden severe hypokalemia in these patients in order to revert the pathophysiology.

Life-Threatening Hypokalemic Paralysis in a Young Bodybuilder

Science.gov (United States)

Cheung, Kitty K. T.; So, Wing-Yee; Kong, Alice P. S.; Ma, Ronald C. W.; Chow, Francis C. C.

2014-01-01

We report a case of life-threatening hypokalemia in a 28-year-old bodybuilder who presented with sudden onset bilateral lower limbs paralysis few days after his bodybuilding competition. His electrocardiogram (ECG) showed typical u-waves due to severe hypokalemia (serum potassium 1.6 mmol/L, reference range (RR) 3.5–5.0 mmol/L). He was admitted to the intensive care unit (ICU) and was treated with potassium replacement. The patient later admitted that he had exposed himself to weight loss agents of unknown nature, purchased online, and large carbohydrate loads in preparation for the competition. He made a full recovery after a few days and discharged himself from the hospital against medical advice. The severe hypokalemia was thought to be caused by several mechanisms to be discussed in this report. With the ever rising number of new fitness centers recently, the ease of online purchasing of almost any drug, and the increasing numbers of youngsters getting into the bodybuilding arena, clinicians should be able to recognize the possible causes of sudden severe hypokalemia in these patients in order to revert the pathophysiology. PMID:24660073

Effect of acute acid-base disturbances on ErbB1/2 tyrosine phosphorylation in rabbit renal proximal tubules.

Science.gov (United States)

Skelton, Lara A; Boron, Walter F

2013-12-15

The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing ∼80% of filtered HCO3(-), the major plasma buffer, into the blood. The PT adapts its rate of HCO3(-) reabsorption (JHCO3(-)) in response to acute acid-base disturbances. Our laboratory previously showed that single isolated perfused PTs adapt JHCO3(-) in response to isolated changes in basolateral (i.e., blood side) CO2 and HCO3(-) concentrations but, surprisingly, not to pH. The response to CO2 concentration can be blocked by the ErbB family tyrosine kinase inhibitor PD-168393. In the present study, we exposed enriched rabbit PT suspensions to five acute acid-base disturbances for 5 and 20 min using a panel of phosphotyrosine (pY)-specific antibodies to determine the influence of each disturbance on pan-pY, ErbB1-specific pY (four sites), and ErbB2-specific pY (two sites). We found that each acid-base treatment generated a distinct temporal pY pattern. For example, the summated responses of the individual ErbB1/2-pY sites to each disturbance showed that metabolic acidosis (normal CO2 concentration and reduced HCO3(-) concentration) produced a transient summated pY decrease (5 vs. 20 min), whereas metabolic alkalosis produced a transient increase. Respiratory acidosis (normal HCO3(-) concentration and elevated CO2 concentration) had little effect on summated pY at 5 min but produced an elevation at 20 min, whereas respiratory alkalosis produced a reduction at 20 min. Our data show that ErbB1 and ErbB2 in the PT respond to acute acid-base disturbances, consistent with the hypothesis that they are part of the signaling cascade.

What is Metabolic Syndrome?

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... Intramural Research Home / Metabolic Syndrome Metabolic Syndrome Also known as What Is Metabolic syndrome ... metabolic risk factors to be diagnosed with metabolic syndrome. Metabolic Risk Factors A Large Waistline Having a large ...

Clinical signs of radiologic pneumonia in under-five hypokalemic diarrheal children admitted to an urban hospital in bangladesh.

Directory of Open Access Journals (Sweden)

Mohammod Jobayer Chisti

Full Text Available BACKGROUND: Clinical signs of pneumonia are often veiled in under-five diarrheal children presenting with hypokalemia, making clinical diagnosis of pneumonia very difficult in such population. However, there is no published report that describes the influences of hypokalemia on the clinical signs of pneumonia in diarrheal children. Our objective was to assess the influences of hypokalemia, and their outcome in such children. METHODS: We prospectively enrolled all under-five diarrheal children (n = 180 admitted to the Special Care Ward of the Dhaka Hospital of icddr,b from September-December 2007 with radiological pneumonia who also had their serum potassium estimated. We compared the clinical features and outcome of the diarrheal children having pneumonia with (cases = 55 and without hypokalemia (controls = 125. RESULTS: The case-fatality among the cases was 2 times higher compared to the controls, but the difference was not statistically significant (p = 0.202. In logistic regression analysis, after adjusting for potential confounders such as age of the patient, clinical dehydration, severe wasting, abnormally sleepy, lower chest wall in-drawing, nasal flaring and inability to drink on admission, under-five diarrheal children with pneumonia who presented with nutritional edema had 3 times more risk to have hypokalemia compared to those without nutritional edema (OR = 2.76, 95% CI = 1.01-7.51 and these hypokalemic children were 64% less likely to present with fast breathing (OR = 0.36, 95% CI = 0.17-0.74. CONCLUSION AND SIGNIFICANCE: The results of our analysis are simple but may have great public health implications and underscore the importance of diligent assessment for pneumonia in under-five diarrheal children having risk of hypokalemia as in children with nutritional edema even in absence of fast breathing, a useful sign of pneumonia. This may help for early initiation of first dose of parental antibiotics

Clinical Signs of Radiologic Pneumonia in Under-Five Hypokalemic Diarrheal Children Admitted to an Urban Hospital in Bangladesh

Science.gov (United States)

Chisti, Mohammod Jobayer; Salam, Mohammed Abdus; Ashraf, Hasan; Faruque, Abu S. G.; Bardhan, Pradip Kumar; Das, Sumon Kumar; Shahunja, K. M.; Shahid, Abu S. M. S. B.; Ahmed, Tahmeed

2013-01-01

Background Clinical signs of pneumonia are often veiled in under-five diarrheal children presenting with hypokalemia, making clinical diagnosis of pneumonia very difficult in such population. However, there is no published report that describes the influences of hypokalemia on the clinical signs of pneumonia in diarrheal children. Our objective was to assess the influences of hypokalemia, and their outcome in such children. Methods We prospectively enrolled all under-five diarrheal children (n = 180) admitted to the Special Care Ward of the Dhaka Hospital of icddr,b from September-December 2007 with radiological pneumonia who also had their serum potassium estimated. We compared the clinical features and outcome of the diarrheal children having pneumonia with (cases = 55) and without hypokalemia (controls = 125). Results The case-fatality among the cases was 2 times higher compared to the controls, but the difference was not statistically significant (p = 0.202). In logistic regression analysis, after adjusting for potential confounders such as age of the patient, clinical dehydration, severe wasting, abnormally sleepy, lower chest wall in-drawing, nasal flaring and inability to drink on admission, under-five diarrheal children with pneumonia who presented with nutritional edema had 3 times more risk to have hypokalemia compared to those without nutritional edema (OR = 2.76, 95% CI = 1.01–7.51) and these hypokalemic children were 64% less likely to present with fast breathing (OR = 0.36, 95% CI = 0.17–0.74). Conclusion and significance The results of our analysis are simple but may have great public health implications and underscore the importance of diligent assessment for pneumonia in under-five diarrheal children having risk of hypokalemia as in children with nutritional edema even in absence of fast breathing, a useful sign of pneumonia. This may help for early initiation of first dose of parental antibiotics along with

Metabolism

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... Are More Common in People With Type 1 Diabetes Metabolic Syndrome Your Child's Weight Healthy Eating Endocrine System Blood Test: Basic Metabolic Panel (BMP) Activity: Endocrine System Growth Disorders Diabetes Center Thyroid Disorders Your Endocrine System Movie: Endocrine ...

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise.

Science.gov (United States)

Hilbert, M; Shushakov, V; Maassen, N

2012-02-01

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO(2) rebreathing, alkalosis by hyperventilation, or control. The Pco(2), pH, K(+) concentration ([K(+)]), and Na(+) concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis (P alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition (P Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.

Giant U waves: an important clinical clue

Directory of Open Access Journals (Sweden)

Verma N

2011-04-01

Full Text Available Nitin Verma, Vincent M Figueredo, Allan M Greenspan, Gregg S PressmanAlbert Einstein Medical Center, Philadelphia, PA, USAAbstract: Electrocardiographic U waves are a common clinical finding, and yet are poorly understood by many physicians. They can be seen in many clinical conditions, most importantly hypokalemia and ischemic heart disease. Over the years, many theories have been put forth to explain their origin. While still not completely understood, it now appears that mechanoelectrical interactions are responsible for normal U waves. Pathologic U waves may be seen in ischemic heart disease where they sometimes point to acute ischemic events. The large U waves of hypokalemia are most likely not true U waves but rather the terminal deflection in a bifid T wave.Keywords: U waves, hypokalemia, myocardial ischemia, electrocardiogram

Episodic seasonal Pseudo-Bartter syndrome in cystic fibrosis.

Science.gov (United States)

Kintu, Brett; Brightwell, Alex

2014-06-01

Pseudo-Bartter syndrome (PBS) describes an uncommon but well recognised complication of cystic fibrosis leading to hypochloraemic, hypokalaemic metabolic alkalosis. Pseudo-Bartter syndrome is usually seen at initial presentation or within the first two years of life in children with cystic fibrosis. Risk factors for development of PBS include warm weather conditions, severe respiratory or pancreatic disease and gastrointestinal losses (e.g. vomiting and diarrhoea). PBS is rare in older children and adolescents although epidemics have been associated with heat wave conditions in warmer climates. In this era of climate change, it is crucial that clinicians consider Pseudo-Bartter syndrome when patients with cystic fibrosis present unwell during summer. Copyright © 2014 Elsevier Ltd. All rights reserved.

A Basic Therapy Gone Awry.

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Galinko, Laura B; Hsu, Steven H; Gauran, Cosmin; Fingerhood, Michael L; Pastores, Stephen M; Halpern, Neil A; Chawla, Sanjay

2017-11-01

Baking soda (sodium bicarbonate) is a common household item that has gained popularity as an alternative cancer treatment. Some have speculated that alkali therapy neutralizes the extracellular acidity of tumor cells that promotes metastases. Internet blogs have touted alkali as a safe and natural alternative to chemotherapy that targets cancer cells without systemic effects. Sodium bicarbonate overdose is uncommon, with few reports of toxic effects in humans. The case described here is the first reported case of severe metabolic alkalosis related to topical use of sodium bicarbonate as a treatment for cancer. This case highlights how a seemingly benign and readily available product can have potentially lethal consequences. ©2017 American Association of Critical-Care Nurses.

Idiopathic Fanconi's syndrome with nephrogenic diabetes insipidus in a child who presented as vitamin D resistant rickets--a case report and review of literature.

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Patra, Soumya; Nadri, Gulnaz; Chowdhary, Harish; Pemde, Harish K; Singh, Varinder; Chandra, Jagdish

2011-01-01

Fanconi's syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycemic glycosuria, tubular proteinuria without hematuria, metabolic acidosis without anion gap and excessive urinary excretion of phosphorous, calcium, uric acid, bicarbonate, sodium, potassium and magnesium. Diabetes insipidus is a disease of collecting tubules and a child mainly presents with dehydration and hypernatremia. We report the first case of idiopathic Fanconi's syndrome along with nephrogenic diabetes insipidus (NDI) in a child who presented to us as resistant rickets. Medline search did not reveal any case of nephrogenic diabetes insipidus associated with idiopathic Fanconi's syndrome. We hypothesized that the NDI may be due to severe hypokalemia induced tubular dysfunction. The child was treated for hypophosphatemic rickets with severe metabolic acidosis and the treatment for NDI was also given. Now he has healed rickets and normal blood pH, sodium and osmolarity.

Modeling of Zymomonas mobilis central metabolism for novel metabolic engineering strategies.

Science.gov (United States)

Kalnenieks, Uldis; Pentjuss, Agris; Rutkis, Reinis; Stalidzans, Egils; Fell, David A

2014-01-01

Mathematical modeling of metabolism is essential for rational metabolic engineering. The present work focuses on several types of modeling approach to quantitative understanding of central metabolic network and energetics in the bioethanol-producing bacterium Zymomonas mobilis. Combined use of Flux Balance, Elementary Flux Mode, and thermodynamic analysis of its central metabolism, together with dynamic modeling of the core catabolic pathways, can help to design novel substrate and product pathways by systematically analyzing the solution space for metabolic engineering, and yields insights into the function of metabolic network, hardly achievable without applying modeling tools.

Metabolism

Science.gov (United States)

... lin), which signals cells to increase their anabolic activities. Metabolism is a complicated chemical process, so it's not ... how those enzymes or hormones work. When the metabolism of body chemicals is ... Hyperthyroidism (pronounced: hi-per-THIGH-roy-dih-zum). Hyperthyroidism ...

Uncovering transcriptional regulation of metabolism by using metabolic network topology

DEFF Research Database (Denmark)

Patil, Kiran Raosaheb; Nielsen, Jens

2005-01-01

in the metabolic network that follow a common transcriptional response. Thus, the algorithm enables identification of so-called reporter metabolites (metabolites around which the most significant transcriptional changes occur) and a set of connected genes with significant and coordinated response to genetic......Cellular response to genetic and environmental perturbations is often reflected and/or mediated through changes in the metabolism, because the latter plays a key role in providing Gibbs free energy and precursors for biosynthesis. Such metabolic changes are often exerted through transcriptional...... therefore developed an algorithm that is based on hypothesis-driven data analysis to uncover the transcriptional regulatory architecture of metabolic networks. By using information on the metabolic network topology from genome-scale metabolic reconstruction, we show that it is possible to reveal patterns...

[Metabolic acidosis].

Science.gov (United States)

Regolisti, Giuseppe; Fani, Filippo; Antoniotti, Riccardo; Castellano, Giuseppe; Cremaschi, Elena; Greco, Paolo; Parenti, Elisabetta; Morabito, Santo; Sabatino, Alice; Fiaccadori, Enrico

2016-01-01

Metabolic acidosis is frequently observed in clinical practice, especially among critically ill patients and/or in the course of renal failure. Complex mechanisms are involved, in most cases identifiable by medical history, pathophysiology-based diagnostic reasoning and measure of some key acid-base parameters that are easily available or calculable. On this basis the bedside differential diagnosis of metabolic acidosis should be started from the identification of the two main subtypes of metabolic acidosis: the high anion gap metabolic acidosis and the normal anion gap (or hyperchloremic) metabolic acidosis. Metabolic acidosis, especially in its acute forms with elevated anion gap such as is the case of lactic acidosis, diabetic and acute intoxications, may significantly affect metabolic body homeostasis and patients hemodynamic status, setting the stage for true medical emergencies. The therapeutic approach should be first aimed at early correction of concurrent clinical problems (e.g. fluids and hemodynamic optimization in case of shock, mechanical ventilation in case of concomitant respiratory failure, hemodialysis for acute intoxications etc.), in parallel to the formulation of a diagnosis. In case of severe acidosis, the administration of alkalizing agents should be carefully evaluated, taking into account the risk of side effects, as well as the potential need of renal replacement therapy.

Warfighter Physiological and Environmental Monitoring: A Study for the U.S. Army Research Institute in Environmental Medicine and the Soldier Systems Center

Science.gov (United States)

2004-11-01

should scale accordingly. Any deviation from this ratio would result in either respiratory alkalosis (minute rate too high) or acidosis (minute rate too...low). In combat situations, hyperventilation may occur, and thus some degree of respiratory alkalosis is expected. If the minute rate were to fall...Derived information including a. Blood volume b. Blunt trauma events and localization c. Burn trauma events and localization d. Respiratory distress

Pulmonary metabolism of foreign compounds: Its role in metabolic activation

International Nuclear Information System (INIS)

Cohen, G.M.

1990-01-01

The lung has the potential of metabolizing many foreign chemicals to a vast array of metabolites with different pharmacological and toxicological properties. Because many chemicals require metabolic activation in order to exert their toxicity, the cellular distribution of the drug-metabolizing enzymes in a heterogeneous tissue, such as the lung, and the balance of metabolic activation and deactivation pathways in any particular cell are key factors in determining the cellular specificity of many pulmonary toxins. Environmental factors such as air pollution, cigarette smoking, and diet markedly affect the pulmonary metabolism of some chemicals and, thereby, possibly affect their toxicity

Global Metabolic Reconstruction and Metabolic Gene Evolution in the Cattle Genome

Science.gov (United States)

Kim, Woonsu; Park, Hyesun; Seo, Seongwon

2016-01-01

The sequence of cattle genome provided a valuable opportunity to systematically link genetic and metabolic traits of cattle. The objectives of this study were 1) to reconstruct genome-scale cattle-specific metabolic pathways based on the most recent and updated cattle genome build and 2) to identify duplicated metabolic genes in the cattle genome for better understanding of metabolic adaptations in cattle. A bioinformatic pipeline of an organism for amalgamating genomic annotations from multiple sources was updated. Using this, an amalgamated cattle genome database based on UMD_3.1, was created. The amalgamated cattle genome database is composed of a total of 33,292 genes: 19,123 consensus genes between NCBI and Ensembl databases, 8,410 and 5,493 genes only found in NCBI or Ensembl, respectively, and 266 genes from NCBI scaffolds. A metabolic reconstruction of the cattle genome and cattle pathway genome database (PGDB) was also developed using Pathway Tools, followed by an intensive manual curation. The manual curation filled or revised 68 pathway holes, deleted 36 metabolic pathways, and added 23 metabolic pathways. Consequently, the curated cattle PGDB contains 304 metabolic pathways, 2,460 reactions including 2,371 enzymatic reactions, and 4,012 enzymes. Furthermore, this study identified eight duplicated genes in 12 metabolic pathways in the cattle genome compared to human and mouse. Some of these duplicated genes are related with specific hormone biosynthesis and detoxifications. The updated genome-scale metabolic reconstruction is a useful tool for understanding biology and metabolic characteristics in cattle. There has been significant improvements in the quality of cattle genome annotations and the MetaCyc database. The duplicated metabolic genes in the cattle genome compared to human and mouse implies evolutionary changes in the cattle genome and provides a useful information for further research on understanding metabolic adaptations of cattle. PMID

[Comparative studies on toxicity of various dielectrics, petroleum derivatives, used in electroerosion technology. IV. Morphological and cytoenzymatic changes in the lungs and acid-base imbalance in rats chronically exposed to petroleum hydrocarbons].

Science.gov (United States)

Starek, A; Kamiński, M

1981-01-01

In rats exposed to odourless kerosene of 75 and 300 mg/m3 concentration, for 14 weeks, morphologic and cytoenzymatic examinations of lungs have been carried out and acid-base equilibrium indices in blood have been determined. Passive congestion of lung parenchyma, subpleural blood extravasation, atelectasis foci, thickened interalveolar septa with infiltrates from neutrophils, lymphocytes, eosinophils and macrophages have been found. In addition a decrease in succinic dehydrogenase activity, NADPH -- tetrazolium reductase, and Mg++-ATP-ase and increase in acid phosphatase activity have been revealed. Those have been focal changes, involving, apart from bronchial tree (low exposure -- 75 mg/m3), the remaining lung parenchyma segments (high exposure -- 300 mg/m3). In addition, disturbances in acid-base equilibrium in form of compensated metabolic alkalosis (75 mg/m3) and compensated metabolic acidosis (300 mg/m3) have occurred. The obtained results demonstrate toxic effects of kerosene hydrocarbons on the function and structure of lungs.

Precision metabolic engineering: The design of responsive, selective, and controllable metabolic systems.

Science.gov (United States)

McNerney, Monica P; Watstein, Daniel M; Styczynski, Mark P

2015-09-01

Metabolic engineering is generally focused on static optimization of cells to maximize production of a desired product, though recently dynamic metabolic engineering has explored how metabolic programs can be varied over time to improve titer. However, these are not the only types of applications where metabolic engineering could make a significant impact. Here, we discuss a new conceptual framework, termed "precision metabolic engineering," involving the design and engineering of systems that make different products in response to different signals. Rather than focusing on maximizing titer, these types of applications typically have three hallmarks: sensing signals that determine the desired metabolic target, completely directing metabolic flux in response to those signals, and producing sharp responses at specific signal thresholds. In this review, we will first discuss and provide examples of precision metabolic engineering. We will then discuss each of these hallmarks and identify which existing metabolic engineering methods can be applied to accomplish those tasks, as well as some of their shortcomings. Ultimately, precise control of metabolic systems has the potential to enable a host of new metabolic engineering and synthetic biology applications for any problem where flexibility of response to an external signal could be useful. Copyright © 2015 International Metabolic Engineering Society. Published by Elsevier Inc. All rights reserved.

Metabolic learning and memory formation by the brain influence systemic metabolic homeostasis

Science.gov (United States)

Zhang, Yumin; Liu, Gang; Yan, Jingqi; Zhang, Yalin; Li, Bo; Cai, Dongsheng

2015-01-01

Metabolic homeostasis is regulated by the brain, whether this regulation involves learning and memory of metabolic information remains unexplored. Here we use a calorie-based, taste-independent learning/memory paradigm to show that Drosophila form metabolic memories that help balancing food choice with caloric intake; however, this metabolic learning or memory is lost under chronic high-calorie feeding. We show that loss of individual learning/memory-regulating genes causes a metabolic learning defect, leading to elevated trehalose and lipids levels. Importantly, this function of metabolic learning requires not only the mushroom body but the hypothalamus-like pars intercerebralis, while NF-κB activation in the pars intercerebralis mimics chronic overnutrition in that it causes metabolic learning impairment and disorders. Finally, we evaluate this concept of metabolic learning/memory in mice, suggesting the hypothalamus is involved in a form of nutritional learning and memory, which is critical for determining resistance or susceptibility to obesity. In conclusion, our data indicate the brain, and potentially the hypothalamus, direct metabolic learning and the formation of memories, which contribute to the control of systemic metabolic homeostasis. PMID:25848677

Engineering Cellular Metabolism

DEFF Research Database (Denmark)

Nielsen, Jens; Keasling, Jay

2016-01-01

Metabolic engineering is the science of rewiring the metabolism of cells to enhance production of native metabolites or to endow cells with the ability to produce new products. The potential applications of such efforts are wide ranging, including the generation of fuels, chemicals, foods, feeds...... of metabolic engineering and will discuss how new technologies can enable metabolic engineering to be scaled up to the industrial level, either by cutting off the lines of control for endogenous metabolism or by infiltrating the system with disruptive, heterologous pathways that overcome cellular regulation....

Actionable Metabolic Pathways in Heart Failure and Cancer—Lessons From Cancer Cell Metabolism

Directory of Open Access Journals (Sweden)

Anja Karlstaedt

2018-06-01

Full Text Available Recent advances in cancer cell metabolism provide unprecedented opportunities for a new understanding of heart metabolism and may offer new approaches for the treatment of heart failure. Key questions driving the cancer field to understand how tumor cells reprogram metabolism and to benefit tumorigenesis are also applicable to the heart. Recent experimental and conceptual advances in cancer cell metabolism provide the cardiovascular field with the unique opportunity to target metabolism. This review compares cancer cell metabolism and cardiac metabolism with an emphasis on strategies of cellular adaptation, and how to exploit metabolic changes for therapeutic benefit.

Carbohydrate Metabolism Disorders

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... metabolic disorder, something goes wrong with this process. Carbohydrate metabolism disorders are a group of metabolic disorders. Normally your enzymes break carbohydrates down into glucose (a type of sugar). If ...

Annual Progress Report, Fiscal Year 1982.

Science.gov (United States)

1982-10-01

incompletely compensated respiratory alkalosis . This condition is accompanied ’ an increase in the excretion of urinary bicarbonate and an elevation of urinary...interfering with the respiratory alkalosis which develops at altitude or by altering the chemical environment of the working muscles. In one study...Orthopedic (32.9%); Respiratory Infection (17.19%); Dermatological (9.4%); Ear, Eye, Nose and Throat (9.4%); Gastrointestinal (7.5); and Adverse Weather Injry

Metabolic learning and memory formation by the brain influence systemic metabolic homeostasis.

Science.gov (United States)

Zhang, Yumin; Liu, Gang; Yan, Jingqi; Zhang, Yalin; Li, Bo; Cai, Dongsheng

2015-04-07

Metabolic homeostasis is regulated by the brain, but whether this regulation involves learning and memory of metabolic information remains unexplored. Here we use a calorie-based, taste-independent learning/memory paradigm to show that Drosophila form metabolic memories that help in balancing food choice with caloric intake; however, this metabolic learning or memory is lost under chronic high-calorie feeding. We show that loss of individual learning/memory-regulating genes causes a metabolic learning defect, leading to elevated trehalose and lipid levels. Importantly, this function of metabolic learning requires not only the mushroom body but also the hypothalamus-like pars intercerebralis, while NF-κB activation in the pars intercerebralis mimics chronic overnutrition in that it causes metabolic learning impairment and disorders. Finally, we evaluate this concept of metabolic learning/memory in mice, suggesting that the hypothalamus is involved in a form of nutritional learning and memory, which is critical for determining resistance or susceptibility to obesity. In conclusion, our data indicate that the brain, and potentially the hypothalamus, direct metabolic learning and the formation of memories, which contribute to the control of systemic metabolic homeostasis.

Animal metabolism

International Nuclear Information System (INIS)

Walburg, H.E.

1977-01-01

Studies on placental transport included the following: clearance of tritiated water as a baseline measurement for transport of materials across perfused placentas; transport of organic and inorganic mercury across the perfused placenta of the guinea pig in late gestation; and transport of cadmium across the perfused placenta of the guinea pig in late gestation. Studies on cadmium absorption and metabolism included the following: intestinal absorption and retention of cadmium in neonatal rats; uptake and distribution of an oral dose of cadmium in postweanling male and female, iron-deficient and normal rats; postnatal viability and growth in rat pups after oral cadmium administration during gestation; and the effect of calcium and phosphorus on the absorption and toxicity of cadmium. Studies on gastrointestinal absorption and mineral metabolism included: uptake and distribution of orally administered plutonium complex compounds in male mice; gastrointestinal absorption of 144 Ce in the newborn mouse, rat, and pig; and gastrointestinal absorption of 95 Nb by rats of different ages. Studies on iodine metabolism included the following: influence of thyroid status and thiocyanate on iodine metabolism in the bovine; effects of simulated fallout radiation on iodine metabolism in dairy cattle; and effects of feeding iodine binding agents on iodine metabolism in the calf

Metabolic Myopathies.

Science.gov (United States)

Tarnopolsky, Mark A

2016-12-01

Metabolic myopathies are genetic disorders that impair intermediary metabolism in skeletal muscle. Impairments in glycolysis/glycogenolysis (glycogen-storage disease), fatty acid transport and oxidation (fatty acid oxidation defects), and the mitochondrial respiratory chain (mitochondrial myopathies) represent the majority of known defects. The purpose of this review is to develop a diagnostic and treatment algorithm for the metabolic myopathies. The metabolic myopathies can present in the neonatal and infant period as part of more systemic involvement with hypotonia, hypoglycemia, and encephalopathy; however, most cases present in childhood or in adulthood with exercise intolerance (often with rhabdomyolysis) and weakness. The glycogen-storage diseases present during brief bouts of high-intensity exercise, whereas fatty acid oxidation defects and mitochondrial myopathies present during a long-duration/low-intensity endurance-type activity or during fasting or another metabolically stressful event (eg, surgery, fever). The clinical examination is often normal between acute events, and evaluation involves exercise testing, blood testing (creatine kinase, acylcarnitine profile, lactate, amino acids), urine organic acids (ketones, dicarboxylic acids, 3-methylglutaconic acid), muscle biopsy (histology, ultrastructure, enzyme testing), MRI/spectroscopy, and targeted or untargeted genetic testing. Accurate and early identification of metabolic myopathies can lead to therapeutic interventions with lifestyle and nutritional modification, cofactor treatment, and rapid treatment of rhabdomyolysis.

Microalgal Metabolic Network Model Refinement through High-Throughput Functional Metabolic Profiling

International Nuclear Information System (INIS)

Chaiboonchoe, Amphun; Dohai, Bushra Saeed; Cai, Hong; Nelson, David R.; Jijakli, Kenan; Salehi-Ashtiani, Kourosh

2014-01-01

Metabolic modeling provides the means to define metabolic processes at a systems level; however, genome-scale metabolic models often remain incomplete in their description of metabolic networks and may include reactions that are experimentally unverified. This shortcoming is exacerbated in reconstructed models of newly isolated algal species, as there may be little to no biochemical evidence available for the metabolism of such isolates. The phenotype microarray (PM) technology (Biolog, Hayward, CA, USA) provides an efficient, high-throughput method to functionally define cellular metabolic activities in response to a large array of entry metabolites. The platform can experimentally verify many of the unverified reactions in a network model as well as identify missing or new reactions in the reconstructed metabolic model. The PM technology has been used for metabolic phenotyping of non-photosynthetic bacteria and fungi, but it has not been reported for the phenotyping of microalgae. Here, we introduce the use of PM assays in a systematic way to the study of microalgae, applying it specifically to the green microalgal model species Chlamydomonas reinhardtii. The results obtained in this study validate a number of existing annotated metabolic reactions and identify a number of novel and unexpected metabolites. The obtained information was used to expand and refine the existing COBRA-based C. reinhardtii metabolic network model iRC1080. Over 254 reactions were added to the network, and the effects of these additions on flux distribution within the network are described. The novel reactions include the support of metabolism by a number of d-amino acids, l-dipeptides, and l-tripeptides as nitrogen sources, as well as support of cellular respiration by cysteamine-S-phosphate as a phosphorus source. The protocol developed here can be used as a foundation to functionally profile other microalgae such as known microalgae mutants and novel isolates.

Microalgal Metabolic Network Model Refinement through High-Throughput Functional Metabolic Profiling

Energy Technology Data Exchange (ETDEWEB)

Chaiboonchoe, Amphun; Dohai, Bushra Saeed; Cai, Hong; Nelson, David R. [Division of Science and Math, New York University Abu Dhabi, Abu Dhabi (United Arab Emirates); Center for Genomics and Systems Biology (CGSB), New York University Abu Dhabi Institute, Abu Dhabi (United Arab Emirates); Jijakli, Kenan [Division of Science and Math, New York University Abu Dhabi, Abu Dhabi (United Arab Emirates); Center for Genomics and Systems Biology (CGSB), New York University Abu Dhabi Institute, Abu Dhabi (United Arab Emirates); Engineering Division, Biofinery, Manhattan, KS (United States); Salehi-Ashtiani, Kourosh, E-mail: ksa3@nyu.edu [Division of Science and Math, New York University Abu Dhabi, Abu Dhabi (United Arab Emirates); Center for Genomics and Systems Biology (CGSB), New York University Abu Dhabi Institute, Abu Dhabi (United Arab Emirates)

2014-12-10

Metabolic modeling provides the means to define metabolic processes at a systems level; however, genome-scale metabolic models often remain incomplete in their description of metabolic networks and may include reactions that are experimentally unverified. This shortcoming is exacerbated in reconstructed models of newly isolated algal species, as there may be little to no biochemical evidence available for the metabolism of such isolates. The phenotype microarray (PM) technology (Biolog, Hayward, CA, USA) provides an efficient, high-throughput method to functionally define cellular metabolic activities in response to a large array of entry metabolites. The platform can experimentally verify many of the unverified reactions in a network model as well as identify missing or new reactions in the reconstructed metabolic model. The PM technology has been used for metabolic phenotyping of non-photosynthetic bacteria and fungi, but it has not been reported for the phenotyping of microalgae. Here, we introduce the use of PM assays in a systematic way to the study of microalgae, applying it specifically to the green microalgal model species Chlamydomonas reinhardtii. The results obtained in this study validate a number of existing annotated metabolic reactions and identify a number of novel and unexpected metabolites. The obtained information was used to expand and refine the existing COBRA-based C. reinhardtii metabolic network model iRC1080. Over 254 reactions were added to the network, and the effects of these additions on flux distribution within the network are described. The novel reactions include the support of metabolism by a number of d-amino acids, l-dipeptides, and l-tripeptides as nitrogen sources, as well as support of cellular respiration by cysteamine-S-phosphate as a phosphorus source. The protocol developed here can be used as a foundation to functionally profile other microalgae such as known microalgae mutants and novel isolates.

Two-Scale 13C Metabolic Flux Analysis for Metabolic Engineering.

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Ando, David; Garcia Martin, Hector

2018-01-01

Accelerating the Design-Build-Test-Learn (DBTL) cycle in synthetic biology is critical to achieving rapid and facile bioengineering of organisms for the production of, e.g., biofuels and other chemicals. The Learn phase involves using data obtained from the Test phase to inform the next Design phase. As part of the Learn phase, mathematical models of metabolic fluxes give a mechanistic level of comprehension to cellular metabolism, isolating the principle drivers of metabolic behavior from the peripheral ones, and directing future experimental designs and engineering methodologies. Furthermore, the measurement of intracellular metabolic fluxes is specifically noteworthy as providing a rapid and easy-to-understand picture of how carbon and energy flow throughout the cell. Here, we present a detailed guide to performing metabolic flux analysis in the Learn phase of the DBTL cycle, where we show how one can take the isotope labeling data from a 13 C labeling experiment and immediately turn it into a determination of cellular fluxes that points in the direction of genetic engineering strategies that will advance the metabolic engineering process.For our modeling purposes we use the Joint BioEnergy Institute (JBEI) Quantitative Metabolic Modeling (jQMM) library, which provides an open-source, python-based framework for modeling internal metabolic fluxes and making actionable predictions on how to modify cellular metabolism for specific bioengineering goals. It presents a complete toolbox for performing different types of flux analysis such as Flux Balance Analysis, 13 C Metabolic Flux Analysis, and it introduces the capability to use 13 C labeling experimental data to constrain comprehensive genome-scale models through a technique called two-scale 13 C Metabolic Flux Analysis (2S- 13 C MFA) [1]. In addition to several other capabilities, the jQMM is also able to predict the effects of knockouts using the MoMA and ROOM methodologies. The use of the jQMM library is

Comprehensive metabolic panel

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Metabolic panel - comprehensive; Chem-20; SMA20; Sequential multi-channel analysis with computer-20; SMAC20; Metabolic panel 20 ... Chernecky CC, Berger BJ. Comprehensive metabolic panel (CMP) - blood. In: ... Tests and Diagnostic Procedures . 6th ed. St Louis, MO: ...

Apparent mineralocorticoid excess syndrome: report of one family with three affected children.

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Al-Harbi, Taiba; Al-Shaikh, Adnan

2012-01-01

The syndrome of apparent mineralocorticoid excess (AME) is an autosomal recessive disorder characterized by hypertension, hypokalemia, low renin, and hypoaldosteronism. It is caused by deficiency of 11β-hydroxysteroid dehydrogenase, which results in a defect of the peripheral metabolism of cortisol to cortisone. As a consequence, the serum cortisol half-life (T½) is prolonged, ACTH is suppressed, and serum cortisol concentration is normal. The hormonal diagnosis of the disorder is made by the increased ratio of urine-free cortisol to cortisone. In patients with AME, this ratio is 5-18, while in normal individuals it is syndrome of AME. We report three siblings - two female and one male - with the syndrome of apparent mineralocorticoid excess who presented with hypertension, hypokalemia, low renin, and low aldosterone levels. The finding of abnormally high ratios of 24-h urine-free cortisol to cortisone in our three patients (case 1, 8.4; case 2, 25; and case 3, 7.5) confirmed the diagnosis of apparent mineralocorticoid excess syndrome in these children. They were treated with oral potassium supplements. The addition of spironolactone resulted in a decrease in blood pressure, rise in serum potassium and a gradual increase in plasma renin activity in all three. In this study, the genetic testing of those three siblings with the typical clinical features of AME has detected missense mutation c.662C>T (p.Arg208Cys) in exon 3 of the HSD11B2 gene in the homozygous state.

A young man with polyuria and lethargy.

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Imtiaz, Salman; Qayyum, Shahid; Kafouri, Hala; Al Khoiter, Mohammad; Askar, Akram

2011-07-01

We report a 20-year-old man who presented to our emergency room with a history of polyuria, weakness, constipation, nausea, and vomiting of two months duration. History and clinical examination revealed a significant weight loss and mild hepatomegaly. Laboratory investigations revealed hypokalemia, hypernatremia, and severe metabolic acidosis and anemia. Ultra-sound of the abdomen revealed enlarged kidneys without hydronerphrosis. The patient developed paralysis due to further decline in serum potassium level, which improved after an aggressive fluid and electrolyte management. He was investigated extensively for polyuria and type of acidosis. The kidney biopsy showed interstitial leukemic infiltration. He was managed accordingly and recovered from the condition. This case demonstrates an unusual presentation of a hematological malignancy, which was a diagnostic as well as a management challenge.

Fluoroacetylcarnitine: metabolism and metabolic effects in mitochondria

Energy Technology Data Exchange (ETDEWEB)

Bremer, J; Davis, E J

1973-01-01

The metabolism and metabolic effects of fluoroacetylcarnitine have been investigated. Carnitineacetyltransferase transfers the fluoro-acetyl group of fluoroacetylcarnitine nearly as rapidly to CoA as the acetyl group of acetylcarnitine. Fluorocitrate is then formed by citrate synthase, but this second reaction is relatively slow. The fluorocitrate formed intramitochondrially inhibits the metabolism of citrate. In heart and skeletal muscle mitochondria the accumulated citrate inhibits citrate synthesis and the ..beta..-oxidation of fatty acids. Free acetate is formed, presumably because accumulated acetyl-CoA is hydrolyzed. In liver mitochondria the accumulation of citrate leads to a relatively increased rate of ketogenesis. Increased ketogenesis is obtained also upon the addition of citrate to the reaction mixture.

Osmolality and respiratory regulation in humans: respiratory compensation for hyperchloremic metabolic acidosis is absent after infusion of hypertonic saline in healthy volunteers.

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Moen, Vibeke; Brudin, Lars; Rundgren, Mats; Irestedt, Lars

2014-10-01

Several animal studies show that changes in plasma osmolality may influence ventilation. Respiratory depression caused by increased plasma osmolality is interpreted as inhibition of water-dependent thermoregulation because conservation of body fluid predominates at the cost of increased core temperature. Respiratory alkalosis, on the other hand, is associated with a decrease in plasma osmolality and strong ion difference (SID) during human pregnancy. We investigated the hypothesis that osmolality would influence ventilation, so that increased osmolality will decrease ventilation and decreased osmolality will stimulate ventilation in both men and women. Our study participants were healthy volunteers of both sexes (ASA physical status I). Ten men (mean 28 years; range 20-40) and 9 women (mean 33 years; range 22-43) were included. All women participated in both the follicular and luteal phases of the menstrual cycle. Hyperosmolality was induced by IV infusion of hypertonic saline 3%, and hypoosmolality by drinking tap water. Arterial blood samples were collected for analysis of electrolytes, osmolality, and blood gases. Sensitivity to CO2 was determined by rebreathing tests performed before and after the fluid-loading procedures. Infusion of hypertonic saline caused hyperchloremic metabolic acidosis with decreased SID in all subjects. Analysis of pooled data showed absence of respiratory compensation. Baseline arterial PCO2 (PaCO2) mean (SD) 37.8 (2.9) mm Hg remained unaltered, with lowest PaCO2 37.8 (2.9) mm Hg after 100 minutes, P = 0.70, causing a decrease in pH from mean (SD) 7.42 (0.02) to 7.38 (0.02), P acidosis was also observed during water loading. Pooled results show that PaCO2 decreased from 38.2 (3.3) mm Hg at baseline to 35.7 (2.8) mm Hg after 80 minutes of drinking water, P = 0.002, and pH remained unaltered: pH 7.43 (0.02) at baseline to pH 7.42 (0.02), P = 0.14, mean difference (confidence interval) = pH -0.007 (-0.017 to 0.003). Our results indicate

Nitrogen metabolism, acid-base regulation, and molecular responses to ammonia and acid infusions in the spiny dogfish shark (Squalus acanthias).

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Nawata, C Michele; Walsh, Patrick J; Wood, Chris M

2015-07-01

Although they are ureotelic, marine elasmobranchs express Rh glycoproteins, putative ammonia channels. To address questions raised by a recent study on high environmental ammonia (HEA) exposure, dogfish were intravascularly infused for 24 h at 3 ml kg(-1) h(-1) with isosmotic NaCl (500 mmol l(-1), control), NH4HCO3 (500 mmol l(-1)), NH4Cl (500 mmol l(-1)), or HCl (as 125 mmol l(-1) HCl + 375 mmol l(-1) NaCl). While NaCl had no effect on arterial acid-base status, NH4HCO3 caused mild alkalosis, NH4Cl caused strong acidosis, and HCl caused lesser acidosis, all predominantly metabolic in nature. Total plasma ammonia (T(Amm)) and excretion rates of ammonia (J(Amm)) and urea-N (J(Urea-N)) were unaffected by NaCl or HCl. However, despite equal loading rates, plasma T(Amm) increased to a greater extent with NH4Cl, while J(Amm) increased to a greater extent with NH4HCO3 due to much greater increases in blood-to-water PNH3 gradients. As with HEA, both treatments caused large (90%) elevations of J(Urea-N), indicating that urea-N synthesis by the ornithine-urea cycle (OUC) is driven primarily by ammonia rather than HCO3(-). Branchial mRNA expressions of Rhbg and Rhp2 were unaffected by NH4HCO3 or NH4Cl, but v-type H(+)-ATPase was down-regulated by both treatments, and Rhbg and Na(+)/H(+) exchanger NHE2 were up-regulated by HCl. In the kidney, Rhbg was unresponsive to all treatments, but Rhp2 was up-regulated by HCl, and the urea transporter UT was up-regulated by HCl and NH4Cl. These responses are discussed in the context of current ideas about branchial, renal, and OUC function in this nitrogen-limited predator.

A case of thyrotoxic periodic paralysis as initial manifestation of Graves' disease in a 16-year-old Korean adolescent

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Se Yong Jung

2014-09-01

Full Text Available Thyrotoxic periodic paralysis (TPP is a rare complication of hyperthyroidism, with recurrent muscle paralysis and hypokalemia that are caused by an intracellular shift of potassium. TPP is relatively common in Asian males, but is extremely rare in children and adolescents, even for those of Asian descent. We describe a 16-year-old Korean adolescent presenting with a two-week history of episodic leg weakness in the morning. He showed sinus tachycardia, lower leg weakness, and hypokalemia. Thyroid function test showed hyperthyroidism, and thyroid ultrasonography revealed a diffuse enlarged thyroid with increased vascularity, consistent with Graves' disease. He was treated with β-adrenergic blocker and antithyroid drugs. He has been symptom free for one year, as his hyperthyroidism has been controlled well with antithyroid drugs. TPP should be considered in children and adolescents with acute paralysis of the lower extremities and hypokalemia.

Hypoxia and Its Acid-Base Consequences: From Mountains to Malignancy.

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Swenson, Erik R

Hypoxia, depending upon its magnitude and circumstances, evokes a spectrum of mild to severe acid-base changes ranging from alkalosis to acidosis, which can alter many responses to hypoxia at both non-genomic and genomic levels, in part via altered hypoxia-inducible factor (HIF) metabolism. Healthy people at high altitude and persons hyperventilating to non-hypoxic stimuli can become alkalotic and alkalemic with arterial pH acutely rising as high as 7.7. Hypoxia-mediated respiratory alkalosis reduces sympathetic tone, blunts hypoxic pulmonary vasoconstriction and hypoxic cerebral vasodilation, and increases hemoglobin oxygen affinity. These effects and others can be salutary or counterproductive to tissue oxygen delivery and utilization, based upon magnitude of each effect and summation. With severe hypoxia either in the setting of profound arterial hemoglobin desaturation and reduced O2 content or poor perfusion (ischemia) at the global or local level, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8. Although conventionally considered to be injurious and deleterious to cell function and survival, both acidoses may be cytoprotective by various anti-inflammatory, antioxidant, and anti-apoptotic mechanisms which limit total hypoxic or ischemic-reperfusion injury. Attempts to correct acidosis by giving bicarbonate or other alkaline agents under these circumstances ahead of or concurrent with reoxygenation efforts may be ill advised. Better understanding of this so-called "pH paradox" or permissive acidosis may offer therapeutic possibilities. Rapidly growing cancers often outstrip their vascular supply compromising both oxygen and nutrient delivery and metabolic waste disposal, thus limiting their growth and metastatic potential. However, their excessive glycolysis and lactate formation may not necessarily represent oxygen insufficiency, but rather the Warburg effect-an attempt to provide a large amount

Drug discovery strategies in the field of tumor energy metabolism: Limitations by metabolic flexibility and metabolic resistance to chemotherapy.

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Amoedo, N D; Obre, E; Rossignol, R

2017-08-01

The search for new drugs capable of blocking the metabolic vulnerabilities of human tumors has now entered the clinical evaluation stage, but several projects already failed in phase I or phase II. In particular, very promising in vitro studies could not be translated in vivo at preclinical stage and beyond. This was the case for most glycolysis inhibitors that demonstrated systemic toxicity. A more recent example is the inhibition of glutamine catabolism in lung adenocarcinoma that failed in vivo despite a strong addiction of several cancer cell lines to glutamine in vitro. Such contradictory findings raised several questions concerning the optimization of drug discovery strategies in the field of cancer metabolism. For instance, the cell culture models in 2D or 3D might already show strong limitations to mimic the tumor micro- and macro-environment. The microenvironment of tumors is composed of cancer cells of variegated metabolic profiles, supporting local metabolic exchanges and symbiosis, but also of immune cells and stroma that further interact with and reshape cancer cell metabolism. The macroenvironment includes the different tissues of the organism, capable of exchanging signals and fueling the tumor 'a distance'. Moreover, most metabolic targets were identified from their increased expression in tumor transcriptomic studies, or from targeted analyses looking at the metabolic impact of particular oncogenes or tumor suppressors on selected metabolic pathways. Still, very few targets were identified from in vivo analyses of tumor metabolism in patients because such studies are difficult and adequate imaging methods are only currently being developed for that purpose. For instance, perfusion of patients with [ 13 C]-glucose allows deciphering the metabolomics of tumors and opens a new area in the search for effective targets. Metabolic imaging with positron emission tomography and other techniques that do not involve [ 13 C] can also be used to evaluate tumor

Transcriptional and metabolic effects of glucose on Streptococcus pneumoniae sugar metabolism

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Laura ePaixão

2015-10-01

Full Text Available Streptococcus pneumoniae is a strictly fermentative human pathogen that relies on carbohydrate metabolism to generate energy for growth. The nasopharynx colonised by the bacterium is poor in free sugars, but mucosa lining glycans can provide a source of sugar. In blood and inflamed tissues glucose is the prevailing sugar. As a result during progression from colonisation to disease S. pneumoniae has to cope with a pronounced shift in carbohydrate nature and availability. Thus, we set out to assess the pneumococcal response to sugars found in glycans and the influence of glucose (Glc on this response at the transcriptional, physiological and metabolic levels. Galactose (Gal, N-acetylglucosamine (GlcNAc and mannose (Man affected the expression of 8 to 14% of the genes covering cellular functions including central carbon metabolism and virulence. The pattern of end-products as monitored by in vivo 13C-NMR is in good agreement with the fermentation profiles during growth, while the pools of phosphorylated metabolites are consistent with the type of fermentation observed (homolactic vs. mixed and regulation at the metabolic level. Furthermore, the accumulation of α-Gal6P and Man6P indicate metabolic bottlenecks in the metabolism of Gal and Man, respectively. Glc added to cells actively metabolizing other sugar(s was readily consumed and elicited a metabolic shift towards a homolactic profile. The transcriptional response to Glc was large (over 5% of the genome. In central carbon metabolism (most represented category, Glc exerted mostly negative regulation. The smallest response to Glc was observed on a sugar mix, suggesting that exposure to varied sugars improves the fitness of S. pneumoniae. The expression of virulence factors was negatively controlled by Glc in a sugar-dependent manner. Overall, our results shed new light on the link between carbohydrate metabolism, adaptation to host niches and virulence.

Transcriptional and metabolic effects of glucose on Streptococcus pneumoniae sugar metabolism.

Science.gov (United States)

Paixão, Laura; Caldas, José; Kloosterman, Tomas G; Kuipers, Oscar P; Vinga, Susana; Neves, Ana R

2015-01-01

Streptococcus pneumoniae is a strictly fermentative human pathogen that relies on carbohydrate metabolism to generate energy for growth. The nasopharynx colonized by the bacterium is poor in free sugars, but mucosa lining glycans can provide a source of sugar. In blood and inflamed tissues glucose is the prevailing sugar. As a result during progression from colonization to disease S. pneumoniae has to cope with a pronounced shift in carbohydrate nature and availability. Thus, we set out to assess the pneumococcal response to sugars found in glycans and the influence of glucose (Glc) on this response at the transcriptional, physiological, and metabolic levels. Galactose (Gal), N-acetylglucosamine (GlcNAc), and mannose (Man) affected the expression of 8 to 14% of the genes covering cellular functions including central carbon metabolism and virulence. The pattern of end-products as monitored by in vivo (13)C-NMR is in good agreement with the fermentation profiles during growth, while the pools of phosphorylated metabolites are consistent with the type of fermentation observed (homolactic vs. mixed) and regulation at the metabolic level. Furthermore, the accumulation of α-Gal6P and Man6P indicate metabolic bottlenecks in the metabolism of Gal and Man, respectively. Glc added to cells actively metabolizing other sugar(s) was readily consumed and elicited a metabolic shift toward a homolactic profile. The transcriptional response to Glc was large (over 5% of the genome). In central carbon metabolism (most represented category), Glc exerted mostly negative regulation. The smallest response to Glc was observed on a sugar mix, suggesting that exposure to varied sugars improves the fitness of S. pneumoniae. The expression of virulence factors was negatively controlled by Glc in a sugar-dependent manner. Overall, our results shed new light on the link between carbohydrate metabolism, adaptation to host niches and virulence.

Hippocampal electrical activity of adult rabbits during moderate passive hyperventilation

International Nuclear Information System (INIS)

Touchard, Francoise

1982-01-01

The effects of a moderate passive hyperventilation (HV) were studied in immobilized un-anesthetized rabbits. Hypocapnia (PCO 2 = 23.3 ± 2.8 mm Hg) and alkalosis (pH = 7.54 ± 0.07) were measured on arterial samples. PO 2 remained stable. The following results were obtained. From the onset of HV, the mean discharge rate (F) of the pyramidal cells (CA 1 ) was modified. Several types of cellular behaviours were defined according to whether F decreased (51 pc of the neurons), increased (39 pc) or remained stable (6 pc). The most marked effect was observed 15 min after HV onset when 87 pc of cells showed a discharge rate lower than in controls. Whatever F variations, the temporal organization of the action potentials remained unchanged in 71 pc of cases. The evoked response resulting from the stimulation of the commissural inputs corresponded with the activity of GABA inhibitory neurons (basket cells). The response threshold, amplitude and latency were not modified by HV. Only the facilitation process resulting from paired pulses was modified in its late stage. These results as well as those concerning unit activity do not support various assumption such as trouble of the neuronal energetic metabolism due to hypoxia, modification of ionic exchanges (Na + , K + , Ca ++ ), or variations of neurotransmitter concentrations (especially GABA). The effects observed could be ascribed to modifications of neuronal membrane resting potential resulting from direct action of CO 2 and alkalosis. (author) [fr

Forty Years Abuse of Baking Soda, Rhabdomyolysis, Glomerulonephritis, Hypertension Leading to Renal Failure: A Case Report

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Terje Forslund M.D., Ph.D.

2008-01-01

Full Text Available We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

A typical presentation of acute myeloid leukemia

Directory of Open Access Journals (Sweden)

Udayakumar N

2006-01-01

Full Text Available A young man who presented with fever, altered sensorium and sudden onset tachypnea, is described. Arterial blood gas analysis, revealed the presence of severe high anion gap metabolic acidosis, with compensatory respiratory alkalosis and normal oxygen saturation. A detailed neurological, nephrological, biochemical and hematological evaluation, revealed the presence of Acute myeloid leukemia, with lactic acidosis and hyponatremia. There are very few reports of presentation of leukemia as lactic acidosis. This case report highlights the need for emergency room physicians, to consider the possibility of lactic acidosis, as one of the causes of high anion gap acidosis and to meticulously investigate the cause of lactic acidosis. We describe a rare clinical instance of lactic acidosis as the presenting manifestation of Acute myeloid leukemia.

Forty years abuse of baking soda, rhabdomyolysis, glomerulonephritis, hypertension leading to renal failure: a case report.

Science.gov (United States)

Forslund, Terje; Koistinen, Arvo; Anttinen, Jorma; Wagner, Bodo; Miettinen, Marja

2008-01-01

We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

Metabolic Syndrome

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Metabolic syndrome is a group of conditions that put you at risk for heart disease and diabetes. These conditions ... agree on the definition or cause of metabolic syndrome. The cause might be insulin resistance. Insulin is ...

Metabolic syndrome and menopause

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Jouyandeh Zahra

2013-01-01

Full Text Available Abstract Background The metabolic syndrome is defined as an assemblage of risk factors for cardiovascular diseases, and menopause is associated with an increase in metabolic syndrome prevalence. The aim of this study was to assess the prevalence of metabolic syndrome and its components among postmenopausal women in Tehran, Iran. Methods In this cross-sectional study in menopause clinic in Tehran, 118 postmenopausal women were investigated. We used the adult treatment panel 3 (ATP3 criteria to classify subjects as having metabolic syndrome. Results Total prevalence of metabolic syndrome among our subjects was 30.1%. Waist circumference, HDL-cholesterol, fasting blood glucose, diastolic blood pressure ,Systolic blood pressure, and triglyceride were significantly higher among women with metabolic syndrome (P-value Conclusions Our study shows that postmenopausal status is associated with an increased risk of metabolic syndrome. Therefore, to prevent cardiovascular disease there is a need to evaluate metabolic syndrome and its components from the time of the menopause.

Enantiomeric metabolic interactions and stereoselective human methadone metabolism.

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Totah, Rheem A; Allen, Kyle E; Sheffels, Pamela; Whittington, Dale; Kharasch, Evan D

2007-04-01

Methadone is administered as a racemate, although opioid activity resides in the R-enantiomer. Methadone disposition is stereoselective, with considerable unexplained variability in clearance and plasma R/S ratios. N-Demethylation of methadone in vitro is predominantly mediated by cytochrome P450 CYP3A4 and CYP2B6 and somewhat by CYP2C19. This investigation evaluated stereoselectivity, models, and kinetic parameters for methadone N-demethylation by recombinant CYP2B6, CYP3A4, and CYP2C19, and the potential for interactions between enantiomers during racemate metabolism. CYP2B6 metabolism was stereoselective. CYP2C19 was less active, and stereoselectivity was opposite that for CYP2B6. CYP3A4 was not stereoselective. With all three isoforms, enantiomer N-dealkylation rates in the racemate were lower than those of (R)-(6-dimethyamino-4,4-diphenyl-heptan-3-one) hydrochloride (R-methadone) or (S)-(6-dimethyamino-4,4-diphenyl-heptan-3-one) hydrochloride (S-methadone) alone, suggesting an enantiomeric interaction and mutual metabolic inhibition. For CYP2B6, the interaction between enantiomers was stereoselective, with S-methadone as a more potent inhibitor of R-methadone N-demethylation than R-of S-methadone. In contrast, enantiomer interactions were not stereoselective with CYP2C19 or CYP3A4. For all three cytochromes P450, methadone N-demethylation was best described by two-site enzyme models with competitive inhibition. There were minor model differences between cytochromes P450 to account for stereoselectivity of metabolism and enantiomeric interactions. Changes in plasma R/S methadone ratios observed after rifampin or troleandomycin pretreatment in humans in vivo were successfully predicted by CYP2B6- but not CYP3A4-catalyzed methadone N-demethylation. CYP2B6 is a predominant catalyst of stereoselective methadone metabolism in vitro. In vivo, CYP2B6 may be a major determinant of methadone metabolism and disposition, and CYP2B6 activity and stereoselective metabolic

Metabolic regulation of inflammation.

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Gaber, Timo; Strehl, Cindy; Buttgereit, Frank

2017-05-01

Immune cells constantly patrol the body via the bloodstream and migrate into multiple tissues where they face variable and sometimes demanding environmental conditions. Nutrient and oxygen availability can vary during homeostasis, and especially during the course of an immune response, creating a demand for immune cells that are highly metabolically dynamic. As an evolutionary response, immune cells have developed different metabolic programmes to supply them with cellular energy and biomolecules, enabling them to cope with changing and challenging metabolic conditions. In the past 5 years, it has become clear that cellular metabolism affects immune cell function and differentiation, and that disease-specific metabolic configurations might provide an explanation for the dysfunctional immune responses seen in rheumatic diseases. This Review outlines the metabolic challenges faced by immune cells in states of homeostasis and inflammation, as well as the variety of metabolic configurations utilized by immune cells during differentiation and activation. Changes in cellular metabolism that contribute towards the dysfunctional immune responses seen in rheumatic diseases are also briefly discussed.

Aquaporin-2 regulation in health and disease

DEFF Research Database (Denmark)

Radin, M J; Yu, Ming-Jiun; Stødkilde-Jørgensen, Lene

2012-01-01

Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with di......Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity...

Metabolic Diet App Suite for inborn errors of amino acid metabolism.

Science.gov (United States)

Ho, Gloria; Ueda, Keiko; Houben, Roderick F A; Joa, Jeff; Giezen, Alette; Cheng, Barbara; van Karnebeek, Clara D M

2016-03-01

An increasing number of rare inborn errors of metabolism (IEMs) are amenable to targeted metabolic nutrition therapy. Daily adherence is important to attain metabolic control and prevent organ damage. This is challenging however, given the lack of information of disorder specific nutrient content of foods, the limited availability and cost of specialty products as well as difficulties in reliable calculation and tracking of dietary intake and targets. To develop apps for all inborn errors of amino acid metabolism for which the mainstay of treatment is a medical diet, and obtain patient and family feedback throughout the process to incorporate this into subsequent versions. The Metabolic Diet App Suite was created with input from health care professionals as a free, user-friendly, online tool for both mobile devices and desktop computers (http://www.metabolicdietapp.org) for 15 different IEMs. General information is provided for each IEM with links to useful online resources. Nutrient information is based on the MetabolicPro™, a North American food database compiled by the Genetic Metabolic Dietitians International (GMDI) Technology committee. After user registration, a personalized dashboard and management plan including specific nutrient goals are created. Each Diet App has a user-friendly interface and the functions include: nutrient intake counts, adding your own foods and homemade recipes and, managing a daily food diary. Patient and family feedback was overall positive and specific suggestions were used to further improve the App Suite. The Metabolic Diet App Suite aids individuals affected by IEMs to track and plan their meals. Future research should evaluate its impact on patient adherence, metabolic control, quality of life and health-related outcomes. The Suite will be updated and expanded to Apps for other categories of IEMs. Finally, this Suite is a support tool only, and does not replace medical/metabolic nutrition professional advice. Copyright �

Metabolic Control of Redox and Redox Control of Metabolism in Plants

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Fernie, Alisdair R.

2014-01-01

Abstract Significance: Reduction-oxidation (Redox) status operates as a major integrator of subcellular and extracellular metabolism and is simultaneously itself regulated by metabolic processes. Redox status not only dominates cellular metabolism due to the prominence of NAD(H) and NADP(H) couples in myriad metabolic reactions but also acts as an effective signal that informs the cell of the prevailing environmental conditions. After relay of this information, the cell is able to appropriately respond via a range of mechanisms, including directly affecting cellular functioning and reprogramming nuclear gene expression. Recent Advances: The facile accession of Arabidopsis knockout mutants alongside the adoption of broad-scale post-genomic approaches, which are able to provide transcriptomic-, proteomic-, and metabolomic-level information alongside traditional biochemical and emerging cell biological techniques, has dramatically advanced our understanding of redox status control. This review summarizes redox status control of metabolism and the metabolic control of redox status at both cellular and subcellular levels. Critical Issues: It is becoming apparent that plastid, mitochondria, and peroxisome functions influence a wide range of processes outside of the organelles themselves. While knowledge of the network of metabolic pathways and their intraorganellar redox status regulation has increased in the last years, little is known about the interorganellar redox signals coordinating these networks. A current challenge is, therefore, synthesizing our knowledge and planning experiments that tackle redox status regulation at both inter- and intracellular levels. Future Directions: Emerging tools are enabling ever-increasing spatiotemporal resolution of metabolism and imaging of redox status components. Broader application of these tools will likely greatly enhance our understanding of the interplay of redox status and metabolism as well as elucidating and

Altered metabolism in cancer

Directory of Open Access Journals (Sweden)

Locasale Jason W

2010-06-01

Full Text Available Abstract Cancer cells have different metabolic requirements from their normal counterparts. Understanding the consequences of this differential metabolism requires a detailed understanding of glucose metabolism and its relation to energy production in cancer cells. A recent study in BMC Systems Biology by Vasquez et al. developed a mathematical model to assess some features of this altered metabolism. Here, we take a broader look at the regulation of energy metabolism in cancer cells, considering their anabolic as well as catabolic needs. See research article: http://www.biomedcentral.com/1752-0509/4/58/

Soluble adenylyl cyclase is an acid-base sensor in epithelial base-secreting cells.

Science.gov (United States)

Roa, Jinae N; Tresguerres, Martin

2016-08-01

Blood acid-base regulation by specialized epithelia, such as gills and kidney, requires the ability to sense blood acid-base status. Here, we developed primary cultures of ray (Urolophus halleri) gill cells to study mechanisms for acid-base sensing without the interference of whole animal hormonal regulation. Ray gills have abundant base-secreting cells, identified by their noticeable expression of vacuolar-type H(+)-ATPase (VHA), and also express the evolutionarily conserved acid-base sensor soluble adenylyl cyclase (sAC). Exposure of cultured cells to extracellular alkalosis (pH 8.0, 40 mM HCO3 (-)) triggered VHA translocation to the cell membrane, similar to previous reports in live animals experiencing blood alkalosis. VHA translocation was dependent on sAC, as it was blocked by the sAC-specific inhibitor KH7. Ray gill base-secreting cells also express transmembrane adenylyl cyclases (tmACs); however, tmAC inhibition by 2',5'-dideoxyadenosine did not prevent alkalosis-dependent VHA translocation, and tmAC activation by forskolin reduced the abundance of VHA at the cell membrane. This study demonstrates that sAC is a necessary and sufficient sensor of extracellular alkalosis in ray gill base-secreting cells. In addition, this study indicates that different sources of cAMP differentially modulate cell biology. Copyright © 2016 the American Physiological Society.

Mycobacterium tuberculosis Metabolism

Science.gov (United States)

Warner, Digby F.

2015-01-01

Metabolism underpins the physiology and pathogenesis of Mycobacterium tuberculosis. However, although experimental mycobacteriology has provided key insights into the metabolic pathways that are essential for survival and pathogenesis, determining the metabolic status of bacilli during different stages of infection and in different cellular compartments remains challenging. Recent advances—in particular, the development of systems biology tools such as metabolomics—have enabled key insights into the biochemical state of M. tuberculosis in experimental models of infection. In addition, their use to elucidate mechanisms of action of new and existing antituberculosis drugs is critical for the development of improved interventions to counter tuberculosis. This review provides a broad summary of mycobacterial metabolism, highlighting the adaptation of M. tuberculosis as specialist human pathogen, and discusses recent insights into the strategies used by the host and infecting bacillus to influence the outcomes of the host–pathogen interaction through modulation of metabolic functions. PMID:25502746

Dysregulated metabolism contributes to oncogenesis

Science.gov (United States)

Hirschey, Matthew D.; DeBerardinis, Ralph J.; Diehl, Anna Mae E.; Drew, Janice E.; Frezza, Christian; Green, Michelle F.; Jones, Lee W.; Ko, Young H.; Le, Anne; Lea, Michael A.; Locasale, Jason W.; Longo, Valter D.; Lyssiotis, Costas A.; McDonnell, Eoin; Mehrmohamadi, Mahya; Michelotti, Gregory; Muralidhar, Vinayak; Murphy, Michael P.; Pedersen, Peter L.; Poore, Brad; Raffaghello, Lizzia; Rathmell, Jeffrey C.; Sivanand, Sharanya; Vander Heiden, Matthew G.; Wellen, Kathryn E.

2015-01-01

Cancer is a disease characterized by unrestrained cellular proliferation. In order to sustain growth, cancer cells undergo a complex metabolic rearrangement characterized by changes in metabolic pathways involved in energy production and biosynthetic processes. The relevance of the metabolic transformation of cancer cells has been recently included in the updated version of the review “Hallmarks of Cancer”, where the dysregulation of cellular metabolism was included as an emerging hallmark. While several lines of evidence suggest that metabolic rewiring is orchestrated by the concerted action of oncogenes and tumor suppressor genes, in some circumstances altered metabolism can play a primary role in oncogenesis. Recently, mutations of cytosolic and mitochondrial enzymes involved in key metabolic pathways have been associated with hereditary and sporadic forms of cancer. Together, these results suggest that aberrant metabolism, once seen just as an epiphenomenon of oncogenic reprogramming, plays a key role in oncogenesis with the power to control both genetic and epigenetic events in cells. In this review, we discuss the relationship between metabolism and cancer, as part of a larger effort to identify a broad-spectrum of therapeutic approaches. We focus on major alterations in nutrient metabolism and the emerging link between metabolism and epigenetics. Finally, we discuss potential strategies to manipulate metabolism in cancer and tradeoffs that should be considered. More research on the suite of metabolic alterations in cancer holds the potential to discover novel approaches to treat it. PMID:26454069

MetaFluxNet: the management of metabolic reaction information and quantitative metabolic flux analysis.

Science.gov (United States)

Lee, Dong-Yup; Yun, Hongsoek; Park, Sunwon; Lee, Sang Yup

2003-11-01

MetaFluxNet is a program package for managing information on the metabolic reaction network and for quantitatively analyzing metabolic fluxes in an interactive and customized way. It allows users to interpret and examine metabolic behavior in response to genetic and/or environmental modifications. As a result, quantitative in silico simulations of metabolic pathways can be carried out to understand the metabolic status and to design the metabolic engineering strategies. The main features of the program include a well-developed model construction environment, user-friendly interface for metabolic flux analysis (MFA), comparative MFA of strains having different genotypes under various environmental conditions, and automated pathway layout creation. http://mbel.kaist.ac.kr/ A manual for MetaFluxNet is available as PDF file.

Perspectives in metabolic engineering: understanding cellular regulation towards the control of metabolic routes.

Science.gov (United States)

Zadran, Sohila; Levine, Raphael D

2013-01-01

Metabolic engineering seeks to redirect metabolic pathways through the modification of specific biochemical reactions or the introduction of new ones with the use of recombinant technology. Many of the chemicals synthesized via introduction of product-specific enzymes or the reconstruction of entire metabolic pathways into engineered hosts that can sustain production and can synthesize high yields of the desired product as yields of natural product-derived compounds are frequently low, and chemical processes can be both energy and material expensive; current endeavors have focused on using biologically derived processes as alternatives to chemical synthesis. Such economically favorable manufacturing processes pursue goals related to sustainable development and "green chemistry". Metabolic engineering is a multidisciplinary approach, involving chemical engineering, molecular biology, biochemistry, and analytical chemistry. Recent advances in molecular biology, genome-scale models, theoretical understanding, and kinetic modeling has increased interest in using metabolic engineering to redirect metabolic fluxes for industrial and therapeutic purposes. The use of metabolic engineering has increased the productivity of industrially pertinent small molecules, alcohol-based biofuels, and biodiesel. Here, we highlight developments in the practical and theoretical strategies and technologies available for the metabolic engineering of simple systems and address current limitations.

Altered drug metabolism during pregnancy: hormonal regulation of drug-metabolizing enzymes.

Science.gov (United States)

Jeong, Hyunyoung

2010-06-01

Medication use during pregnancy is prevalent, but pharmacokinetic information of most drugs used during pregnancy is lacking in spite of known effects of pregnancy on drug disposition. Accurate pharmacokinetic information is essential for optimal drug therapy in mother and fetus. Thus, understanding how pregnancy influences drug disposition is important for better prediction of pharmacokinetic changes of drugs in pregnant women. Pregnancy is known to affect hepatic drug metabolism, but the underlying mechanisms remain unknown. Physiological changes accompanying pregnancy are probably responsible for the reported alteration in drug metabolism during pregnancy. These include elevated concentrations of various hormones such as estrogen, progesterone, placental growth hormones and prolactin. This review covers how these hormones influence expression of drug-metabolizing enzymes (DMEs), thus potentially responsible for altered drug metabolism during pregnancy. The reader will gain a greater understanding of the altered drug metabolism in pregnant women and the regulatory effects of pregnancy hormones on expression of DMEs. In-depth studies in hormonal regulatory mechanisms as well as confirmatory studies in pregnant women are warranted for systematic understanding and prediction of the changes in hepatic drug metabolism during pregnancy.

A 13 year old girl with muscle weakness and ventricular tachycardia

International Nuclear Information System (INIS)

Rauf, M.; Zeb, S.; Adil, M.; Gul, A.M.; Hafizullah, M.

2012-01-01

Gitelman's syndrome is characterized by hypokalemia, hypomagnesemia and hypocalciuria. It is an autosomal recessive renal disorder and mostly present with asymptomatic hypokalemia but muscle cramps, dizziness, fatigue, muscle weakness and arrhythmias are the usual presentation. Same is the case with us, young girl presented with multiple symptoms and arrhythmia was worked up for electrolyte imbalance. Long term prognosis in terms of maintaining growth, renal function and life expectancy is excellent. Family screening is important for its early detection and treatment. This needs future genetic studies. (author)

Genome scale metabolic modeling of cancer

DEFF Research Database (Denmark)

Nilsson, Avlant; Nielsen, Jens

2017-01-01

of metabolism which allows simulation and hypotheses testing of metabolic strategies. It has successfully been applied to many microorganisms and is now used to study cancer metabolism. Generic models of human metabolism have been reconstructed based on the existence of metabolic genes in the human genome......Cancer cells reprogram metabolism to support rapid proliferation and survival. Energy metabolism is particularly important for growth and genes encoding enzymes involved in energy metabolism are frequently altered in cancer cells. A genome scale metabolic model (GEM) is a mathematical formalization...

[Menopause and metabolic syndrome].

Science.gov (United States)

Meirelles, Ricardo M R

2014-03-01

The incidence of cardiovascular disease increases considerably after the menopause. One reason for the increased cardiovascular risk seems to be determined by metabolic syndrome, in which all components (visceral obesity, dyslipidemia, hypertension, and glucose metabolism disorder) are associated with higher incidence of coronary artery disease. After menopause, metabolic syndrome is more prevalent than in premenopausal women, and may plays an important role in the occurrence of myocardial infarction and other atherosclerotic and cardiovascular morbidities. Obesity, an essential component of the metabolic syndrome, is also associated with increased incidence of breast, endometrial, bowel, esophagus, and kidney cancer. The treatment of metabolic syndrome is based on the change in lifestyle and, when necessary, the use of medication directed to its components. In the presence of symptoms of the climacteric syndrome, hormonal therapy, when indicated, will also contribute to the improvement of the metabolic syndrome.

Relationships among personality traits, metabolic syndrome, and metabolic syndrome scores: The Kakegawa cohort study.

Science.gov (United States)

Ohseto, Hisashi; Ishikuro, Mami; Kikuya, Masahiro; Obara, Taku; Igarashi, Yuko; Takahashi, Satomi; Kikuchi, Daisuke; Shigihara, Michiko; Yamanaka, Chizuru; Miyashita, Masako; Mizuno, Satoshi; Nagai, Masato; Matsubara, Hiroko; Sato, Yuki; Metoki, Hirohito; Tachibana, Hirofumi; Maeda-Yamamoto, Mari; Kuriyama, Shinichi

2018-04-01

Metabolic syndrome and the presence of metabolic syndrome components are risk factors for cardiovascular disease (CVD). However, the association between personality traits and metabolic syndrome remains controversial, and few studies have been conducted in East Asian populations. We measured personality traits using the Japanese version of the Eysenck Personality Questionnaire (Revised Short Form) and five metabolic syndrome components-elevated waist circumference, elevated triglycerides, reduced high-density lipoprotein cholesterol, elevated blood pressure, and elevated fasting glucose-in 1322 participants aged 51.1±12.7years old from Kakegawa city, Japan. Metabolic syndrome score (MS score) was defined as the number of metabolic syndrome components present, and metabolic syndrome as having the MS score of 3 or higher. We performed multiple logistic regression analyses to examine the relationship between personality traits and metabolic syndrome components and multiple regression analyses to examine the relationship between personality traits and MS scores adjusted for age, sex, education, income, smoking status, alcohol use, and family history of CVD and diabetes mellitus. We also examine the relationship between personality traits and metabolic syndrome presence by multiple logistic regression analyses. "Extraversion" scores were higher in those with metabolic syndrome components (elevated waist circumference: P=0.001; elevated triglycerides: P=0.01; elevated blood pressure: P=0.004; elevated fasting glucose: P=0.002). "Extraversion" was associated with the MS score (coefficient=0.12, P=0.0003). No personality trait was significantly associated with the presence of metabolic syndrome. Higher "extraversion" scores were related to higher MS scores, but no personality trait was significantly associated with the presence of metabolic syndrome. Copyright © 2018 Elsevier Inc. All rights reserved.

Metabolic Syndrome in Children: Clinical Picture, Features of Lipid and Carbohydrate Metabolism

Directory of Open Access Journals (Sweden)

O.S. Bobrykovych

2013-09-01

Full Text Available The study included 225 children aged from 14 to 18 years with various manifestations of the metabolic syndrome in neighborhoods, different by iodine provision. The physical development (height, weight, body mass index, waist and hip circumferences has been examined. Biochemical investigations are focused on the study of lipid and carbohydrate metabolism in children. It is found that children who live in mountains have more severe obesity. In parallel with the increase of the degree of obesity, disorders of lipid and carbohydrate metabolism aggravate in children with sings of metabolic syndrome.

Physiologic and Pharmacokinetic Changes in Pregnancy

Directory of Open Access Journals (Sweden)

Maged eCostantine

2014-04-01

Full Text Available Physiologic changes in pregnancy induce profound alterations to the pharmacokinetic properties of many medications. These changes affect distribution, absorption, metabolism, and excretion of drugs, and thus may impact their pharmacodynamic properties during pregnancy. Pregnant women undergo several adaptations in many organ systems. Some adaptations are secondary to hormonal changes in pregnancy, while others occur to support the gravid woman and her developing fetus. Some of the changes in maternal physiology during pregnancy include, for example, increased maternal fat and total body water, decreased plasma protein concentrations, especially albumin, increased maternal blood volume, cardiac output and blood flow to the kidneys and uteroplacental unit, and decreased blood pressure. The maternal blood volume expansion occurs at a larger proportion than the increase in red blood cell mass, which results in physiologic anemia and hemodilution. Other physiologic changes include increased tidal volume, partially compensated respiratory alkalosis, delayed gastric emptying and gastrointestinal motility, and altered activity of hepatic drug metabolizing enzymes. Understating these changes and their profound impact on the pharmacokinetic properties of drugs in pregnancy is essential to optimize maternal and fetal health.

Sleep and Metabolism: An Overview

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Sunil Sharma

2010-01-01

Full Text Available Sleep and its disorders are increasingly becoming important in our sleep deprived society. Sleep is intricately connected to various hormonal and metabolic processes in the body and is important in maintaining metabolic homeostasis. Research shows that sleep deprivation and sleep disorders may have profound metabolic and cardiovascular implications. Sleep deprivation, sleep disordered breathing, and circadian misalignment are believed to cause metabolic dysregulation through myriad pathways involving sympathetic overstimulation, hormonal imbalance, and subclinical inflammation. This paper reviews sleep and metabolism, and how sleep deprivation and sleep disorders may be altering human metabolism.

A case report of nephrogenic diabetes insipidus with idiopathic Fanconi syndrome in a child who presented with vitamin D resistant rickets.

Science.gov (United States)

Patra, Soumya; Nadri, Gulnaz; Chowdhary, Harish; Pemde, Harish K; Singh, Varinder; Chandra, Jagdish

2014-05-01

Fanconi syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells, occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycemic glycosuria, tubular proteinuria without hematuria, metabolic acidosis without anion gap and excessive urinary excretion of phosphorous, calcium, uric acid, bicarbonate, sodium, potassium and magnesium. Diabetes insipidus is a disease of collecting tubules and children mainly present with dehydration and hypernatremia. We are reporting the first case of idiopathic Fanconi's syndrome along with nephrogenic diabetes insipidus in a child who presented to us with vitamin D resistant rickets. Medline search did not reveal any case of nephrogenic diabetes insipidus (NDI) associated with idiopathic Fanconi syndrome. We hypothesized that the NDI may be due to to severe hypokalemia induced tubular dysfunction.

Molecular cloning of ion channels in Felis catus that are related to periodic paralyses in man: a contribution to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis

Directory of Open Access Journals (Sweden)

Marlyn Zapata

2014-07-01

Full Text Available Neck ventroflexion in cats has different causes; however, the most common is the hypokalemia associated with flaccid paralysis secondary to chronic renal failure. In humans, the most common causes of acute flaccid paralysis are hypokalemia precipitated by thyrotoxicosis and familial forms linked to mutations in sodium, potassium, and calcium channel genes. Here, we describe the sequencing and analysis of skeletal muscle ion channels in Felis catus that could be related to periodic paralyses in humans, contributing to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis. We studied genomic DNA from eleven cats, including five animals that were hyperthyroid with hypokalemia, although only one presented with muscle weakness, and six healthy control domestic cats. We identified the ion channel ortholog genes KCNJ2, KCNJ12, KCNJ14, CACNA1S and SCN4A in the Felis catus genome, together with several polymorphic variants. Upon comparative alignment with other genomes, we found that Felis catus provides evidence for a high genomic conservation of ion channel sequences. Although we hypothesized that neck ventroflexion in cats could be associated with a thyrotoxic or familial periodic paralysis channel mutation, we did not identify any previously detected human channel mutation in the hyperthyroid cat presenting hypokalemia. However, based on the small number of affected cats in this study, we cannot yet rule out this molecular mechanism. Notwithstanding, hyperthyroidism should still be considered as a differential diagnosis in hypokalemic feline paralysis.

Metabolically healthy obesity and risk of mortality: does the definition of metabolic health matter?

Science.gov (United States)

Hinnouho, Guy-Marino; Czernichow, Sébastien; Dugravot, Aline; Batty, G David; Kivimaki, Mika; Singh-Manoux, Archana

2013-08-01

To assess the association of a "metabolically healthy obese" phenotype with mortality using five definitions of metabolic health. Adults (n = 5,269; 71.7% men) aged 39-62 years in 1991 through 1993 provided data on BMI and metabolic health, defined using data from the Adult Treatment Panel-III (ATP-III); criteria from two studies; and the Matsuda and homeostasis model assessment (HOMA) indices. Cross-classification of BMI categories and metabolic status (healthy/unhealthy) created six groups. Cox proportional hazards regression models were used to analyze associations with all-cause and cardiovascular disease (CVD) mortality during a median follow-up of 17.7 years. A total of 638 individuals (12.1% of the cohort) were obese, of whom 9-41% were metabolically healthy, depending on the definition. Regardless of the definition, compared with metabolically healthy, normal-weight individuals, both the metabolically healthy obese (hazard ratios [HRs] ranged from 1.81 [95% CI 1.16-2.84] for ATP-III to 2.30 [1.13-4.70] for the Matsuda index) and the metabolically abnormal obese (HRs ranged from 1.57 [1.08-2.28] for the Matsuda index to 2.05 [1.44-2.92] for criteria defined in a separate study) had an increased risk of mortality. The only exception was the lack of excess risk using the HOMA criterion for the metabolically healthy obese (1.08; 0.67-1.74). Among the obese, the risk of mortality did not vary as a function of metabolic health apart from when using the HOMA criterion (1.93; 1.15-3.22). Similar results were obtained for cardiovascular mortality. For most definitions of metabolic health, both metabolically healthy and unhealthy obese patients carry an elevated risk of mortality.

Clinical update on metabolic syndrome

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Juan Diego Hernández-Camacho

2017-12-01

Full Text Available Metabolic syndrome has been defined as a global issue since it affects a lot of people. Numerous factors are involved in metabolic syndrome development. It has been described that metabolic syndrome has negative consequences on health. Consequently, a lot of treatments have been proposed to palliate it such as drugs, surgery or life style changes where nutritional habits have shown to be an important point in its management. The current study reviews the literature existing about the actual epidemiology of metabolic syndrome, the components involucrate in its appearance and progression, the clinical consequences of metabolic syndrome and the nutritional strategies reported in its remission. A bibliographic search in PubMed and Medline was performed to identify eligible studies. Authors obtained that metabolic syndrome is present in population from developed and undeveloped areas in a huge scale. Environmental and genetic elements are involucrate in metabolic syndrome development. Metabolic syndrome exponentially increased risk of cardiovascular disease, some types of cancers, diabetes mellitus type 2, sleep disturbances, etc. Nutritional treatments play a crucial role in metabolic syndrome prevention, treatment and recovery.

Metabolism and disease

National Research Council Canada - National Science Library

Grodzicker, Terri; Stewart, David J; Stillman, Bruce

2011-01-01

...), cellular, organ system (cardiovascular, bone), and organismal (timing and life span) scales. Diseases impacted by metabolic imbalance or dysregulation that were covered in detail included diabetes, obesity, metabolic syndrome, and cancer...

The association between the metabolic syndrome and metabolic syndrome score and pulmonary function in non-smoking adults.

Science.gov (United States)

Yoon, Hyun; Gi, Mi Young; Cha, Ju Ae; Yoo, Chan Uk; Park, Sang Muk

2018-03-01

This study assessed the association of metabolic syndrome and metabolic syndrome score with the predicted forced vital capacity and predicted forced expiratory volume in 1 s (predicted forced expiratory volume in 1 s) values in Korean non-smoking adults. We analysed data obtained from 6684 adults during the 2013-2015 Korean National Health and Nutrition Examination Survey. After adjustment for related variables, metabolic syndrome ( p metabolic syndrome score ( p metabolic syndrome score with metabolic syndrome score 0 as a reference group showed no significance for metabolic syndrome score 1 [1.061 (95% confidence interval, 0.755-1.490)] and metabolic syndrome score 2 [1.247 (95% confidence interval, 0.890-1.747)], but showed significant for metabolic syndrome score 3 [1.433 (95% confidence interval, 1.010-2.033)] and metabolic syndrome score ⩾ 4 [1.760 (95% confidence interval, 1.216-2.550)]. In addition, the odds ratio of restrictive pulmonary disease of the metabolic syndrome [1.360 (95% confidence interval, 1.118-1.655)] was significantly higher than those of non-metabolic syndrome. Metabolic syndrome and metabolic syndrome score were inversely associated with the predicted forced vital capacity and forced expiratory volume in 1 s values in Korean non-smoking adults. In addition, metabolic syndrome and metabolic syndrome score were positively associated with the restrictive pulmonary disease.

Metabolic interrelationships software application: Interactive learning tool for intermediary metabolism

NARCIS (Netherlands)

A.J.M. Verhoeven (Adrie); M. Doets (Mathijs); J.M.J. Lamers (Jos); J.F. Koster (Johan)

2005-01-01

textabstractWe developed and implemented the software application titled Metabolic Interrelationships as a self-learning and -teaching tool for intermediary metabolism. It is used by undergraduate medical students in an integrated organ systems-based and disease-oriented core curriculum, which

Metabolic control of feed intake: implications for metabolic disease of fresh cows.

Science.gov (United States)

Allen, Michael S; Piantoni, Paola

2013-07-01

The objective of this article is to discuss metabolic control of feed intake in the peripartum period and its implications for metabolic disease of fresh cows. Understanding how feed intake is controlled during the transition from gestation to lactation is critical to both reduce risk and successfully treat many metabolic diseases. Copyright © 2013. Published by Elsevier Inc.

[Metabolic myopathies].

Science.gov (United States)

Papazian, Óscar; Rivas-Chacón, Rafael

2013-09-06

To review the metabolic myopathies manifested only by crisis of myalgias, cramps and rigidity of the muscles with decreased voluntary contractions and normal inter crisis neurologic examination in children and adolescents. These metabolic myopathies are autosomic recessive inherited enzymatic deficiencies of the carbohydrates and lipids metabolisms. The end result is a reduction of intra muscle adenosine triphosphate, mainly through mitochondrial oxidative phosphorylation, with decrease of available energy for muscle contraction. The one secondary to carbohydrates intra muscle metabolism disorders are triggered by high intensity brief (fatty acids metabolism disorders are triggered by low intensity prolonged (> 10 min) exercises. The conditions in the first group in order of decreasing frequency are the deficiencies of myophosforilase (GSD V), muscle phosphofructokinase (GSD VII), phosphoglycerate mutase 1 (GSD X) and beta enolase (GSD XIII). The conditions in the second group in order of decreasing frequency are the deficiencies of carnitine palmitoyl transferase II and very long chain acyl CoA dehydrogenase. The differential characteristics of patients in each group and within each group will allow to make the initial presumptive clinical diagnosis in the majority and then to order only the necessary tests to achieve the final diagnosis. Treatment during the crisis includes hydration, glucose and alkalinization of urine if myoglobin in blood and urine are elevated. Prevention includes avoiding exercise which may induce the crisis and fasting. The prognosis is good with the exception of rare cases of acute renal failure due to hipermyoglobinemia because of severe rabdomyolisis.

Fatty acid metabolism: target for metabolic syndrome

OpenAIRE

Wakil, Salih J.; Abu-Elheiga, Lutfi A.

2009-01-01

Fatty acids are a major energy source and important constituents of membrane lipids, and they serve as cellular signaling molecules that play an important role in the etiology of the metabolic syndrome. Acetyl-CoA carboxylases 1 and 2 (ACC1 and ACC2) catalyze the synthesis of malonyl-CoA, the substrate for fatty acid synthesis and the regulator of fatty acid oxidation. They are highly regulated and play important roles in the energy metabolism of fatty acids in animals, including humans. They...

Concentration of Potassium in Plasma, Erythrocytes, and Muscle Tissue in Cows with Decreased Feed Intake and Gastrointestinal Ileus.

Science.gov (United States)

Schneider, S; Müller, A; Wittek, T

2016-01-01

Healthy cows consume large amounts of potassium and a sudden loss in appetite can lead to hypokalemia. The routine method to evaluate potassium homeostasis is the measurement of the extracellular potassium in plasma or serum, but this does not provide information about the intracellular potassium pool. To evaluate potassium homeostasis by comparing the extracellular and intracellular potassium concentration in cows with reduced feed intake and gastrointestinal ileus. Twenty cows 1-3 days postpartum (group 1) and 20 cows with gastrointestinal ileus (group 2). Observational cross-sectional study. Plasma potassium was measured by using an ion-sensitive electrode. Intracellular potassium was measured in erythrocytes and muscle tissue (muscle biopsy) by using inductively coupled plasma optical emission spectroscopy. Cows of group 1 did not have hypokalemia. Overall cows with gastrointestinal ileus were hypokalemic (mean ± SD, 2.9 mmol/L ± 0.78), but potassium concentration in erythrocytes and muscle tissue was not lower than in postpartum cows. Intracellular potassium in erythrocytes varied very widely; group 1: 3497-10735 mg/kg (5559 ± 2002 mg/kg), group 2: 4139-21678 mg/kg (7473 ± 4034 mg/kg). Potassium in muscle tissue did not differ between group 1 (3356 ± 735 mg/kg wet weight) and group 2 (3407 ± 1069 mg/kg wet weight). No association between extracellular and intracellular potassium concentrations was detected. That measurement of plasma potassium concentration is not sufficient to evaluate potassium metabolism of cows. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.

Intranasal Insulin Restores Metabolic Parameters and Insulin Sensitivity in Rats with Metabolic Syndrome.

Science.gov (United States)

Derkach, K V; Ivantsov, A O; Chistyakova, O V; Sukhov, I B; Buzanakov, D M; Kulikova, A A; Shpakov, A O

2017-06-01

We studied the effect of 10-week treatment with intranasal insulin (0.5 IU/day) on glucose tolerance, glucose utilization, lipid metabolism, functions of pancreatic β cells, and insulin system in the liver of rats with cafeteria diet-induced metabolic syndrome. The therapy reduced body weight and blood levels of insulin, triglycerides, and atherogenic cholesterol that are typically increased in metabolic syndrome, normalized glucose tolerance and its utilization, and increased activity of insulin signaling system in the liver, thus reducing insulin resistance. The therapy did not affect the number of pancreatic islets and β cells. The study demonstrates prospects of using intranasal insulin for correction of metabolic parameters and reduction of insulin resistance in metabolic syndrome.

Gitelman's syndrome in pregnancy: case report and review of the literature.

LENUS (Irish Health Repository)

McCarthy, Fergus P

2012-01-31

Gitelman\\'s syndrome (GS), a rare renal disorder, results in hypokalaemia, hypomagnesaemia, hypocalciuria and a metabolic alkalosis. It is unclear if an alteration in management is necessary or beneficial during pregnancy. A 32-year-old woman with GS was managed in her second pregnancy. Antenatally, the patient required 39 (principally day case) admissions to the hospital for intravenous (IV) therapy and received a cumulative total of 47 l of IV 0.9% saline solution, 47 doses of 20 mmol magnesium chloride and 46 doses of 80 mmol potassium chloride. She delivered a 2940-g female infant in excellent condition by caesarean section. We would suggest that close attention to maternal weight gain during pregnancy is an easily available clinical tool to assess adequacy of fluid and electrolyte repletion in this condition.

Infantile variant of Bartter syndrome and sensorineural deafness: A new autosomal recessive disorder

Energy Technology Data Exchange (ETDEWEB)

Landau, D.; Shalev, H.; Carmi, Rivka; Ohaly, M. [Univ. of the Negev, Ashkelon (Israel)

1995-12-04

The infantile variant of Bartter syndrome (IBS) is usually associated with maternal polyhydramnios, premature birth, postnatal polyuria and hypokalemic hypochloremic metabolic alkalosis and a typical appearance. IBS is thought to be an autosomal recessive trait. Several congenital tubular defects are associated with sensorineural deafness (SND). However, an association between the IBS and SND has not been reported so far. Here we describe 5 children of an extended consanguineous Bedouin family with IBS and SND. In 3 of the cases, the typical electrolyte imbalance and facial appearance were detected neonatally. SND was detected as early as age 1 month, suggesting either coincidental homozygotization of 2 recessive genes or a pleiotropic effect of one autosomal recessive gene. This association suggests that evaluation of SND is warranted in every case of IBS. 35 refs., 2 figs., 2 tabs.

Drug metabolism in birds

Science.gov (United States)

Pan, Huo Ping; Fouts, James R.

1979-01-01

Papers published over 100 years since the beginning of the scientific study of drug metabolism in birds were reviewed. Birds were found to be able to accomplish more than 20 general biotransformation reactions in both functionalization and conjugation. Chickens were the primary subject of study but over 30 species of birds were used. Large species differences in drug metabolism exist between birds and mammals as well as between various birds, these differences were mostly quantitative. Qualitative differences were rare. On the whole, drug metabolism studies in birds have been neglected as compared with similar studies on insects and mammals. The uniqueness of birds and the advantages of using birds in drug metabolism studies are discussed. Possible future studies of drug metabolism in birds are recommended.

Metabolic Mechanisms in Obesity and Type 2 Diabetes: Insights from Bariatric/Metabolic Surgery

Directory of Open Access Journals (Sweden)

Adriana Florinela Cătoi

2015-11-01

Full Text Available Obesity and the related diabetes epidemics represent a real concern worldwide. Bariatric/metabolic surgery emerged in last years as a valuable therapeutic option for obesity and related diseases, including type 2 diabetes mellitus (T2DM. The complicated network of mechanisms involved in obesity and T2DM have not completely defined yet. There is still a debate on which would be the first metabolic defect leading to metabolic deterioration: insulin resistance or hyperinsulinemia? Insight into the metabolic effects of bariatric/metabolic surgery has revealed that, beyond weight loss and food restriction, other mechanisms can be activated by the rearrangements of the gastrointestinal tract, such as the incretinic/anti-incretinic system, changes in bile acid composition and flow, and modifications of gut microbiota; all of them possibly involved in the remission of T2DM. The complete elucidation of these mechanisms will lead to a better understanding of the pathogenesis of this disease. Our aim was to review some of the metabolic mechanisms involved in the development of T2DM in obese patients as well as in the remission of this condition in patients submitted to bariatric/metabolic surgery.

Serum Potassium Levels Inversely Correlate with D-Dimer In Patients with Acute-Onset Atrial Fibrillation

International Nuclear Information System (INIS)

Cervellin, Gianfranco; Bonfanti, Laura; Picanza, Alessandra; Lippi, Giuseppe

2015-01-01

D-dimer values are frequently increased in patients with atrial fibrillation (AF) compared to subjects in sinus rhythm. Hypokalemia plays a role in several cardiovascular diseases, but little is known about the association with AF. D-dimer values are frequently increased in patients with atrial fibrillation (AF) compared with subjects in sinus rhythm. Hypokalemia plays a role in several cardiovascular diseases, but little is known about the association with AF. The aim of this study was to investigate correlations between D-dimer and serum potassium in acute-onset AF (AAF). To investigate the potential correlation between the values of serum potassium and D-dimer in patients with AAF, we retrospectively reviewed clinical and laboratory data of all emergency department visits for AAF in 2013. Among 271 consecutive AAF patients with D-dimer assessments, those with hypokalemia (n = 98) had significantly higher D-dimer values than normokalemic patients (139 versus 114 ng/mL, p = 0.004). The rate of patients with D-dimer values exceeding the diagnostic cut-off was higher in the group of patients with hypokalemia than in those with normal serum potassium (26.5% versus 16.2%; p = 0.029). An inverse and highly significant correlation was found between serum potassium and D-dimer (r = −0.21; p < 0.001), even after adjustments for age and sex (beta coefficient −94.8; p = 0.001). The relative risk for a positive D-dimer value attributed to hypokalemia was 1.64 (95% CI, 1.02 to 2.63; p = 0.040). The correlation remained statistically significant in patients free from antihypertensive drugs (r = −0.25; p = 0.018), but not in those taking angiotensin-receptor blockers, angiotensin-converting enzyme inhibitors, or diuretics. The inverse correlation between values of potassium and D-dimer in patients with AAF provides important and complementary information about the thromboembolic risk of these patients

Serum Potassium Levels Inversely Correlate with D-Dimer In Patients with Acute-Onset Atrial Fibrillation

Energy Technology Data Exchange (ETDEWEB)

Cervellin, Gianfranco, E-mail: gcervellin@ao.pr.it; Bonfanti, Laura; Picanza, Alessandra; Lippi, Giuseppe [1Academic Hospital of Parma (Italy)

2015-03-15

D-dimer values are frequently increased in patients with atrial fibrillation (AF) compared to subjects in sinus rhythm. Hypokalemia plays a role in several cardiovascular diseases, but little is known about the association with AF. D-dimer values are frequently increased in patients with atrial fibrillation (AF) compared with subjects in sinus rhythm. Hypokalemia plays a role in several cardiovascular diseases, but little is known about the association with AF. The aim of this study was to investigate correlations between D-dimer and serum potassium in acute-onset AF (AAF). To investigate the potential correlation between the values of serum potassium and D-dimer in patients with AAF, we retrospectively reviewed clinical and laboratory data of all emergency department visits for AAF in 2013. Among 271 consecutive AAF patients with D-dimer assessments, those with hypokalemia (n = 98) had significantly higher D-dimer values than normokalemic patients (139 versus 114 ng/mL, p = 0.004). The rate of patients with D-dimer values exceeding the diagnostic cut-off was higher in the group of patients with hypokalemia than in those with normal serum potassium (26.5% versus 16.2%; p = 0.029). An inverse and highly significant correlation was found between serum potassium and D-dimer (r = −0.21; p < 0.001), even after adjustments for age and sex (beta coefficient −94.8; p = 0.001). The relative risk for a positive D-dimer value attributed to hypokalemia was 1.64 (95% CI, 1.02 to 2.63; p = 0.040). The correlation remained statistically significant in patients free from antihypertensive drugs (r = −0.25; p = 0.018), but not in those taking angiotensin-receptor blockers, angiotensin-converting enzyme inhibitors, or diuretics. The inverse correlation between values of potassium and D-dimer in patients with AAF provides important and complementary information about the thromboembolic risk of these patients.

NAD(+) metabolism: A therapeutic target for age-related metabolic disease

NARCIS (Netherlands)

Mouchiroud, Laurent; Houtkooper, Riekelt H.; Auwerx, Johan

2013-01-01

Abstract Nicotinamide adenine dinucleotide (NAD) is a central metabolic cofactor by virtue of its redox capacity, and as such regulates a wealth of metabolic transformations. However, the identification of the longevity protein silent regulator 2 (Sir2), the founding member of the sirtuin protein

Tumor Metabolism of Malignant Gliomas

Energy Technology Data Exchange (ETDEWEB)

Ru, Peng; Williams, Terence M.; Chakravarti, Arnab; Guo, Deliang, E-mail: deliang.guo@osumc.edu [Department of Radiation Oncology, Ohio State University Comprehensive Cancer Center & Arthur G James Cancer Hospital, Columbus, OH 43012 (United States)

2013-11-08

Constitutively activated oncogenic signaling via genetic mutations such as in the EGFR/PI3K/Akt and Ras/RAF/MEK pathways has been recognized as a major driver for tumorigenesis in most cancers. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA and RNA, leading to enhanced growth of human tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. In malignant gliomas, metabolism pathways of glucose, glutamine and lipid are significantly reprogrammed. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. In this review, we will summarize recent studies revealing critical gene alterations that lead to metabolic changes in malignant gliomas, and also discuss promising therapeutic strategies via targeting the key players in metabolic regulation.

Tumor Metabolism of Malignant Gliomas

International Nuclear Information System (INIS)

Ru, Peng; Williams, Terence M.; Chakravarti, Arnab; Guo, Deliang

2013-01-01

Constitutively activated oncogenic signaling via genetic mutations such as in the EGFR/PI3K/Akt and Ras/RAF/MEK pathways has been recognized as a major driver for tumorigenesis in most cancers. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA and RNA, leading to enhanced growth of human tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. In malignant gliomas, metabolism pathways of glucose, glutamine and lipid are significantly reprogrammed. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. In this review, we will summarize recent studies revealing critical gene alterations that lead to metabolic changes in malignant gliomas, and also discuss promising therapeutic strategies via targeting the key players in metabolic regulation

Metabolic Adaptation to Muscle Ischemia

Science.gov (United States)

Cabrera, Marco E.; Coon, Jennifer E.; Kalhan, Satish C.; Radhakrishnan, Krishnan; Saidel, Gerald M.; Stanley, William C.

2000-01-01

Although all tissues in the body can adapt to varying physiological/pathological conditions, muscle is the most adaptable. To understand the significance of cellular events and their role in controlling metabolic adaptations in complex physiological systems, it is necessary to link cellular and system levels by means of mechanistic computational models. The main objective of this work is to improve understanding of the regulation of energy metabolism during skeletal/cardiac muscle ischemia by combining in vivo experiments and quantitative models of metabolism. Our main focus is to investigate factors affecting lactate metabolism (e.g., NADH/NAD) and the inter-regulation between carbohydrate and fatty acid metabolism during a reduction in regional blood flow. A mechanistic mathematical model of energy metabolism has been developed to link cellular metabolic processes and their control mechanisms to tissue (skeletal muscle) and organ (heart) physiological responses. We applied this model to simulate the relationship between tissue oxygenation, redox state, and lactate metabolism in skeletal muscle. The model was validated using human data from published occlusion studies. Currently, we are investigating the difference in the responses to sudden vs. gradual onset ischemia in swine by combining in vivo experimental studies with computational models of myocardial energy metabolism during normal and ischemic conditions.

[Metabolic functions and sport].

Science.gov (United States)

Riviere, Daniel

2004-01-01

Current epidemiological studies emphasize the increased of metabolic diseases of the adults, such as obesity, type-2 diabetes and metabolic syndromes. Even more worrying is the rising prevalence of obesity in children. It is due more to sedentariness, caused more by inactivity (television, video, games, etc.) than by overeating. Many studies have shown that regular physical activities benefit various bodily functions including metabolism. After dealing with the major benefits of physical exercise on some adult metabolic disorders, we focus on the prime role played by physical activity in combating the public health problem of childhood obesity.

Metabolic disorders in menopause

Directory of Open Access Journals (Sweden)

Grzegorz Stachowiak

2015-04-01

Full Text Available Metabolic disorders occurring in menopause, including dyslipidemia, disorders of carbohydrate metabolism (impaired glucose tolerance – IGT, type 2 diabetes mellitus – T2DM or components of metabolic syndrome, constitute risk factors for cardiovascular disease in women. A key role could be played here by hyperinsulinemia, insulin resistance and visceral obesity, all contributing to dyslipidemia, oxidative stress, inflammation, alter coagulation and atherosclerosis observed during the menopausal period. Undiagnosed and untreated, metabolic disorders may adversely affect the length and quality of women’s life. Prevention and treatment preceded by early diagnosis should be the main goal for the physicians involved in menopausal care. This article represents a short review of the current knowledge concerning metabolic disorders (e.g. obesity, polycystic ovary syndrome or thyroid diseases in menopause, including the role of a tailored menopausal hormone therapy (HT. According to current data, HT is not recommend as a preventive strategy for metabolic disorders in menopause. Nevertheless, as part of a comprehensive strategy to prevent chronic diseases after menopause, menopausal hormone therapy, particularly estrogen therapy may be considered (after balancing benefits/risks and excluding women with absolute contraindications to this therapy. Life-style modifications, with moderate physical activity and healthy diet at the forefront, should be still the first choice recommendation for all patients with menopausal metabolic abnormalities.

Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.

Science.gov (United States)

Anandhan, Annadurai; Jacome, Maria S; Lei, Shulei; Hernandez-Franco, Pablo; Pappa, Aglaia; Panayiotidis, Mihalis I; Powers, Robert; Franco, Rodrigo

2017-07-01

The loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of protein inclusions (Lewy bodies) are the pathological hallmarks of Parkinson's disease (PD). PD is triggered by genetic alterations, environmental/occupational exposures and aging. However, the exact molecular mechanisms linking these PD risk factors to neuronal dysfunction are still unclear. Alterations in redox homeostasis and bioenergetics (energy failure) are thought to be central components of neurodegeneration that contribute to the impairment of important homeostatic processes in dopaminergic cells such as protein quality control mechanisms, neurotransmitter release/metabolism, axonal transport of vesicles and cell survival. Importantly, both bioenergetics and redox homeostasis are coupled to neuro-glial central carbon metabolism. We and others have recently established a link between the alterations in central carbon metabolism induced by PD risk factors, redox homeostasis and bioenergetics and their contribution to the survival/death of dopaminergic cells. In this review, we focus on the link between metabolic dysfunction, energy failure and redox imbalance in PD, making an emphasis in the contribution of central carbon (glucose) metabolism. The evidence summarized here strongly supports the consideration of PD as a disorder of cell metabolism. Copyright © 2017 Elsevier Inc. All rights reserved.

Fluid, electrolyte, and acid-base balances in three-day, combined-training horses.

Science.gov (United States)

White, S L

1998-04-01

Horses competing in 3-day, combined-training events develop a metabolic acidosis that is partially compensated for by a respiratory alkalosis immediately after phases B and D. By the end of phase C and 30 minutes to 2 hours after phase D, the acidosis is resolved by the oxidation of lactate, and a metabolic alkalosis prevails. A reduction in TBW and cation content occurs, which often is not replenished 12 to 24 hours after the event, even though the serum or plasma concentration of various constituents may be within normal limits. Hypochloremia and hypocalcemia, however, may persist 12 or more hours after the speed and endurance test. All of the data cited in this article are from horses that successfully completed their respective tests. Nevertheless, some horses developed substantial fluid and cation losses. In horses that are not well conditioned or in competitions in which terrain, footing, or hot environments increase the thermal load or decrease heat loss, greater losses of fluids and electrolytes can be expected. Body weight losses exceeding 5% and cation losses exceeding 4000 mEq/L occur in endurance horses suffering from exhaustion and synchronous diaphragmatic flutter. In one study, two thirds of the Na+ lost during exercise-induced sweating in cool, dry conditions was replenished from salt supplements added to a balanced forage and concentrated diet. Consequently, horses in regular training and competition may benefit from salt supplementation. The composition of the salt supplement and the amount fed should be based on the composition of the horse's diet, degree of work, and environmental conditions. Horses competing in a 3-day, combined-training event may be expected to have persistent losses of weight and cations, particularly if conditions result in heavy sweating. Many horses in the field studies had minimal changes in weight and cation balance compared with pre-event values. The diet and electrolyte supplementation of the horses in the majority of

Metabolic Engineering X Conference

Energy Technology Data Exchange (ETDEWEB)

Flach, Evan [American Institute of Chemical Engineers

2015-05-07

The International Metabolic Engineering Society (IMES) and the Society for Biological Engineering (SBE), both technological communities of the American Institute of Chemical Engineers (AIChE), hosted the Metabolic Engineering X Conference (ME-X) on June 15-19, 2014 at the Westin Bayshore in Vancouver, British Columbia. It attracted 395 metabolic engineers from academia, industry and government from around the globe.

Pyruvate Kinase Triggers a Metabolic Feedback Loop that Controls Redox Metabolism in Respiring Cells

NARCIS (Netherlands)

Grüning, N.M.; Rinnerthaler, M.; Bluemlein, K.; Mulleder, M.; Wamelink, M.M.C.; Lehrach, H.; Jakobs, C.A.J.M.; Breitenbach, M.; Ralser, M.

2011-01-01

In proliferating cells, a transition from aerobic to anaerobic metabolism is known as the Warburg effect, whose reversal inhibits cancer cell proliferation. Studying its regulator pyruvate kinase (PYK) in yeast, we discovered that central metabolism is self-adapting to synchronize redox metabolism

Fatty liver as a risk factor for progression from metabolically healthy to metabolically abnormal in non-overweight individuals.

Science.gov (United States)

Hashimoto, Yoshitaka; Hamaguchi, Masahide; Fukuda, Takuya; Ohbora, Akihiro; Kojima, Takao; Fukui, Michiaki

2017-07-01

Recent studies identified that metabolically abnormal non-obese phenotype is a risk factor for cardiovascular diseases. However, little is known about risk factor for progression from metabolically healthy non-overweight to metabolically abnormal phenotype. We hypothesized that fatty liver had a clinical impact on progression from metabolically healthy non-overweight to metabolically abnormal phenotype. In this retrospective cohort study, 14,093 Japanese (7557 men and 6736 women), who received the health-checkup program from 2004 to 2012, were enrolled. Overweight and obesity were defined as body mass index 23.0-25.0 and ≥25.0 kg/m 2 . Four metabolic factors (impaired fasting glucose, hypertension, hypertriglyceridemia and low high density lipoprotein-cholesterol concentration) were used for definition of metabolically healthy (less than two factors) or metabolically abnormal (two or more). We divided the participants into three groups: metabolically healthy non-overweight (9755 individuals, men/women = 4290/5465), metabolically healthy overweight (2547 individuals, 1800/747) and metabolically healthy obesity (1791 individuals, 1267/524). Fatty liver was diagnosed by ultrasonography. Over the median follow-up period of 5.3 years, 873 metabolically healthy non-overweight, 512 metabolically healthy overweight and 536 metabolically healthy obesity individuals progressed to metabolically abnormal. The adjusted hazard risks of fatty liver on progression were 1.49 (95% confidence interval 1.20-1.83, p = 0.005) in metabolically healthy non-overweight, 1.37 (1.12-1.66, p = 0.002) in metabolically healthy overweight and 1.38 (1.15-1.66, p overweight individuals.

Aspects of astrocyte energy metabolism, amino acid neurotransmitter homoeostasis and metabolic compartmentation

DEFF Research Database (Denmark)

Kreft, Marko; Bak, Lasse Kristoffer; Waagepetersen, Helle S

2012-01-01

Astrocytes are key players in brain function; they are intimately involved in neuronal signalling processes and their metabolism is tightly coupled to that of neurons. In the present review, we will be concerned with a discussion of aspects of astrocyte metabolism, including energy......-generating pathways and amino acid homoeostasis. A discussion of the impact that uptake of neurotransmitter glutamate may have on these pathways is included along with a section on metabolic compartmentation....

Sleep and Metabolism: An Overview

OpenAIRE

Sharma, Sunil; Kavuru, Mani

2010-01-01

Sleep and its disorders are increasingly becoming important in our sleep deprived society. Sleep is intricately connected to various hormonal and metabolic processes in the body and is important in maintaining metabolic homeostasis. Research shows that sleep deprivation and sleep disorders may have profound metabolic and cardiovascular implications. Sleep deprivation, sleep disordered breathing, and circadian misalignment are believed to cause metabolic dysregulation through myriad pathways i...

Metabolic imaging using PET

International Nuclear Information System (INIS)

Kudo, Takashi

2007-01-01

There is growing evidence that myocardial metabolism plays a key role not only in ischaemic heart disease but also in a variety of diseases which involve myocardium globally, such as heart failure and diabetes mellitus. Understanding myocardial metabolism in such diseases helps to elucidate the pathophysiology and assists in making therapeutic decisions. As well as providing information on regional changes, PET can deliver quantitative information about both regional and global changes in metabolism. This capability of quantitative measurement is one of the major advantages of PET along with physiological positron tracers, especially relevant in evaluating diseases which involve the whole myocardium. This review discusses major PET tracers for metabolic imaging and their clinical applications and contributions to research regarding ischaemic heart disease and other diseases such as heart failure and diabetic heart disease. Future applications of positron metabolic tracers for the detection of vulnerable plaque are also highlighted briefly. (orig.)

Metabolic Engineering VII Conference

Energy Technology Data Exchange (ETDEWEB)

Kevin Korpics

2012-12-04

The aims of this Metabolic Engineering conference are to provide a forum for academic and industrial researchers in the field; to bring together the different scientific disciplines that contribute to the design, analysis and optimization of metabolic pathways; and to explore the role of Metabolic Engineering in the areas of health and sustainability. Presentations, both written and oral, panel discussions, and workshops will focus on both applications and techniques used for pathway engineering. Various applications including bioenergy, industrial chemicals and materials, drug targets, health, agriculture, and nutrition will be discussed. Workshops focused on technology development for mathematical and experimental techniques important for metabolic engineering applications will be held for more in depth discussion. This 2008 meeting will celebrate our conference tradition of high quality and relevance to both industrial and academic participants, with topics ranging from the frontiers of fundamental science to the practical aspects of metabolic engineering.

Astrocytes and energy metabolism.

Science.gov (United States)

Prebil, Mateja; Jensen, Jørgen; Zorec, Robert; Kreft, Marko

2011-05-01

Astrocytes are glial cells, which play a significant role in a number of processes, including the brain energy metabolism. Their anatomical position between blood vessels and neurons make them an interface for effective glucose uptake from blood. After entering astrocytes, glucose can be involved in different metabolic pathways, e.g. in glycogen production. Glycogen in the brain is localized mainly in astrocytes and is an important energy source in hypoxic conditions and normal brain functioning. The portion of glucose metabolized into glycogen molecules in astrocytes is as high as 40%. It is thought that the release of gliotransmitters (such as glutamate, neuroactive peptides and ATP) into the extracellular space by regulated exocytosis supports a significant part of communication between astrocytes and neurons. On the other hand, neurotransmitter action on astrocytes has a significant role in brain energy metabolism. Therefore, understanding the astrocytes energy metabolism may help understanding neuron-astrocyte interactions.

Genetic and environmental relationships of metabolic and weight phenotypes to metabolic syndrome and diabetes: the healthy twin study.

Science.gov (United States)

Song, Yun-Mi; Sung, Joohon; Lee, Kayoung

2015-02-01

We aimed to examine the relationships, including genetic and environmental correlations, between metabolic and weight phenotypes and factors related to diabetes and metabolic syndrome. Participants of the Healthy Twin Study without diabetes (n=2687; 895 monozygotic and 204 dizygotic twins, and 1588 nontwin family members; mean age, 42.5±13.1 years) were stratified according to body mass index (BMI) (metabolic syndrome categories at baseline. The metabolic traits, namely diabetes and metabolic syndrome, metabolic syndrome components, glycated hemoglobin (HbA1c) level, and homeostasis model assessment of insulin resistance (HOMA-IR), were assessed after 2.5±2.1 years. In a multivariate-adjusted model, those who had metabolic syndrome or overweight phenotypes at baseline were more likely to have higher HbA1C and HOMA-IR levels and abnormal metabolic syndrome components at follow-up as compared to the metabolically healthy normal weight subgroup. The incidence of diabetes was 4.4-fold higher in the metabolically unhealthy but normal weight individuals and 3.3-fold higher in the metabolically unhealthy and overweight individuals as compared with the metabolically healthy normal weight individuals. The heritability of the metabolic syndrome/weight phenotypes was 0.40±0.03. Significant genetic and environmental correlations were observed between the metabolic syndrome/weight phenotypes at baseline and the metabolic traits at follow-up, except for incident diabetes, which only had a significant common genetic sharing with the baseline phenotypes. The genetic and environmental relationships between the metabolic and weight phenotypes at baseline and the metabolic traits at follow-up suggest pleiotropic genetic mechanisms and the crucial role of lifestyle and behavioral factors.

Analysis of postoperative biochemical values and clinical outcomes after adrenalectomy for primary aldosteronism.

Science.gov (United States)

Swearingen, Andrew J; Kahramangil, Bora; Monteiro, Rosebel; Krishnamurthy, Vikram; Jin, Judy; Shin, Joyce; Siperstein, Allan; Berber, Eren

2018-04-01

Primary aldosteronism causes hypertension and hypokalemia and is often surgically treatable. Diagnosis includes elevated plasma aldosterone, suppressed plasma renin activity, and elevated aldosterone renin ratio. Adrenalectomy improves hypertension and hypokalemia. Postoperative plasma aldosterone and plasma renin activity may be useful in documenting cure or failure. A retrospective analysis of patients who underwent adrenalectomy for primary aldosteronism from 2010 to 2016 was performed, analyzing preoperative and postoperative plasma aldosterone, plasma renin activity, hypertension, and hypokalemia. The utility of postoperative testing was assessed. Clinical cure was defined as improved hypertension control and resolution of potassium loss. Biochemical cure was defined as aldosterone renin ratio reduction to <23.6. Forty-four patients were included; 20 had plasma aldosterone and plasma renin activity checked on postoperative day 1. In the study, 40/44 (91%) were clinically cured. All clinical failures had of biochemical failure at follow-up. Postoperative day 1aldosterone renin ratio <23.6 had PPV of 95% for clinical cure. Cured patients had mean plasma aldosterone drop of 33.1 ng/dL on postoperative day 1; noncured patient experienced 3.9 ng/dL increase. A cutoff of plasma aldosterone decrease of 10 ng/dL had high positive predictive value for clinical cure. Changes in plasma aldosterone and plasma renin activity after adrenalectomy correlate with improved hypertension and hypokalemia. The biochemical impact of adrenalectomy manifests as early as postoperative day 1. We propose a plasma aldosterone decrease of 10 ng/dL as a criterion to predict clinical cure. Copyright © 2017 Elsevier Inc. All rights reserved.

Metabolic routes along digestive system of licorice: multicomponent sequential metabolism method in rat.

Science.gov (United States)

Zhang, Lei; Zhao, Haiyu; Liu, Yang; Dong, Honghuan; Lv, Beiran; Fang, Min; Zhao, Huihui

2016-06-01

This study was conducted to establish the multicomponent sequential metabolism (MSM) method based on comparative analysis along the digestive system following oral administration of licorice (Glycyrrhiza uralensis Fisch., leguminosae), a traditional Chinese medicine widely used for harmonizing other ingredients in a formulae. The licorice water extract (LWE) dissolved in Krebs-Ringer buffer solution (1 g/mL) was used to carry out the experiments and the comparative analysis was performed using HPLC and LC-MS/MS methods. In vitro incubation, in situ closed-loop and in vivo blood sampling were used to measure the LWE metabolic profile along the digestive system. The incubation experiment showed that the LWE was basically stable in digestive juice. A comparative analysis presented the metabolic profile of each prototype and its corresponding metabolites then. Liver was the major metabolic organ for LWE, and the metabolism by the intestinal flora and gut wall was also an important part of the process. The MSM method was practical and could be a potential method to describe the metabolic routes of multiple components before absorption into the systemic blood stream. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.

Metabolic syndrome, diet and exercise.

Science.gov (United States)

De Sousa, Sunita M C; Norman, Robert J

2016-11-01

Polycystic ovary syndrome (PCOS) is associated with a range of metabolic complications including insulin resistance (IR), obesity, dyslipidaemia, hypertension, obstructive sleep apnoea (OSA) and non-alcoholic fatty liver disease. These compound risks result in a high prevalence of metabolic syndrome and possibly increased cardiovascular (CV) disease. As the cardiometabolic risk of PCOS is shared amongst the different diagnostic systems, all women with PCOS should undergo metabolic surveillance though the precise approach differs between guidelines. Lifestyle interventions consisting of increased physical activity and caloric restriction have been shown to improve both metabolic and reproductive outcomes. Pharmacotherapy and bariatric surgery may be considered in resistant metabolic disease. Issues requiring further research include the natural history of PCOS-associated metabolic disease, absolute CV risk and comparative efficacy of lifestyle interventions. Copyright © 2016 Elsevier Ltd. All rights reserved.

Metabolic Reprogramming in Thyroid Carcinoma

Directory of Open Access Journals (Sweden)

Raquel Guimaraes Coelho

2018-03-01

Full Text Available Among all the adaptations of cancer cells, their ability to change metabolism from the oxidative to the glycolytic phenotype is a hallmark called the Warburg effect. Studies on tumor metabolism show that improved glycolysis and glutaminolysis are necessary to maintain rapid cell proliferation, tumor progression, and resistance to cell death. Thyroid neoplasms are common endocrine tumors that are more prevalent in women and elderly individuals. The incidence of thyroid cancer has increased in the Past decades, and recent findings describing the metabolic profiles of thyroid tumors have emerged. Currently, several drugs are in development or clinical trials that target the altered metabolic pathways of tumors are undergoing. We present a review of the metabolic reprogramming in cancerous thyroid tissues with a focus on the factors that promote enhanced glycolysis and the possible identification of promising metabolic targets in thyroid cancer.

Metabolic Reprogramming in Thyroid Carcinoma

Science.gov (United States)

Coelho, Raquel Guimaraes; Fortunato, Rodrigo S.; Carvalho, Denise P.

2018-01-01

Among all the adaptations of cancer cells, their ability to change metabolism from the oxidative to the glycolytic phenotype is a hallmark called the Warburg effect. Studies on tumor metabolism show that improved glycolysis and glutaminolysis are necessary to maintain rapid cell proliferation, tumor progression, and resistance to cell death. Thyroid neoplasms are common endocrine tumors that are more prevalent in women and elderly individuals. The incidence of thyroid cancer has increased in the Past decades, and recent findings describing the metabolic profiles of thyroid tumors have emerged. Currently, several drugs are in development or clinical trials that target the altered metabolic pathways of tumors are undergoing. We present a review of the metabolic reprogramming in cancerous thyroid tissues with a focus on the factors that promote enhanced glycolysis and the possible identification of promising metabolic targets in thyroid cancer. PMID:29629339

Clinical characteristics of chronic kidney disease of nontraditional causes in Salvadoran farming communities.

Science.gov (United States)

Herrera, Raúl; Orantes, Carlos M; Almaguer, Miguel; Alfonso, Pedro; Bayarre, Héctor D; Leiva, Irma M; Smith, Magaly J; Cubias, Ricardo A; Torres, Carlos G; Almendárez, Walter O; Cubias, Francisco R; Morales, Fabrizio E; Magaña, Salvador; Amaya, Juan C; Perdomo, Edgard; Ventura, Mercedes C; Villatoro, Juan F; Vela, Xavier F; Zelaya, Susana M; Granados, Delmy V; Vela, Eduardo; Orellana, Patricia; Hevia, Reynaldo; Fuentes, E Jackeline; Mañalich, Reinaldo; Bacallao, Raymed; Ugarte, Mario; Arias, María I; Chávez, Jackelin; Flores, Nelson E; Aparicio, Claudia E

2014-04-01

: hypermagnesuria (100%), hyperphosphaturia (50%), hypernatriuria (45.7%), hyperkaluria (23.9%), hypercalciuria (17.4%), electrolyte polyuria (43.5%), metabolic alkalosis (45.7%), hyponatremia (47.8%), hypocalcemia (39.1%), hypokalemia (30.4%), hypomagnesemia (19.6%). Imaging: Ultrasound showed fatty liver (93.5%) and vascular Doppler showed tibial artery damage (66.7%). Neurological symptoms: abnormal tendon reflexes (45.6%), Babinski sign and myoclonus (6.5%), sensorineural hearing loss (56.5%). This chronic kidney disease studied behaves clinically like chronic tubulointerstitial nephropathy, but with systemic manifestations not attributable to kidney disease. While male agricultural workers predominated, women and adolescents were also affected. Findings support a hypothesis of multifactorial etiology with a key role played by nephrotoxic environmental agents.

Fat and Sugar Metabolism During Exercise in Patients With Metabolic Myopathy

Science.gov (United States)

2017-08-31

Metabolism, Inborn Errors; Lipid Metabolism, Inborn Errors; Carbohydrate Metabolism, Inborn Errors; Long-Chain 3-Hydroxyacyl-CoA Dehydrogenase Deficiency; Glycogenin-1 Deficiency (Glycogen Storage Disease Type XV); Carnitine Palmitoyl Transferase 2 Deficiency; VLCAD Deficiency; Medium-chain Acyl-CoA Dehydrogenase Deficiency; Multiple Acyl-CoA Dehydrogenase Deficiency; Carnitine Transporter Deficiency; Neutral Lipid Storage Disease; Glycogen Storage Disease Type II; Glycogen Storage Disease Type III; Glycogen Storage Disease Type IV; Glycogen Storage Disease Type V; Muscle Phosphofructokinase Deficiency; Phosphoglucomutase 1 Deficiency; Phosphoglycerate Mutase Deficiency; Phosphoglycerate Kinase Deficiency; Phosphorylase Kinase Deficiency; Beta Enolase Deficiency; Lactate Dehydrogenase Deficiency; Glycogen Synthase Deficiency

Imaging metabolic heterogeneity in cancer.

Science.gov (United States)

Sengupta, Debanti; Pratx, Guillem

2016-01-06

As our knowledge of cancer metabolism has increased, it has become apparent that cancer metabolic processes are extremely heterogeneous. The reasons behind this heterogeneity include genetic diversity, the existence of multiple and redundant metabolic pathways, altered microenvironmental conditions, and so on. As a result, methods in the clinic and beyond have been developed in order to image and study tumor metabolism in the in vivo and in vitro regimes. Both regimes provide unique advantages and challenges, and may be used to provide a picture of tumor metabolic heterogeneity that is spatially and temporally comprehensive. Taken together, these methods may hold the key to appropriate cancer diagnoses and treatments in the future.

Maternal cardiac metabolism in pregnancy

Science.gov (United States)

Liu, Laura X.; Arany, Zolt

2014-01-01

Pregnancy causes dramatic physiological changes in the expectant mother. The placenta, mostly foetal in origin, invades maternal uterine tissue early in pregnancy and unleashes a barrage of hormones and other factors. This foetal ‘invasion’ profoundly reprogrammes maternal physiology, affecting nearly every organ, including the heart and its metabolism. We briefly review here maternal systemic metabolic changes during pregnancy and cardiac metabolism in general. We then discuss changes in cardiac haemodynamic during pregnancy and review what is known about maternal cardiac metabolism during pregnancy. Lastly, we discuss cardiac diseases during pregnancy, including peripartum cardiomyopathy, and the potential contribution of aberrant cardiac metabolism to disease aetiology. PMID:24448314

Understanding specificity in metabolic pathways-Structural biology of human nucleotide metabolism

International Nuclear Information System (INIS)

Welin, Martin; Nordlund, Paer

2010-01-01

Interactions are the foundation of life at the molecular level. In the plethora of activities in the cell, the evolution of enzyme specificity requires the balancing of appropriate substrate affinity with a negative selection, in order to minimize interactions with other potential substrates in the cell. To understand the structural basis for enzyme specificity, the comparison of structural and biochemical data between enzymes within pathways using similar substrates and effectors is valuable. Nucleotide metabolism is one of the largest metabolic pathways in the human cell and is of outstanding therapeutic importance since it activates and catabolises nucleoside based anti-proliferative drugs and serves as a direct target for anti-proliferative drugs. In recent years the structural coverage of the enzymes involved in human nucleotide metabolism has been dramatically improved and is approaching completion. An important factor has been the contribution from the Structural Genomics Consortium (SGC) at Karolinska Institutet, which recently has solved 33 novel structures of enzymes and enzyme domains in human nucleotide metabolism pathways and homologs thereof. In this review we will discuss some of the principles for substrate specificity of enzymes in human nucleotide metabolism illustrated by a selected set of enzyme families where a detailed understanding of the structural determinants for specificity is now emerging.

Metabolic imaging using SPECT

International Nuclear Information System (INIS)

Taki, Junichi; Matsunari, Ichiro

2007-01-01

In normal condition, the heart obtains more than two-thirds of its energy from the oxidative metabolism of long chain fatty acids, although a wide variety of substrates such as glucose, lactate, ketone bodies and amino acids are also utilised. In ischaemic myocardium, on the other hand, oxidative metabolism of free fatty acid is suppressed and anaerobic glucose metabolism plays a major role in residual oxidative metabolism. Therefore, metabolic imaging can be an important technique for the assessment of various cardiac diseases and conditions. In SPECT, several iodinated fatty acid traces have been introduced and studied. Of these, 123 I-labelled 15-(p-iodophenyl)3-R, S-methylpentadecanoic acid (BMIPP) has been the most commonly used tracer in clinical studies, especially in some of the European countries and Japan. In this review article, several fatty acid tracers for SPECT are characterised, and the mechanism of uptake and clinical utility of BMIPP are discussed in detail. (orig.)

Metabolic surgery: quo vadis?

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Ramos-Leví, Ana M; Rubio Herrera, Miguel A

2014-01-01

The impact of bariatric surgery beyond its effect on weight loss has entailed a change in the way of regarding it. The term metabolic surgery has become more popular to designate those interventions that aim at resolving diseases that have been traditionally considered as of exclusive medical management, such as type 2 diabetes mellitus (T2D). Recommendations for metabolic surgery have been largely addressed and discussed in worldwide meetings, but no definitive consensus has been reached yet. Rates of diabetes remission after metabolic surgery have been one of the most debated hot topics, with heterogeneity being a current concern. This review aims to identify and clarify controversies regarding metabolic surgery, by focusing on a critical analysis of T2D remission rates achieved with different bariatric procedures, and using different criteria for its definition. Indications for metabolic surgery for patients with T2D who are not morbidly obese are also discussed. Copyright © 2013 SEEN. Published by Elsevier Espana. All rights reserved.

Energy Metabolism in the Liver

OpenAIRE

Rui, Liangyou

2014-01-01

The liver is an essential metabolic organ, and its metabolic activity is tightly controlled by insulin and other metabolic hormones. Glucose is metabolized into pyruvate through glycolysis in the cytoplasm, and pyruvate is completely oxidized to generate ATP through the TCA cycle and oxidative phosphorylation in the mitochondria. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, p...

Hypokalemic muscular paralysis causing acute respiratory failure due to rhabdomyolysis with renal tubular acidosis in a chronic glue sniffer.

Science.gov (United States)

Kao, K C; Tsai, Y H; Lin, M C; Huang, C C; Tsao, C Y; Chen, Y C

2000-01-01

A 34-year-old male was admitted to the emergency department with the development of quadriparesis and respiratory failure due to hypokalemia after prolonged glue sniffing. The patient was subsequently given mechanical ventilatory support for respiratory failure. He was weaned from the ventilator 4 days later after potassium replacement. Toluene is an aromatic hydrocarbon found in glues, cements, and solvents. It is known to be toxic to the nervous system, hematopoietic system, and causes acid-base and electrolyte disorders. Acute respiratory failure with hypokalemia and rhabdomyolysis with acute renal failure should be considered as potential events in a protracted glue sniffing.

Symptoms and Diagnosis of Metabolic Syndrome

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... Thromboembolism Aortic Aneurysm More Symptoms and Diagnosis of Metabolic Syndrome Updated:Apr 13,2017 What are the symptoms ... Syndrome? This content was last reviewed August 2016. Metabolic Syndrome • Home • About Metabolic Syndrome • Why Metabolic Syndrome Matters • ...

DNA Damage, Repair, and Cancer Metabolism

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Turgeon, Marc-Olivier; Perry, Nicholas J. S.; Poulogiannis, George

2018-01-01

Although there has been a renewed interest in the field of cancer metabolism in the last decade, the link between metabolism and DNA damage/DNA repair in cancer has yet to be appreciably explored. In this review, we examine the evidence connecting DNA damage and repair mechanisms with cell metabolism through three principal links. (1) Regulation of methyl- and acetyl-group donors through different metabolic pathways can impact DNA folding and remodeling, an essential part of accurate double strand break repair. (2) Glutamine, aspartate, and other nutrients are essential for de novo nucleotide synthesis, which dictates the availability of the nucleotide pool, and thereby influences DNA repair and replication. (3) Reactive oxygen species, which can increase oxidative DNA damage and hence the load of the DNA-repair machinery, are regulated through different metabolic pathways. Interestingly, while metabolism affects DNA repair, DNA damage can also induce metabolic rewiring. Activation of the DNA damage response (DDR) triggers an increase in nucleotide synthesis and anabolic glucose metabolism, while also reducing glutamine anaplerosis. Furthermore, mutations in genes involved in the DDR and DNA repair also lead to metabolic rewiring. Links between cancer metabolism and DNA damage/DNA repair are increasingly apparent, yielding opportunities to investigate the mechanistic basis behind potential metabolic vulnerabilities of a substantial fraction of tumors. PMID:29459886

What is Nutrition & Metabolism?

Directory of Open Access Journals (Sweden)

Feinman Richard D

2004-08-01

Full Text Available Abstract A new Open Access journal, Nutrition & Metabolism (N&M will publish articles that integrate nutrition with biochemistry and molecular biology. The open access process is chosen to provide rapid and accessible dissemination of new results and perspectives in a field that is of great current interest. Manuscripts in all areas of nutritional biochemistry will be considered but three areas of particular interest are lipoprotein metabolism, amino acids as metabolic signals, and the effect of macronutrient composition of diet on health. The need for the journal is identified in the epidemic of obesity, diabetes, dyslipidemias and related diseases, and a sudden increase in popular diets, as well as renewed interest in intermediary metabolism.

Mathematical modelling of metabolism

DEFF Research Database (Denmark)

Gombert, Andreas Karoly; Nielsen, Jens

2000-01-01

Mathematical models of the cellular metabolism have a special interest within biotechnology. Many different kinds of commercially important products are derived from the cell factory, and metabolic engineering can be applied to improve existing production processes, as well as to make new processes...... availability of genomic information and powerful analytical techniques, mathematical models also serve as a tool for understanding the cellular metabolism and physiology....... available. Both stoichiometric and kinetic models have been used to investigate the metabolism, which has resulted in defining the optimal fermentation conditions, as well as in directing the genetic changes to be introduced in order to obtain a good producer strain or cell line. With the increasing...

microRNAs and lipid metabolism

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Aryal, Binod; Singh, Abhishek K.; Rotllan, Noemi; Price, Nathan; Fernández-Hernando, Carlos

2017-01-01

Purpose of review Work over the last decade has identified the important role of microRNAs (miRNAS) in regulating lipoprotein metabolism and associated disorders including metabolic syndrome, obesity and atherosclerosis. This review summarizes the most recent findings in the field, highlighting the contribution of miRNAs in controlling low-density lipoprotein (LDL) and high-density lipoprotein (HDL) metabolism. Recent findings A number of miRNAs have emerged as important regulators of lipid metabolism, including miR-122 and miR-33. Work over the last two years has identified additional functions of miR-33 including the regulation of macrophage activation and mitochondrial metabolism. Moreover, it has recently been shown that miR-33 regulates vascular homeostasis and cardiac adaptation in response to pressure overload. In addition to miR-33 and miR-122, recent GWAS have identified single nucleotide polymorphisms (SNP) in the proximity of miRNAs genes associated with abnormal levels of circulating lipids in humans. Several of these miRNA, such as miR-148a and miR-128-1, target important proteins that regulate cellular cholesterol metabolism, including the low-density lipoprotein receptor (LDLR) and the ATP-binding cassette A1 (ABCA1). Summary microRNAs have emerged as critical regulators of cholesterol metabolism and promising therapeutic targets for treating cardiometabolic disorders including atherosclerosis. Here, we discuss the recent findings in the field highlighting the novel mechanisms by which miR-33 controls lipid metabolism and atherogenesis and the identification of novel miRNAs that regulate LDL metabolism. Finally, we summarize the recent findings that identified miR-33 as an important non-coding RNA that controls cardiovascular homeostasis independent of its role in regulating lipid metabolism. PMID:28333713

Quantification of patterns of regional cardiac metabolism

International Nuclear Information System (INIS)

Lear, J.L.; Ackermann, R.F.

1990-01-01

To quantitatively map and compare patterns of regional cardiac metabolism with greater spatial resolution than is possible with positron emission tomography (PET), the authors developed autoradiographic techniques for use with combinations of radiolabeled fluorodeoxyglucose (FDG), glucose (GLU), and acetate (ACE) and applied the techniques to normal rats. Kinetic models were developed to compare GLU-based oxidative glucose metabolism with FDG-based total glucose metabolism (oxidative plus anaerobic) and to compare ACE-based overall oxidative metabolism with FDG-based total glucose metabolism. GLU-based metabolism generally paralleled FDG-based metabolism, but divergence occurred in certain structures such as the papillary muscles, where FDG-based metabolism was much greater. ACE-based metabolism also generally paralleled FDG-based metabolism, but again, the papillary muscles had relatively greater FDG-based metabolism. These discrepancies between FDG-based metabolism and GLU- or ACE-based metabolism suggest the presence of high levels of anaerobic glycolysis. Thus, the study indicates that anaerobic glycolysis, in addition to occurring in ischemic or stunned myocardium (as has been shown in recent PET studies), occurs normally in specific cardiac regions, despite the presence of abundant oxygen

Energy Metabolism in the Liver

Science.gov (United States)

Rui, Liangyou

2014-01-01

The liver is an essential metabolic organ, and its metabolic activity is tightly controlled by insulin and other metabolic hormones. Glucose is metabolized into pyruvate through glycolysis in the cytoplasm, and pyruvate is completely oxidized to generate ATP through the TCA cycle and oxidative phosphorylation in the mitochondria. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, phospholipids, and cholesterol esters in hepatocytes, and these complex lipids are stored in lipid droplets and membrane structures, or secreted into the circulation as VLDL particles. In the fasted state, the liver secretes glucose through both breakdown of glycogen (glycogenolysis) and de novo glucose synthesis (gluconeogenesis). During pronged fasting, hepatic gluconeogenesis is the primary source of endogenous glucose production. Fasting also promotes lipolysis in adipose tissue to release nonesterified fatty acids which are converted into ketone bodies in the liver though mitochondrial β oxidation and ketogenesis. Ketone bodies provide a metabolic fuel for extrahepatic tissues. Liver metabolic processes are tightly regulated by neuronal and hormonal systems. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis, but suppresses gluconeogenesis; glucagon counteracts insulin action. Numerous transcription factors and coactivators, including CREB, FOXO1, ChREBP, SREBP, PGC-1α, and CRTC2, control the expression of the enzymes which catalyze the rate-limiting steps of liver metabolic processes, thus controlling liver energy metabolism. Aberrant energy metabolism in the liver promotes insulin resistance, diabetes, and nonalcoholic fatty liver diseases (NAFLD). PMID:24692138

Metabolic Regulation of a Bacterial Cell System with Emphasis on Escherichia coli Metabolism

Science.gov (United States)

Shimizu, Kazuyuki

2013-01-01

It is quite important to understand the overall metabolic regulation mechanism of bacterial cells such as Escherichia coli from both science (such as biochemistry) and engineering (such as metabolic engineering) points of view. Here, an attempt was made to clarify the overall metabolic regulation mechanism by focusing on the roles of global regulators which detect the culture or growth condition and manipulate a set of metabolic pathways by modulating the related gene expressions. For this, it was considered how the cell responds to a variety of culture environments such as carbon (catabolite regulation), nitrogen, and phosphate limitations, as well as the effects of oxygen level, pH (acid shock), temperature (heat shock), and nutrient starvation. PMID:25937963

Noise effect in metabolic networks

International Nuclear Information System (INIS)

Zheng-Yan, Li; Zheng-Wei, Xie; Tong, Chen; Qi, Ouyang

2009-01-01

Constraint-based models such as flux balance analysis (FBA) are a powerful tool to study biological metabolic networks. Under the hypothesis that cells operate at an optimal growth rate as the result of evolution and natural selection, this model successfully predicts most cellular behaviours in growth rate. However, the model ignores the fact that cells can change their cellular metabolic states during evolution, leaving optimal metabolic states unstable. Here, we consider all the cellular processes that change metabolic states into a single term 'noise', and assume that cells change metabolic states by randomly walking in feasible solution space. By simulating a state of a cell randomly walking in the constrained solution space of metabolic networks, we found that in a noisy environment cells in optimal states tend to travel away from these points. On considering the competition between the noise effect and the growth effect in cell evolution, we found that there exists a trade-off between these two effects. As a result, the population of the cells contains different cellular metabolic states, and the population growth rate is at suboptimal states. (cross-disciplinary physics and related areas of science and technology)

Xenobiotic Metabolism and Gut Microbiomes.

Directory of Open Access Journals (Sweden)

Anubhav Das

Full Text Available Humans are exposed to numerous xenobiotics, a majority of which are in the form of pharmaceuticals. Apart from human enzymes, recent studies have indicated the role of the gut bacterial community (microbiome in metabolizing xenobiotics. However, little is known about the contribution of the plethora of gut microbiome in xenobiotic metabolism. The present study reports the results of analyses on xenobiotic metabolizing enzymes in various human gut microbiomes. A total of 397 available gut metagenomes from individuals of varying age groups from 8 nationalities were analyzed. Based on the diversities and abundances of the xenobiotic metabolizing enzymes, various bacterial taxa were classified into three groups, namely, least versatile, intermediately versatile and highly versatile xenobiotic metabolizers. Most interestingly, specific relationships were observed between the overall drug consumption profile and the abundance and diversity of the xenobiotic metabolizing repertoire in various geographies. The obtained differential abundance patterns of xenobiotic metabolizing enzymes and bacterial genera harboring them, suggest their links to pharmacokinetic variations among individuals. Additional analyses of a few well studied classes of drug modifying enzymes (DMEs also indicate geographic as well as age specific trends.

Exercise-induced hypertension in men with metabolic syndrome: anthropometric, metabolic, and hemodynamic features.

Science.gov (United States)

Gaudreault, Valérie; Després, Jean-Pierre; Rhéaume, Caroline; Alméras, Natalie; Bergeron, Jean; Tremblay, Angelo; Poirier, Paul

2013-02-01

Metabolic syndrome is associated with increased cardiac morbidity. The aim of this study was to evaluate exercise-induced hypertension (EIH) in men with metabolic syndrome and to explore potential associations with anthropometric and metabolic variables. A total of 179 normotensive men with metabolic syndrome underwent a maximal symptom-limited treadmill test. Blood pressure was measured at 5-min rest prior to exercise testing (anticipatory blood pressure), at every 3 min during the exercise, and during the recovery period. EIH was defined as maximum systolic blood pressure (SBP) ≥220 mmHg and/or maximum diastolic blood pressure (DBP) ≥100 mmHg. Of the 179 men, 87 (47%) presented EIH. Resting blood pressure values at baseline were 127±10/83±6 mmHg in EIH and 119±9/80±6 mmHg (P=0.01 for both) in normal blood pressure responders to exercise. Anticipatory SBP and DPS were higher in the group with EIH (P=0.001). Subjects with EIH presented higher waist circumference (WC) (Pmetabolic syndrome showed EIH. These men are characterized by a worsened metabolic profile. Our data suggest that a treadmill exercise test may be helpful to identify a potentially higher risk metabolic syndrome subset of subjects.

Metabolic syndrome presenting as abdominal pain

Directory of Open Access Journals (Sweden)

Mohammed Y Al-Dossary

2017-01-01

Full Text Available Metabolic syndrome represents a sum of risk factors that lead to the occurrence of cardiovascular and cerebrovascular events. The early detection of metabolic syndrome is extremely important in adults who are at risk. Although the physiopathological mechanisms of the metabolic syndrome are not yet clear, insulin resistance plays a key role that could explain the development of type 2 diabetes mellitus in untreated metabolic syndrome patients. Here, we present the case of a 26-year-old male who was diagnosed with metabolic syndrome and severe hypertriglyceridemia after presenting with abdominal pain. Although hypertriglyceridemia and hyperglycemia are the most common predictors of metabolic syndrome, clinicians need to be vigilant for unexpected presentations in patients at risk for metabolic syndrome. This case sheds light on the importance of early detection.

Genome-scale modeling for metabolic engineering.

Science.gov (United States)

Simeonidis, Evangelos; Price, Nathan D

2015-03-01

We focus on the application of constraint-based methodologies and, more specifically, flux balance analysis in the field of metabolic engineering, and enumerate recent developments and successes of the field. We also review computational frameworks that have been developed with the express purpose of automatically selecting optimal gene deletions for achieving improved production of a chemical of interest. The application of flux balance analysis methods in rational metabolic engineering requires a metabolic network reconstruction and a corresponding in silico metabolic model for the microorganism in question. For this reason, we additionally present a brief overview of automated reconstruction techniques. Finally, we emphasize the importance of integrating metabolic networks with regulatory information-an area which we expect will become increasingly important for metabolic engineering-and present recent developments in the field of metabolic and regulatory integration.

LakeMetabolizer: An R package for estimating lake metabolism from free-water oxygen using diverse statistical models

Science.gov (United States)

Winslow, Luke; Zwart, Jacob A.; Batt, Ryan D.; Dugan, Hilary; Woolway, R. Iestyn; Corman, Jessica; Hanson, Paul C.; Read, Jordan S.

2016-01-01

Metabolism is a fundamental process in ecosystems that crosses multiple scales of organization from individual organisms to whole ecosystems. To improve sharing and reuse of published metabolism models, we developed LakeMetabolizer, an R package for estimating lake metabolism from in situ time series of dissolved oxygen, water temperature, and, optionally, additional environmental variables. LakeMetabolizer implements 5 different metabolism models with diverse statistical underpinnings: bookkeeping, ordinary least squares, maximum likelihood, Kalman filter, and Bayesian. Each of these 5 metabolism models can be combined with 1 of 7 models for computing the coefficient of gas exchange across the air–water interface (k). LakeMetabolizer also features a variety of supporting functions that compute conversions and implement calculations commonly applied to raw data prior to estimating metabolism (e.g., oxygen saturation and optical conversion models). These tools have been organized into an R package that contains example data, example use-cases, and function documentation. The release package version is available on the Comprehensive R Archive Network (CRAN), and the full open-source GPL-licensed code is freely available for examination and extension online. With this unified, open-source, and freely available package, we hope to improve access and facilitate the application of metabolism in studies and management of lentic ecosystems.

Cerebral Metabolic Changes Related to Oxidative Metabolism in a Model of Bacterial Meningitis Induced by Lipopolysaccharide

DEFF Research Database (Denmark)

Munk, Michael; Rom Poulsen, Frantz; Larsen, Lykke

2018-01-01

BACKGROUND: Cerebral mitochondrial dysfunction is prominent in the pathophysiology of severe bacterial meningitis. In the present study, we hypothesize that the metabolic changes seen after intracisternal lipopolysaccharide (LPS) injection in a piglet model of meningitis is compatible...... with mitochondrial dysfunction and resembles the metabolic patterns seen in patients with bacterial meningitis. METHODS: Eight pigs received LPS injection in cisterna magna, and four pigs received NaCl in cisterna magna as a control. Biochemical variables related to energy metabolism were monitored by intracerebral...... dysfunction with increasing cerebral LPR due to increased lactate and normal pyruvate, PbtO2, and ICP. The metabolic pattern resembles the one observed in patients with bacterial meningitis. Metabolic monitoring in these patients is feasible to monitor for cerebral metabolic derangements otherwise missed...

Nitrile Metabolizing Yeasts

Science.gov (United States)

Bhalla, Tek Chand; Sharma, Monica; Sharma, Nitya Nand

Nitriles and amides are widely distributed in the biotic and abiotic components of our ecosystem. Nitrile form an important group of organic compounds which find their applications in the synthesis of a large number of compounds used as/in pharmaceutical, cosmetics, plastics, dyes, etc>. Nitriles are mainly hydro-lyzed to corresponding amide/acid in organic chemistry. Industrial and agricultural activities have also lead to release of nitriles and amides into the environment and some of them pose threat to human health. Biocatalysis and biotransformations are increasingly replacing chemical routes of synthesis in organic chemistry as a part of ‘green chemistry’. Nitrile metabolizing organisms or enzymes thus has assumed greater significance in all these years to convert nitriles to amides/ acids. The nitrile metabolizing enzymes are widely present in bacteria, fungi and yeasts. Yeasts metabolize nitriles through nitrilase and/or nitrile hydratase and amidase enzymes. Only few yeasts have been reported to possess aldoxime dehydratase. More than sixty nitrile metabolizing yeast strains have been hither to isolated from cyanide treatment bioreactor, fermented foods and soil. Most of the yeasts contain nitrile hydratase-amidase system for metabolizing nitriles. Transformations of nitriles to amides/acids have been carried out with free and immobilized yeast cells. The nitrilases of Torulopsis candida>and Exophiala oligosperma>R1 are enantioselec-tive and regiospecific respectively. Geotrichum>sp. JR1 grows in the presence of 2M acetonitrile and may have potential for application in bioremediation of nitrile contaminated soil/water. The nitrilase of E. oligosperma>R1 being active at low pH (3-6) has shown promise for the hydroxy acids. Immobilized yeast cells hydrolyze some additional nitriles in comparison to free cells. It is expected that more focus in future will be on purification, characterization, cloning, expression and immobilization of nitrile metabolizing

Metabolic syndrome and menopause

OpenAIRE

Jouyandeh, Zahra; Nayebzadeh, Farnaz; Qorbani, Mostafa; Asadi, Mojgan

2013-01-01

Abstract Background The metabolic syndrome is defined as an assemblage of risk factors for cardiovascular diseases, and menopause is associated with an increase in metabolic syndrome prevalence. The aim of this study was to assess the prevalence of metabolic syndrome and its components among postmenopausal women in Tehran, Iran. Methods In this cross-sectional study in menopause clinic in Tehran, 118 postmenopausal women were investigated. We used the adult treatment panel 3 (ATP3) criteria t...

Vertigo and metabolic disorders.

Science.gov (United States)