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Sample records for acidosis

  1. Metabolic acidosis

    Acidosis - metabolic ... Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not ... the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ...

  2. Lactic Acidosis

    K.Srikanth

    2012-01-01

    Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poiso...

  3. Lactic Acidosis

    K.Srikanth

    2012-10-01

    Full Text Available Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia. Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction.

  4. Acidosis and Urinary Calcium Excretion

    Alexander, R Todd; Cordat, Emmanuelle; Chambrey, Régine;

    2016-01-01

    Metabolic acidosis is associated with increased urinary calcium excretion and related sequelae, including nephrocalcinosis and nephrolithiasis. The increased urinary calcium excretion induced by metabolic acidosis predominantly results from increased mobilization of calcium out of bone and...... renal tubule and then discuss why not all gene defects that cause renal tubular acidosis are associated with hypercalciuria and nephrocalcinosis....

  5. Renal tubular acidosis and nerve deafness.

    Dunger, D B; Brenton, D. P.; Cain, A R

    1980-01-01

    Two brothers are described with renal tubular acidosis and nerve deafness: the elder also had rickets and hypokalaemia. The parents were unaffected. Studies of urinary acidification and bicarbonate excretion were consistent with a distal tubular abnormality. This report strengthens the view previously proposed in similar cases that nerve deafness and renal tubular acidosis constitute a genetic entity. Examination for nerve deafness is indicated in any child with renal tubular acidosis.

  6. Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

    Berg, van den Else; Engberink, M.F.; Brink, E.J.; Baak, van M.A.; Joosten, M.M.; Gans, R.O.B.; Navis, G.; Bakker, S.J.L.

    2012-01-01

    Background and objectives Acidosis is prevalent among renal transplant recipients (RTRs) and adversely affects cardiometabolic processes. Factors contributing to acidosis are graft dysfunction and immunosuppressive drugs. Little is known about the potential influence of diet on acidosis in RTRs. Thi

  7. D-Lactic Acidosis in Humans: Review of Update

    Kang, Kyung Pyo; Lee, Sik; Kang, Sung Kyew

    2006-01-01

    D-Lactic acidosis has been well documented in ruminants. In humans, D-lactic acidosis is very rare, but D-lactic acidosis may be more common than generally believed and should be looked for in a case of metabolic acidosis in which the cause of acidosis is not apparent. The clinical presentation of D-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The entity should be considered as a diagnosis in a patient who presents with metabolic acidosis accompanied ...

  8. [Hypokalemic pareses secondary to renal tubular acidosis].

    Gøransson, L G; Apeland, T; Omdal, R

    2000-01-30

    A 24 year old woman presented with flaccid paralysis, severe hypokalaemia and hyperchloremia, metabolic acidosis. Immunological tests and labial glandular biopsy indicated primary Sjögren's syndrome as the underlying cause of her distal renal tubular acidosis. The patient recovered after alkali and potassium substitution and was put on oral treatment with potassium citrate. PMID:10827521

  9. Acidosis láctica

    Caridad Soler Morejón

    2000-06-01

    Full Text Available Se conoce que el ácido láctico es un producto terminal del metabolismo anaeróbico de la glucosa, que, en condiciones normales, los niveles séricos alcanzan las 2 mEq/L o menos. La mayor parte del lactato se elimina de forma muy eficaz por el hígado y se utiliza en la gluconeogénesis o para obtener energía. Si se producen incrementos considerables de las cifras de lactato sérico con disminución del metabolismo de conversión de lactato a piruvato se instala un cuadro de acidosis metabólica, a menudo grave, que puede llevar al paciente a la muerte. Desde el punto de vista clínico se debe sospechar ante un paciente con acidosis metabólica no bien explicada y anión Gap elevado, el cual se encuentra por encima de 25-30 mEq/L, aún en presencia de insuficiencia renal, de cetoacidosis o de la ingestión de un tóxico. La prevención de la hipoxia hística desempeña un papel importantísimo y en este sentido todas las medidas que contribuyen a garantizar una buena perfusión hística. Se señala la importancia del control adecuado de la diabetes mellitus, la selección más adecuada de hipoglicemiantes, el aporte de tiamina en los pacientes de riesgo, entre otras medidasIt is know that lactic acid is a last product of glucose anaerobic metabolism, that, in normal conditions, serum levels reach 2 mEq/L or less. Most of lactate is released in a very efficacious way by liver and is used in gluconeogenesis or to obtain energy. If there are significant increases of serum lactate figures with a decrease of metabolism of the conversion of lactate in pyruvate, a situation of metabolic acidosis frequently serious will present, which may provoke death of patient. From the clinical point of view, it must be suspected in a patient with non well explained metabolic acidosis and a high anion gap, which is over 25-30 mEq/L, even in presence of renal failure, ketoacidosis or ingestion of a toxic agent. That prevention of tissue hypoxia play a very

  10. Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

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

    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 ...

  11. Understanding lactic acidosis in paracetamol (acetaminophen) poisoning

    Shah, Anoop D; Wood, David M; Dargan, Paul I

    2011-01-01

    Paracetamol (acetaminophen) is one of the most commonly taken drugs in overdose in many areas of the world, and the most common cause of acute liver failure in both the UK and USA. Paracetamol poisoning can result in lactic acidosis in two different scenarios. First, early in the course of poisoning and before the onset of hepatotoxicity in patients with massive ingestion; a lactic acidosis is usually associated with coma. Experimental evidence from studies in whole animals, perfused liver sl...

  12. Moduretic-induced metabolic acidosis and hyperkalaemia.

    Wan, H. H.; Lye, M. D.

    1980-01-01

    A patient who developed significant metabolic acidosis and severe hyperkalaemia while taking Moduretic (amiloride and hydrochlorothiazide) is reported. During the period of hyperkalaemia (maximum potassium 7-6 mmol/l) the patient's whole body potassium content was normal. His acid-base balance and serum potassium returned to normal some 10 days after stopping the drug. The possible mechanism of acidosis and hyperkalaemia in this patient is discussed.

  13. Clinical profile of distal renal tubular acidosis

    Ratan Jha; Muthukrishnan, J.; Shekhar Shiradhonkar; Kiran Patro; Harikumar KVS; Modi, K.D.

    2011-01-01

    To determine the clinical profile and progression of renal dysfunction in distal renal tubular acidosis (dRTA), we retrospectively studied 96 consecutive cases of dRTA diagnosed at our center. Patients with unexplained metabolic bone disease, short stature, hypokalemia, re-current renal stones, chronic obstructive uropathy or any primary autoimmune condition known to cause dRTA were screened. Distal RTA was diagnosed on the basis of systemic metabolic acidosis with urine pH >5.5 and positive ...

  14. The genomic analysis of lactic acidosis and acidosis response in human cancers.

    Julia Ling-Yu Chen

    2008-12-01

    Full Text Available The tumor microenvironment has a significant impact on tumor development. Two important determinants in this environment are hypoxia and lactic acidosis. Although lactic acidosis has long been recognized as an important factor in cancer, relatively little is known about how cells respond to lactic acidosis and how that response relates to cancer phenotypes. We develop genome-scale gene expression studies to dissect transcriptional responses of primary human mammary epithelial cells to lactic acidosis and hypoxia in vitro and to explore how they are linked to clinical tumor phenotypes in vivo. The resulting experimental signatures of responses to lactic acidosis and hypoxia are evaluated in a heterogeneous set of breast cancer datasets. A strong lactic acidosis response signature identifies a subgroup of low-risk breast cancer patients having distinct metabolic profiles suggestive of a preference for aerobic respiration. The association of lactic acidosis response with good survival outcomes may relate to the role of lactic acidosis in directing energy generation toward aerobic respiration and utilization of other energy sources via inhibition of glycolysis. This "inhibition of glycolysis" phenotype in tumors is likely caused by the repression of glycolysis gene expression and Akt inhibition. Our study presents a genomic evaluation of the prognostic information of a lactic acidosis response independent of the hypoxic response. Our results identify causal roles of lactic acidosis in metabolic reprogramming, and the direct functional consequence of lactic acidosis pathway activity on cellular responses and tumor development. The study also demonstrates the utility of genomic analysis that maps expression-based findings from in vitro experiments to human samples to assess links to in vivo clinical phenotypes.

  15. Metabolic acidosis: neo-considerations for general surgeons.

    Martin, L C E; Abah, U; Bean, E; Gupta, S

    2012-11-01

    Hyperchloraemic metabolic acidosis is a documented complication of neobladder formation. However, it usually improves with time and is mild. Severe and persistent metabolic acidosis may manifest when patients undergo further surgery for other reasons. Neobladder formation following radical cystectomy or cystoprostatectomy is becoming increasingly common, and surgeons treating patients with neobladders should recognise and treat metabolic acidosis with intravenous fluids and bicarbonate. PMID:23131216

  16. Late Metabolic Acidosis Caused by Renal Tubular Acidosis in Acute Salicylate Poisoning.

    Sakai, Norihiro; Hirose, Yasuo; Sato, Nobuhiro; Kondo, Daisuke; Shimada, Yuko; Hori, Yasushi

    2016-01-01

    A 16-year-old man was transferred to our emergency department seven hours after ingesting 486 aspirin tablets. His blood salicylate level was 83.7 mg/dL. He was treated with fluid resuscitation and sodium bicarbonate infusion, and his condition gradually improved, with a decline in the blood salicylate level. However, eight days after admission, he again reported nausea, a venous blood gas revealed metabolic acidosis with a normal anion gap. The blood salicylate level was undetectable, and a urinalysis showed glycosuria, proteinuria and elevated beta-2 microglobulin and n-acetyl glucosamine levels, with a normal urinary pH despite the acidosis. We diagnosed him with relapse of metabolic acidosis caused by renal tubular acidosis. PMID:27181539

  17. Lactic Acidosis: Current Treatments and Future Directions.

    Kraut, Jeffrey A; Madias, Nicolaos E

    2016-09-01

    Mortality rates associated with severe lactic acidosis (blood pHreduce mortality. This failure has been attributed to both reduction in serum calcium concentration and generation of excess carbon dioxide with intracellular acidification. In animal studies, hyperventilation and infusion of calcium during sodium bicarbonate administration improves cardiovascular function, suggesting that this approach could allow expression of the positive aspects of sodium bicarbonate. Other buffers, such as THAM or Carbicarb, or dialysis might also provide base with fewer untoward effects. Examination of these therapies in humans is warranted. The cellular injury associated with lactic acidosis is partly due to activation of NHE1, a cell-membrane Na(+)/H(+) exchanger. In animal studies, selective NHE1 inhibitors improve cardiovascular function, ameliorate lactic acidosis, and reduce mortality, supporting future research into their possible use in humans. Two main mechanisms contribute to lactic acid accumulation in sepsis and low-flow states: tissue hypoxia and epinephrine-induced stimulation of aerobic glycolysis. Targeting these mechanisms could allow for more specific therapy. This Acid-Base and Electrolyte Teaching Case presents a patient with acute lactic acidosis and describes current and future approaches to treatment. PMID:27291485

  18. Renal tubular acidosis complicated with hypokalemic periodic paralysis.

    Chang, Y C; Huang, C C; Chiou, Y Y; Yu, C Y

    1995-07-01

    Three Chinese girls with hypokalemic periodic paralysis secondary to different types of renal tubular acidosis are presented. One girl has primary distal renal tubular acidosis complicated with nephrocalcinosis. Another has primary Sjögren syndrome with distal renal tubular acidosis, which occurs rarely with hypokalemic periodic paralysis in children. The third has an isolated proximal renal tubular acidosis complicated with multiple organ abnormalities, unilateral carotid artery stenosis, respiratory failure, and consciousness disturbance. The diagnostic evaluation and emergent and prophylactic treatment for these three types of renal tubular acidosis are discussed. PMID:7575850

  19. Distal renal tubular acidosis and amelogenesis imperfecta: A rare association

    Ravi, P.; Ekambaranath, T. S.; Arasi, S. Ellil; Fernando, E.

    2013-01-01

    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, previ...

  20. Drug-Induced Metabolic Acidosis [version 1; referees: 3 approved

    Amy Quynh Trang Pham

    2015-12-01

    Full Text Available Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs’ characteristics.

  1. Distal renal tubular acidosis in recurrent renal stone formers

    Osther, P J; Hansen, A B; Røhl, H F

    1989-01-01

    metabolic disturbances in renal stone formers. Distal renal tubular acidosis (dRTA) was relatively more common in female stone formers and most often found in patients with bilateral stone disease (36%). Since prophylactic treatment in renal stone formers with renal acidification defects is available, this...... (1.1%) had complete distal renal tubular acidosis and 14 (15.5%) incomplete distal renal tubular acidosis. Our results confirm that distal renal tubular acidification defects are associated with a more severe form of stone disease and make distal renal tubular acidosis one of the most frequent...

  2. Distal Renal Tubular Acidosis and Calcium Nephrolithiasis

    Moe, Orson W.; Fuster, Daniel G.; Xie, Xiao-Song

    2008-09-01

    Calcium stones are commonly encountered in patients with congenital distal renal tubular acidosis, a disease of renal acidification caused by mutations in either the vacuolar H+-ATPase (B1 or a4 subunit), anion exchanger-1, or carbonic anhydrase II. Based on the existing database, we present two hypotheses. First, heterozygotes with mutations in B1 subunit of H+-ATPase are not normal but may harbor biochemical abnormalities such as renal acidification defects, hypercalciuria, and hypocitraturia which can predispose them to kidney stone formation. Second, we propose at least two mechanisms by which mutant B1 subunit can impair H+-ATPase: defective pump assembly and defective pump activity.

  3. Type IV renal tubular acidosis associated with Alport's syndrome.

    Tkácová, R.; Roland, R.; Böör, A.; Kovácová, A.; Lazúrová, I.; Tkác, I.; Hildebrand, T.; Sefara, P.

    1993-01-01

    A case of hereditary nephritis with mild reduction of renal function associated with renal tubular acidosis type IV is described. The patient was admitted with life-threatening hyperkalaemia. To our knowledge, type IV renal tubular acidosis has not been reported previously in association with Alport's syndrome in an adult patient.

  4. An unrecognised case of metabolic acidosis following neobladder augmentation cystoplasty

    David Eldred-Evans

    2015-01-01

    Conclusion: Hyperchloremic metabolic acidosis is a well-established complication of urinary diversion. Patient with orthotopic neobladder with high residual urine and large capacity are at even higher risk of metabolic acidosis. This information should be clearly documented in the post-operative discharge documentation to ensure early recognition by non-specialists.

  5. Clinical profile of distal renal tubular acidosis

    Ratan Jha

    2011-01-01

    Full Text Available To determine the clinical profile and progression of renal dysfunction in distal renal tubular acidosis (dRTA, we retrospectively studied 96 consecutive cases of dRTA diagnosed at our center. Patients with unexplained metabolic bone disease, short stature, hypokalemia, re-current renal stones, chronic obstructive uropathy or any primary autoimmune condition known to cause dRTA were screened. Distal RTA was diagnosed on the basis of systemic metabolic acidosis with urine pH >5.5 and positive urine anion gap. In those patients who had fasting urine pH >5.5 with normal baseline systemic pH and bicarbonate levels (incomplete RTA, acid load test with ammonium chloride was done. A cause of dRTA could be established in 53 (54% patients. Urological defect in children (22/44 and autoimmune disease in adults (11/52 were the commonest causes. Hypokalemic paralysis, proximal muscle weakness and voiding difficulty were the common modes of presentation. Doubling of serum creatinine during the study period was noted in 13 out of 27 patients who had GFR 60 mL/min (P <0.005. In conclusion, urological disorders were the commonest cause of dRTA in children while autoimmune disorders were the commonest asso-ciation in adults. Worse baseline renal function, longer duration of disease and greater frequency of nephrolithiasis/nephrocalcinosis and urological disorders were noted in those who had wor-sening of renal dysfunction during the study period.

  6. Clinical profile of distal renal tubular acidosis.

    Jha, Ratan; Muthukrishnan, J; Shiradhonkar, Shekhar; Patro, Kiran; Harikumar, Kvs; Modi, K D

    2011-03-01

    To determine the clinical profile and progression of renal dysfunction in distal renal tubular acidosis (dRTA), we retrospectively studied 96 consecutive cases of dRTA diagnosed at our center. Patients with unexplained metabolic bone disease, short stature, hypokalemia, re-current renal stones, chronic obstructive uropathy or any primary autoimmune condition known to cause dRTA were screened. Distal RTA was diagnosed on the basis of systemic metabolic acidosis with urine pH >5.5 and positive urine anion gap. In those patients who had fasting urine pH >5.5 with normal baseline systemic pH and bicarbonate levels (incomplete RTA), acid load test with ammonium chloride was done. A cause of dRTA could be established in 53 (54%) patients. Urological defect in children (22/44) and autoimmune disease in adults (11/52) were the commonest causes. Hypokalemic paralysis, proximal muscle weakness and voiding difficulty were the common modes of presentation. Doubling of serum creatinine during the study period was noted in 13 out of 27 patients who had GFR 60 mL/min (P <0.005). In conclusion, urological disorders were the commonest cause of dRTA in children while autoimmune disorders were the commonest asso-ciation in adults. Worse baseline renal function, longer duration of disease and greater frequency of nephrolithiasis/nephrocalcinosis and urological disorders were noted in those who had wor-sening of renal dysfunction during the study period. PMID:21422623

  7. Renal tubular acidosis due to the milk-alkali syndrome.

    Rochman, J; Better, O S; Winaver, J; Chaimowitz, C; Barzilai, A; Jacobs, R

    1977-06-01

    A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome. PMID:885714

  8. Distal renal tubular acidosis and amelogenesis imperfecta: A rare association.

    Ravi, P; Ekambaranath, T S; Arasi, S Ellil; Fernando, E

    2013-11-01

    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. PMID:24339526

  9. Lactic Acidosis in a Patient with Type 2 Diabetes Mellitus.

    Weisberg, Lawrence S

    2015-08-01

    Lactic acidosis occurs when lactate production exceeds its metabolism. There are many possible causes of lactic acidosis, and in any given patient, several causes may coexist. This Attending Rounds presents a case in point. Metformin's role in the pathogenesis of lactic acidosis in patients with diabetes mellitus is complex, as the present case illustrates. The treatment of lactic acidosis is controversial, except for the imperative to remedy its underlying cause. The use of sodium bicarbonate to treat the often alarming metabolic derangements may be quite efficacious in that regard but is of questionable benefit to patients. Renal replacement therapies (RRTs) have particular appeal in this setting for a variety of reasons, but their effect on clinical outcomes is untested. PMID:25762524

  10. Side Effects of HIV Medicines: HIV and Lactic Acidosis

    ... HIV medicines. All HIV medicines in the nucleoside reverse transcriptase inhibitor (NRTI) drug class may cause lactic acidosis, but ... some HIV medicines. HIV medicines in the nucleoside reverse transcriptase inhibitor (NRTI) drug class can cause the body to ...

  11. [Primary distal renal tubular acidosis: a case report].

    Abdallah, Jihene Ben; Charfeddine, Bassem; Braham, Imen; Neffati, Souhir; Othmen, Leila Ben; Letaief, Affef; Smach, Mohamed Ali; Bourfifa, Zoheier; Dridi, Hedi; Limem, Khalifa

    2011-01-01

    The primary distal renal tubular acidosis is characterized biochemically by the inability of the kidney to produce appropriately acid urine in the presence of systemic metabolic acidosis or after acid loading (e.g. ammonium chloride). It is secondary to defective excretion of H(+) by the cells of the collecting duct. We report the observation of the child MC, 4-year-old, for whom the association of polyuria-polydipsia syndrome, a failure to thrive, nephrolithiasis, hypercalciuria, and especially a high urine pH in the presence of metabolic acidosis did evoke diagnosis of distal renal tubular acidosis. An urine acidification test with ammonium chloride was performed, the urinary pH was always higher than 5.5, thus confirming the diagnosis. PMID:21464016

  12. Acute Isoniazid Intoxication: Convulsion, Rhabdomyolysis and Metabolic Acidosis

    OKUTUR, Sadi Kerem

    2006-01-01

    Isoniazid is one of the most commonly used antituberculous drugs. Acute intoxication is characterized by repetitious convulsions, high anion gap metabolic acidosis and coma. The basis of therapy consists of parenteral pyridoxine administration in a dose equivalent to that of isoniazid ingested. Here we present a case of acute isoniazid intoxication presenting with convulsions and metabolic acidosis with consequent rhabdomyolysis and discuss the clinical signs and pathophysiology of isoniazid ...

  13. Renal tubular acidosis secondary to jejunoileal bypass for morbid obesity

    Schaffalitzky de Muckadell, O B; Ladefoged, Jens; Thorup, Jørgen Mogens

    1985-01-01

    Renal handling of acid and base was studied in patients with persistent metabolic acidosis 3-9 years after jejunoileal bypass for morbid obesity. Excretion of acid was studied before and after intravenous infusion of NH4Cl and excretion of bicarbonate after infusion of NaHCO3. Bypass patients...... groups. Fractional loss of bicarbonate in urine was higher in controls than in bypass patients. The renal impairment is classified as distal renal tubular acidosis....

  14. Treatment of Lactic Acidosis with Dichloroacetate in Dogs

    Park, Robert; Arieff, Allen I.; Leach, William; Lazarowitz, Virginia C.

    1982-01-01

    Lactic acidosis is a clinical condition due to accumulation of H+ ions from lactic acid, characterized by blood lactate levels >5 mM and arterial pH 60%. Dichloroacetate (DCA) is a compound that lowers blood lactate levels under various conditions in both man and laboratory animals. It acts to increase pyruvate oxidation by activation of pyruvate dehydrogenase. We evaluated the effects of DCA in the treatment of two different models of type B experimental lactic acidosis in diabetic dogs: hep...

  15. Metformin-induced lactic acidosis: a case series

    Silvestre Joana; Carvalho Susana; Mendes Vitor; Coelho Luis; Tapadinhas Camila; Ferreira Pedro; Povoa Pedro; Ceia Fatima

    2007-01-01

    Abstract Introduction Unlike other agents used in the treatment of type 2 diabetes mellitus, metformin has been shown to reduce mortality in obese patients. It is therefore being increasingly used in higher doses. The major concern of many physicians is a possible risk of lactic acidosis. The reported frequency of metformin related lactic acidosis is 0.05 per 1000 patient-years; some authors advocate that this rate is equal in those patients not taking metformin. Case presentation We present ...

  16. Benign duodenocolic fistula. A case presenting with acidosis

    Benn, Marianne; Nielsen, F T; Antonsen, H K

    1997-01-01

    A case of benign duodenocolic fistula as a complication to peptic ulcer disease is presented, the case being interesting for the rarity of the diagnosis and by being complicated with acidosis. The etiology, clinical features, diagnosis, and treatment are reviewed.......A case of benign duodenocolic fistula as a complication to peptic ulcer disease is presented, the case being interesting for the rarity of the diagnosis and by being complicated with acidosis. The etiology, clinical features, diagnosis, and treatment are reviewed....

  17. A distal renal tubular acidosis showing hyperammonemia and hyperlactacidemia

    C. Ripoli; Pinna, A.; Marras, S.; M.L. Fenu; Nurchi, A M

    2012-01-01

    Introduction: distal renal tubular acidosis (dRTA) presents itself with variable clinical manifestations and often with late expressions that impact on prognosis. Case report: A 45-day-old male infant was admitted with stopping growth, difficult feeding and vomiting after meals. Clinical tests and labs revealed a type 1 renal tubular acidosis, even if the first blood tests showed ammonium and lactate increase. We had to exclude metabolic diseases before having a certain diagnosis. Conclusions...

  18. Lactic acidosis induced by metformin: incidence, management and prevention.

    Lalau, Jean-Daniel

    2010-09-01

    Lactic acidosis associated with metformin treatment is a rare but important adverse event, and unravelling the problem is critical. First, this potential event still influences treatment strategies in type 2 diabetes mellitus, particularly in the many patients at risk of kidney failure, in those presenting contraindications to metformin and in the elderly. Second, the relationship between metformin and lactic acidosis is complex, since use of the drug may be causal, co-responsible or coincidental. The present review is divided into three parts, dealing with the incidence, management and prevention of lactic acidosis occurring during metformin treatment. In terms of incidence, the objective of this article is to counter the conventional view of the link between metformin and lactic acidosis, according to which metformin-associated lactic acidosis is rare but is still associated with a high rate of mortality. In fact, the direct metformin-related mortality is close to zero and metformin may even be protective in cases of very severe lactic acidosis unrelated to the drug. Metformin has also inherited a negative class effect, since the early biguanide, phenformin, was associated with more frequent and sometimes fatal lactic acidosis. In the second part of this review, the objective is to identify the most efficient patient management methods based on our knowledge of how metformin acts on glucose/lactate metabolism and how lactic acidosis may occur (at the organ and cellular levels) during metformin treatment. The liver appears to be a key organ for both the antidiabetic effect of metformin and the development of lactic acidosis; the latter is attributed to mitochondrial impairment and subsequent adenosine triphosphate depletion, acceleration of the glycolytic flux, increased glucose uptake and the generation of lactate, which effluxes into the circulation rather than being oxidized further. Haemodialysis should systematically be performed in severe forms of lactic

  19. Metabolic Acidosis with Ophthalmic Dorzolamide in a Neonate.

    Capino, Amanda C; Dannaway, Douglas C; Miller, Jamie L

    2016-01-01

    Carbonic anhydrase inhibitors are a common cause of normal anion gap metabolic acidosis; however, development is less commonly associated with ophthalmic administration of these agents. We report a case of a premature neonate who was being treated at our institution with betaxolol, dorzolamide, and latanoprost ophthalmic products for suspected bilateral congenital glaucoma. In addition, the patient was also receiving caffeine, ursodiol, and acidified liquid human milk fortifier. The patient developed a normal anion gap metabolic acidosis, and both dorzolamide ophthalmic solution and the acidified human milk fortifier were considered potential causes. Upon discontinuation of the dorzolamide ophthalmic solution and the switching of liquid human milk fortifiers, the normal anion gap metabolic acidosis gradually resolved. As a result of the pH and acidity, the acidified liquid human milk fortifier is thought to be associated with an anion gap acidosis; therefore, dorzolamide is suspected to be the primary cause of a normal gap acidosis. This case demonstrates that systemic effects can occur with ophthalmic administration of dorzolamide in a premature neonate. Ophthalmic agents should not be overlooked as a potential cause of systemic toxicity. PMID:27453705

  20. Acidosis Promotes Bcl-2 Family-mediated Evasion of Apoptosis

    Ryder, Christopher; McColl, Karen; Zhong, Fei; Distelhorst, Clark W.

    2012-01-01

    Acidosis arises in solid and lymphoid malignancies secondary to altered nutrient supply and utilization. Tumor acidosis correlates with therapeutic resistance, although the mechanism behind this effect is not fully understood. Here we show that incubation of lymphoma cell lines in acidic conditions (pH 6.5) blocks apoptosis induced by multiple cytotoxic metabolic stresses, including deprivation of glucose or glutamine and treatment with dexamethasone. We sought to examine the role of the Bcl-2 family of apoptosis regulators in this process. Interestingly, we found that acidic culture causes elevation of both Bcl-2 and Bcl-xL, while also attenuating glutamine starvation-induced elevation of p53-up-regulated modulator of apoptosis (PUMA) and Bim. We confirmed with knockdown studies that these shifts direct survival decisions during starvation and acidosis. Importantly, the promotion of a high anti- to pro-apoptotic Bcl-2 family member ratio by acidosis renders cells exquisitely sensitive to the Bcl-2/Bcl-xL antagonist ABT-737, suggesting that acidosis causes Bcl-2 family dependence. This dependence appears to be mediated, in part, by the acid-sensing G protein-coupled receptor, GPR65, via a MEK/ERK pathway. PMID:22685289

  1. Neurological damage arising from intrapartum hypoxia/acidosis.

    Rei, M; Ayres-de-Campos, D; Bernardes, J

    2016-01-01

    Complications occurring at any level of foetal oxygen supply will result in hypoxaemia, and this may ultimately lead to hypoxia/acidosis and neurological damage. Hypoxic-ischaemic encephalopathy (HIE) is the short-term neurological dysfunction caused by intrapartum hypoxia/acidosis, and this diagnosis requires the presence of a number of findings, including the confirmation of newborn metabolic acidosis, low Apgar scores, early imaging evidence of cerebral oedema and the appearance of clinical signs of neurological dysfunction in the first 48 h of life. Cerebral palsy (CP) consists of a heterogeneous group of nonprogressive movement and posture disorders, frequently accompanied by cognitive and sensory impairments, epilepsy, nutritional deficiencies and secondary musculoskeletal lesions. Although CP is the most common long-term neurological complication associated with intrapartum hypoxia/acidosis, >80% of cases are caused by other phenomena. Data on minor long-term neurological deficits are scarce, but they suggest that less serious intellectual and motor impairments may result from intrapartum hypoxia/acidosis. This chapter focuses on the existing evidence of neurological damage associated with poor foetal oxygenation during labour. PMID:26148854

  2. Type B Lactic Acidosis Associated With Venlafaxine Overdose.

    Iragavarapu, Chaitanya; Gupta, Tanush; Chugh, Savneek S; Aronow, Wilbert S; Frishman, William H

    2016-01-01

    Lactic acidosis that is not secondary to tissue hypoperfusion or hypoxemia (type B lactic acidosis) is a rare but potentially fatal condition that has been associated with drugs like metformin, linezolid, and nucleoside reverse-transcriptase inhibitors in patients with HIV. We report the first case of type B lactic acidosis caused by overdose of the serotonin-norepinephrine reuptake inhibitor, venlafaxine. A 55-year-old man with no significant medical history was brought to the emergency department after intentional ingestion of around 80 capsules of venlafaxine (a total dose of over 6000 mg) in an attempt to commit suicide. Complete blood count and comprehensive metabolic panel were unremarkable except for a bicarbonate level of 13 mEq/L and an anion gap of 22 mEq/L. An arterial blood gas revealed a pH of 7.39, partial pressure of CO2 of 19 mm Hg, calculated bicarbonate of 11.5 mEq/L, and a lactate level of 8.6 mmol/L. The patient was started on aggressive intravenous hydration with normal saline along with oral activated charcoal with sorbitol. Repeat laboratory work after 4 hours showed an improvement in anion gap (15 mEq/L) and serum lactate (5.6 mmol/L). The patient remained stable throughout the hospital stay and lactic acidosis resolved in 24 hours. In the absence of hypotension, hypoxemia, kidney or liver dysfunction, myopathy, malignancy, or use of other medications, venlafaxine was the most likely cause of lactic acidosis in our case. Rapid improvement of acidosis was probably related to clearance of the drug. PMID:25405896

  3. Coagulopathy induced by acidosis, hypothermia and hypocalcaemia in severe bleeding.

    De Robertis, E; Kozek-Langenecker, S A; Tufano, R; Romano, G M; Piazza, O; Zito Marinosci, G

    2015-01-01

    Acidosis, hypothermia and hypocalcaemia are determinants for morbidity and mortality during massive hemorrhages. However, precise pathological mechanisms of these environmental factors and their potential additive or synergistic anticoagulant and/or antiplatelet effects are not fully elucidated and are at least in part controversial. Best available evidences from experimental trials indicate that acidosis and hypothermia progressively impair platelet aggregability and clot formation. Considering the cell-based model of coagulation physiology, hypothermia predominantly prolongs the initiation phase, while acidosis prolongs the propagation phase of thrombin generation. Acidosis increases fibrinogen breakdown while hypothermia impairs its synthesis. Acidosis and hypothermia have additive effects. The effect of hypocalcaemia on coagulopathy is less investigated but it appears that below the cut-off of 0.9 mmol/L, several enzymatic steps in the plasmatic coagulation system are blocked while above that cut-off effects remain without clinical sequalae. The impact of environmental factor on hemostasis is underestimated in clinical practice due to our current practice of using routine coagulation laboratory tests such as partial thromboplastin time or prothrombin time, which are performed at standardized test temperature, after pH correction, and upon recalcification. Temperature-adjustments are feasible in viscoelastic point-of-care tests such as thrombelastography and thromboelastometry which may permit quantification of hypothermia-induced coagulopathy. Rewarming hypothermic bleeding patients is highly recommended because it improves patient outcome. Despite the absence of high-quality evidence, calcium supplementation is clinical routine in bleeding management. Buffer administration may not reverse acidosis-induced coagulopathy but may be essential for the efficacy of coagulation factor concentrates such as recombinant activated factor VII. PMID:24608516

  4. Ventilatory response in metabolic acidosis and cerebral blood volume in humans.

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

    2001-01-01

    The relationship between alterations in cerebral blood volume (CBV) and central chemosensitivity regulation was studied under neutral metabolic conditions and during metabolic acidosis. Fifteen healthy subjects (5610 years) were investigated. To induce metabolic acidosis, ammonium chloride (NH(4)Cl)

  5. Type 4 renal tubular acidosis in a kidney transplant recipient.

    Kulkarni, Manjunath

    2016-02-01

    We report a case of a 66-year-old diabetic patient who presented with muscle weakness 2 weeks after kidney transplantation. Her immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and steroids. She was found to have hyperkalemia and normal anion gap metabolic acidosis. Tacrolimus levels were in therapeutic range. All other drugs such as beta blockers and trimethoprim - sulfamethoxazole were stopped. She did not respond to routine antikalemic measures. Further evaluation revealed type 4 renal tubular acidosis. Serum potassium levels returned to normal after starting sodium bicarbonate and fludrocortisone therapy. Though hyperkalemia is common in kidney transplant recipients, determining exact cause can guide specific treatment. PMID:27105603

  6. [5-0xoproline (pyroglutamic acid) acidosis and acetaminophen- a differential diagnosis in high anion gap metabolic acidosis].

    Weiler, Stefan; Bellmann, Romuald; Kullak-Ublick, Gerd A

    2015-12-01

    Rare cases of high anion gap metabolic acidosis during long-term paracetamol administration in therapeutic doses with causative 5-oxoproline (pyroglutamic acid} accumulation have been reported. Other concomitant risk factors such as malnutrition, alcohol abuse, renal or hepatic dysfunction, comedication with flue/oxacillin, vigabatrin, netilmicin or sepsis have been described. The etiology seems to be a drug-induced reversible inhibition of glutathione synthetase or 5-oxoprolinase leading to elevated serum and urine levels of 5-oxoproline. Other more frequent differential diagnoses, such as intoxications, ketoacidosis or lactic acidosis should be excluded. Causative substances should be stopped. 5-oxoproline concentrations in urine can be quantified to establish the diagnosis. Adverse drug reactions, which are not listed or insufficiently described in the respective Swiss product information, should be reported to the regional pharmacovigilance centres for early signal detection. 5-0 xoproline acidosis will be integrated as a potential adverse drug reaction in the Swiss product information for paracetamol. PMID:26654818

  7. Cerebrovascular response to acute metabolic acidosis in humans.

    Ven, M.T.P. van de; Colier, W.N.J.M.; Kersten, B.T.P.; Oeseburg, B.; Folgering, H.T.M.

    2003-01-01

    OBJECTIVES: Evaluation of the cerebrovascular response (delta CBV/delta PaCO2) during baseline metabolic conditions and acute metabolic acidosis. METHODS: 15 healthy subjects, 5 m, 10 f, 56 +/- 10 yrs were investigated. For acidification, NH4Cl was given orally. CBV was measured using Near Infrared

  8. Phenylbutyrate Therapy for Pyruvate Dehydrogenase Complex Deficiency and Lactic Acidosis

    Ferriero, Rosa; Manco, Giuseppe; Lamantea, Eleonora; Nusco, Edoardo; Ferrante, Mariella I.; Sordino, Paolo; Stacpoole, Peter W.; Lee, Brendan; Zeviani, Massimo; Brunetti-Pierri, Nicola

    2014-01-01

    Lactic acidosis is a build-up of lactic acid in the blood and tissues, which can be due to several inborn errors of metabolism as well as nongenetic conditions. Deficiency of pyruvate dehydrogenase complex (PDHC) is the most common genetic disorder leading to lactic acidosis. Phosphorylation of specific serine residues of the E1α subunit of PDHC by pyruvate dehydrogenase kinase (PDK) inactivates the enzyme, whereas dephosphorylation restores PDHC activity. We found that phenylbutyrate enhances PDHC enzymatic activity in vitro and in vivo by increasing the proportion of unphosphorylated enzyme through inhibition of PDK. Phenylbutyrate given to C57B6/L wild-type mice results in a significant increase in PDHC enzyme activity and a reduction of phosphorylated E1α in brain, muscle, and liver compared to saline-treated mice. By means of recombinant enzymes, we showed that phenylbutyrate prevents phosphorylation of E1α through binding and inhibition of PDK, providing a molecular explanation for the effect of phenylbutyrate on PDHC activity. Phenylbutyrate increases PDHC activity in fibroblasts from PDHC-deficient patients harboring various molecular defects and corrects the morphological, locomotor, and biochemical abnormalities in the noam631 zebrafish model of PDHC deficiency. In mice, phenylbutyrate prevents systemic lactic acidosis induced by partial hepatectomy. Because phenylbutyrate is already approved for human use in other diseases, the findings of this study have the potential to be rapidly translated for treatment of patients with PDHC deficiency and other forms of primary and secondary lactic acidosis. PMID:23467562

  9. Metformin-induced lactic acidosis: a case series

    Silvestre Joana

    2007-10-01

    Full Text Available Abstract Introduction Unlike other agents used in the treatment of type 2 diabetes mellitus, metformin has been shown to reduce mortality in obese patients. It is therefore being increasingly used in higher doses. The major concern of many physicians is a possible risk of lactic acidosis. The reported frequency of metformin related lactic acidosis is 0.05 per 1000 patient-years; some authors advocate that this rate is equal in those patients not taking metformin. Case presentation We present two case reports of metformin-associated lactic acidosis. The first case is a 77 year old female with a past medical history of hypertension and type 2 diabetes mellitus who had recently been prescribed metformin (3 g/day, perindopril and acetylsalicylic acid. She was admitted to the emergency department two weeks later with abdominal pain and psychomotor agitation. Physical examination revealed only signs of poor perfusion. Laboratory evaluation revealed hyperkalemia, elevated creatinine and blood urea nitrogen and mild leukocytosis. Arterial blood gases showed severe lactic acidemia. She was admitted to the intensive care unit. Vasopressor and ventilatory support was initiated and continuous venovenous hemodiafiltration was instituted. Twenty-four hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the sixth day. The second patient is a 69 year old male with a past medical history of hypertension, type 2 diabetes mellitus and ischemic heart disease who was on metformin (4 g/day, glycazide, acetylsalicylic acid and isosorbide dinitrate. He was admitted to the emergency department in shock with extreme bradycardia. Initial evaluation revealed severe lactic acidosis and elevated creatinine and urea. The patient was admitted to the Intensive Care Unit and commenced on continuous venovenous hemodiafiltration in addition to other supportive measures. A

  10. Development of diabetes-induced acidosis in the rat retina.

    Dmitriev, Andrey V; Henderson, Desmond; Linsenmeier, Robert A

    2016-08-01

    We hypothesized that the retina of diabetic animals would be unusually acidic due to increased glycolytic metabolism. Acidosis in tumors and isolated retina has been shown to lead to increased VEGF. To test the hypothesis we have measured the transretinal distribution of extracellular H(+) concentration (H(+)-profiles) in retinae of control and diabetic dark-adapted intact Long-Evans rats with ion-selective electrodes. Diabetes was induced by intraperitoneal injection of streptozotocin. Intact rat retinae are normally more acidic than blood with a peak of [H(+)]o in the outer nuclear layer (ONL) that averages 30 nM higher than H(+) in the choroid. Profiles in diabetic animals were similar in shape, but diabetic retinae began to be considerably more acidic after 5 weeks of diabetes. In retinae of 1-3 month diabetics the difference between the ONL and choroid was almost twice as great as in controls. At later times, up to 6 months, some diabetics still demonstrated abnormally high levels of [H(+)]o, but others were even less acidic than controls, so that the average level of acidosis was not different. Greater variability in H(+)-profiles (both between animals and between profiles recorded in one animal) distinguished the diabetic retinae from controls. Within animals, this variability was not random, but exhibited regions of higher and lower H(+). We conclude that retinal acidosis begins to develop at an early stage of diabetes (1-3 months) in rats. However, it does not progress, and the acidity of diabetic rat retina was diminished at later stages (3-6 months). Also the diabetes-induced acidosis has a strongly expressed local character. As result, the diabetic retinas show much wider variability in [H(+)] distribution than controls. pH influences metabolic and neural processes, and these results suggest that local acidosis could play a role in the pathogenesis of diabetic retinopathy. PMID:27262608

  11. Metformin-Associated Acute Kidney Injury and Lactic Acidosis

    David Arroyo

    2011-01-01

    Full Text Available Objectives. Metformin is the preferred oral antidiabetic agent for type 2 diabetes. Lactic acidosis is described as a rare complication, usually during an acute kidney injury (AKI. Material and Methods. We conducted a prospective observational study of metformin-associated AKI cases during four years. 29 cases were identified. Previous renal function, clinical data, and outcomes were recorded. Results. An episode of acute gastroenteritis precipitated the event in 26 cases. Three developed a septic shock. Three patients died, the only related factor being liver dysfunction. More severe metabolic acidosis hyperkalemia and anemia were associated with higher probabilities of RRT requirement. We could not find any relationship between previous renal dysfunction and the outcome of the AKI. Conclusions. AKI associated to an episode of volume depletion due to gastrointestinal losses is a serious complication in type 2 diabetic patients on metformin. Previous renal dysfunction (mild-to-moderate CKD has no influence on the severity or outcome.

  12. A distal renal tubular acidosis showing hyperammonemia and hyperlactacidemia

    C. Ripoli

    2012-08-01

    Full Text Available Introduction: distal renal tubular acidosis (dRTA presents itself with variable clinical manifestations and often with late expressions that impact on prognosis. Case report: A 45-day-old male infant was admitted with stopping growth, difficult feeding and vomiting after meals. Clinical tests and labs revealed a type 1 renal tubular acidosis, even if the first blood tests showed ammonium and lactate increase. We had to exclude metabolic diseases before having a certain diagnosis. Conclusions: blood and urine investigations and genetic tests are fundamental to formulate dRTA diagnosis and to plan follow-up, according to possible phenotypic expressions of recessive and dominant autosomal forms in patients with dRTA.

  13. Acidosis ruminal en bovinos lecheros: implicaciones sobre la producción y la salud animal - Ruminal acidosis in dairy cattle: implications for animal health and production

    Granja Salcedo, Yury Tatiana

    2012-04-01

    Full Text Available ResumenLa acidosis ruminal es un importante problema en la producción de bovinos alimentados con dietas ricas en concentrados, especialmente en vacas de alta producción lechera.AbstractRuminal acidosis is a major problem in the production of cattle fed diets rich in concentrates, especially in cows of high milk production.

  14. Metabolic acidosis may be as protective as hypercapnic acidosis in an ex-vivo model of severe ventilator-induced lung injury: a pilot study

    Patsouris Efstratios

    2011-04-01

    Full Text Available Abstract Background There is mounting experimental evidence that hypercapnic acidosis protects against lung injury. However, it is unclear if acidosis per se rather than hypercapnia is responsible for this beneficial effect. Therefore, we sought to evaluate the effects of hypercapnic (respiratory versus normocapnic (metabolic acidosis in an ex vivo model of ventilator-induced lung injury (VILI. Methods Sixty New Zealand white rabbit ventilated and perfused heart-lung preparations were used. Six study groups were evaluated. Respiratory acidosis (RA, metabolic acidosis (MA and normocapnic-normoxic (Control - C groups were randomized into high and low peak inspiratory pressures, respectively. Each preparation was ventilated for 1 hour according to a standardized ventilation protocol. Lung injury was evaluated by means of pulmonary edema formation (weight gain, changes in ultrafiltration coefficient, mean pulmonary artery pressure changes as well as histological alterations. Results HPC group gained significantly greater weight than HPMA, HPRA and all three LP groups (P = 0.024, while no difference was observed between HPMA and HPRA groups regarding weight gain. Neither group differ on ultrafiltration coefficient. HPMA group experienced greater increase in the mean pulmonary artery pressure at 20 min (P = 0.0276 and 40 min (P = 0.0012 compared with all other groups. Histology scores were significantly greater in HP vs. LP groups (p Conclusions In our experimental VILI model both metabolic acidosis and hypercapnic acidosis attenuated VILI-induced pulmonary edema implying a mechanism other than possible synergistic effects of acidosis with CO2 for VILI attenuation.

  15. Blood Parameters Modification at Different Ruminal Acidosis Conditions

    Roberta De Nardi

    2013-09-01

    Full Text Available This study evaluated the reliability of various blood parameters to assess the ruminal acidosis in cattle. Six whole heifers were fed three experimental rations in a 3 x 3 Latin square design. The diets had different starch levels: high (HS, medium (MS or low (CT. Ruminal pH values were continuously measured using wireless sensors. To evaluate the severity of ruminal acidosis, the amount of time per day that the pH was below 5.8, 5.5 and 5.0 was recorded. Blood samples were analyzed for complete blood count, venous blood gas and biochemical profile at 8:00 and 12:00 h. The data were analyzed according to a mixed model. Feeding on CT, MS and HS led to significant differences in DMI (7.7 vs. 6.9 vs. 5.1 kg/d; P < 0.01 which modified the amount of time per day that the pH was below 5.0 (0 vs. 12 vs. 92 min; P < 0.10. Feeding MS and HS diets led to inflammation as indicated by the significant increment of white blood cells when compared to the CT ones and to blood concentration due to the osmotic pressure at ruminal level. Furthermore a significant decrease of bicarbonate level, CO2 partial pressure and oxyhemoglobin was observed as consequence of the activation of metabolic processes aimed to prevent metabolic acidosis. No differences were observed on blood sampling time, suggesting that one daily blood sample was enough to evaluate the metabolic variations related to ruminal acidosis.

  16. Cellular acidosis inhibits assembly, disassembly, and motility of stress granules.

    Chudinova, E M; Nadezhdina, E S; Ivanov, P A

    2012-11-01

    Stress granules (SGs) are large ribonucleoprotein (RNP)-containing particles that form in cytoplasm in response to a variety of acute changes in the cellular environment. One of the general parameters of the cell environment is pH. In some diseases, as well as in muscle fatigue, tissue acidosis occurs, leading to decrease in intracellular pH. Here we studied whether decrease in pH causes the formation of SGs in cultured animal cells, whether it affects the formation of the SGs under the action of arsenite and, if such effects occur, what are the mechanisms of the influence of acidosis. Acidosis was simulated by decreasing the pH of the culture medium, which acidified the cytoplasm. We found that medium acidification to pH 6.0 in itself did not cause formation of SGs in cells. Moreover, acidification prevented the formation of SGs under treatment with sodium arsenite or sodium arsenite together with the proteasome inhibitor MG132, and it inhibited the dissociation of preformed SGs under the influence of cycloheximide. We established that pH decrease did not affect the phosphorylation of eIF2α that occurs under the action of sodium arsenite, and even caused such phosphorylation by itself. We also found that the velocity of SG motion in cytoplasm at acidic pH was very low, and the mobile fraction of SG-incorporated PABP protein revealed by FRAP was decreased. We suppose that acidic pH impairs biochemical processes favoring assembly of RNPs in stress conditions and RNP dissociation on the termination of stress. Thus, in acidosis the reaction of the cellular translation apparatus to stress is modified. PMID:23240565

  17. Metabolic Acidosis Without Clinical Signs of Dehydration in Young Calves

    Kasari, T R; Naylor, J M

    1984-01-01

    Metabolic acidosis without clinical signs of dehydration was diagnosed in four calves between nine and 21 days of age. In each calf either coma or depression with weakness and ataxia was observed. Two calves had slow deep respirations. Treatment with intravenous administration of solutions of sodium bicarbonate was accompanied by a rise in blood pH and a return to normal demeanor, ambulation and appetites, allowing these calves to return to their respective herds.

  18. Lactic acidosis secondary to metformin overdose: a case report

    Timbrell Simon

    2012-08-01

    Full Text Available Abstract Introduction Metformin is a commonly used treatment modality in type 2 diabetes mellitus, with a well documented side effect of lactic acidosis. In the intensive care setting lactate and pH levels are regularly used as a useful predictor of poor prognosis. In this article we highlight how high lactate levels are not an accurate predictor of mortality in deliberate metformin overdose. Case presentation We present the case of a 70-year-old Caucasian man who took a deliberate metformin overdose of unknown quantity. He had a profound lactic acidosis at presentation with a pH of 6.93 and a lactate level of more than 20mmol/L. These figures would normally correspond with a mortality of more than 80%; however, with appropriate management this patient’s condition improved. Conclusion We provide evidence that the decision to treat severe lactic acidosis in deliberate metformin overdose should not be based on arterial lactate and pH levels, as would be the case in other overdoses. We also demonstrate that appropriate treatment with hemodiafiltration and 8.4% sodium bicarbonate, even in patients with a very high lactate and low pH, can be successful.

  19. Acute phase protein response during acute ruminal acidosis in cattle

    Danscher, A. M.; Thoefner, M. B.; Heegaard, Peter M. H.;

    2011-01-01

    The aim of the study was to describe the acute phase protein and leukocyte responses in dairy heifers during acute, oligofructose-induced ruminal acidosis. The study included 2 trials involving oral oligofructose overload (17g/kg BW) to nonpregnant Danish Holstein heifers. Trial 1 included 12...... performed.Heifers receiving oligofructose developed a profound ruminal and systemic acidosis (in Trial 1 and 2 lowest ruminal pH was 4.3±0.2 and 3.8±0.02, respectively, and minimum SBE was −9.3±4.1 and −8.9±2.8, respectively). In Trial 1, SAA concentrations were higher than baseline concentrations on all...... than control heifers at 18 and 24h after overload (max. 13.7±4.3 billions/L). Feeding had no effect on plasma fibrinogen concentrations or WBC in Trial 1.Acute ruminal and systemic acidosis caused by oligofructose overload resulted in distinct acute phase protein and leukocyte responses in dairy...

  20. Hypokalemic quadriparesis and rhabdomyolysis as a rare presentation of distal renal tubular acidosis.

    Ahmad Bhat, Manzoor; Ahmad Laway, Bashir; Mustafa, Farhat; Shafi Kuchay, Mohammad; Mubarik, Idrees; Ahmad Palla, Nazir

    2014-01-01

    Distal renal tubular acidosis is a syndrome of abnormal urine acidification and is characterized by hyperchloremic metabolic acidosis, hypokalemia, hypercalciurea, nephrocalcinosis and nephrolithiasis. Despite the presence of persistent hypokalemia, acute muscular paralysis is rarely encountered in males. Here, we will report an eighteen year old male patient who presented with flaccid quadriparesis and was subsequently found to have rhabdomyolysis, severe short stature, skeletal deformities and primary distal renal tubular acidosis. PMID:25250276

  1. Postoperative metabolic acidosis following the minimally invasive radiofrequency maze procedure

    Raymond Patrick Hom

    2016-01-01

    Full Text Available Purpose: Atrial fibrillation (AF is the most common arrhythmia treated in the world. While medical treatment with antiarrhythmic drugs remains the primary treatment modality, symptomatic refractory AF often requires treatment with a catheter or surgical ablation. One minimally invasive therapy is the Mini-Maze procedure, which utilizes epicardial radiofrequency ablation via a subxiphoid approach to rid the heart of arrhythmogenic atrial foci without a median sternotomy or cardiopulmonary bypass. The goal of this retrospective cohort study was to identify clinical factors associated with metabolic acidosis following the Mini-Maze procedure. Materials and Methods: After Institutional Review Board approval, we studied patients undergoing the Mini-Maze procedure, off-pump coronary artery bypass grafting or patients conventional Cox-Maze on cardiopulmonary bypass. The first base deficit value obtained in the Intensive Care Unit was used as a measure of metabolic acidosis. Using logistic regression with Akaike information criteria, we analyzed preoperative, intraoperative, and postoperative data to determine the factors associated with changes in base deficit. Results: A multivariable model using stepwise selection demonstrated that diabetes mellitus and weight were associated with a decrease in the base deficit by 2.87 mEq/L (95% CI: −5.55-−0.19 and 0.04 mEq/L (95%CI: −0.08, 0.004, respectively. Furthermore, creatinine was associated with a 1.57 mEq/L (95% CI: 0.14, 2.99 increase in the base deficit. Conclusion: The Mini-Maze procedure was not associated with postoperative metabolic acidosis. Instead, nondiabetic patients and patients with higher creatinine were associated with greater base deficits after undergoing cardiac surgery.

  2. Risk Factors for Developing Metabolic Acidosis after Radical Cystectomy and Ileal Neobladder

    Yoon, Hyun Suk; Yoon, Hana; Chung, Woo Sik; Sim, Bong Suk; Ryu, Dong-Ryeol; Lee, Dong Hyeon

    2016-01-01

    Purpose To investigate the serial changes of metabolic acidosis and identify associated risk factors in patients who underwent radical cystectomy and ileal neobladder. Material and Methods From January 2010 to August 2014, 123 patients who underwent radical cystectomy and ileal neobladder reconstruction for bladder cancer were included in this study. Metabolic acidosis was defined as a serum bicarbonate level less than 22 mEq/L and impaired renal function was defined as a GFR <50ml/min. The presence of metabolic acidosis was evaluated at 1 month, 1 year, and 2 years after surgery. Multivariate logistic regression analysis was conducted to identify risk factors associated with development of metabolic acidosis. Results Metabolic acidosis was observed in 52%, 19.5%, and 7.3% of patients at 1 month, 1 year, and 2 years after surgery, respectively. At 1 month after surgery, impaired renal function was the only independent risk factor associated with metabolic acidosis (OR 3.87, P = 0.046). At 1 year after surgery, diabetes was the only independent risk factor associated with metabolic acidosis (OR 5.68, P = 0.002). At 2 years post-surgery, both age and diabetes were significant risk factors associated with metabolic acidosis. Conclusion Approximately, half of patients experienced metabolic acidosis one month after ileal neobladder reconstruction. Preoperative impaired renal function was the most significant risk factor for developing metabolic acidosis in the early postoperative period. However, the incidence of metabolic acidosis decreased to less than 20% 1 year after surgery, and diabetes was an independent risk factor during this period. PMID:27384686

  3. Reality of severe metformin-induced lactic acidosis in the absence of chronic renal impairment.

    Bruijstens, L.A.; Luin, M. van; Buscher-Jungerhans, P.M.; Bosch, F.H.

    2008-01-01

    BACKGROUND: Lactic acidosis in metformin use is a widely recognised but rare side effect. Case reports usually describe elderly patients with conditions which in themselves can cause lactic acidosis or with known contraindications to metformin. We present cases of an elderly woman, a younger woman a

  4. Type IV renal tubular acidosis and spironolactone therapy in the elderly.

    O'Connell, J. E.; Colledge, N. R.

    1993-01-01

    Spironolactone therapy is a well-known cause of hyperkalaemia, but in susceptible patient, it may also be associated with metabolic acidosis. We report a case of severe renal tubular acidosis (Type IV) with life-threatening hyperkalaemia caused by spironolactone, and discuss the mechanisms by which this may occur.

  5. Hypokalemic quadriparesis and rhabdomyolysis as a rare presentation of distal renal tubular acidosis

    Ahmad Bhat, Manzoor; Ahmad Laway, Bashir; Mustafa, Farhat; Shafi Kuchay, Mohammad; Mubarik, Idrees; Ahmad Palla, Nazir

    2014-01-01

    Distal renal tubular acidosis is a syndrome of abnormal urine acidification and is characterized by hyperchloremic metabolic acidosis, hypokalemia, hypercalciurea, nephrocalcinosis and nephrolithiasis. Despite the presence of persistent hypokalemia, acute muscular paralysis is rarely encountered in males. Here, we will report an eighteen year old male patient who presented with flaccid quadriparesis and was subsequently found to have rhabdomyolysis, severe short stature, skeletal deformities ...

  6. A perspective on Serum Lactic acid, Lactic Acidosis in a Critical Care Unit

    Agela A.Elbadri

    2013-06-01

    Full Text Available Breast cancer is one of the major surgical problems encountered in Libya. Lactic acidosis is a universal complication in breast cancer patients and can be considered a possible prognostic marker. Therefore, it will be beneficial to correctly understand and review the biochemistry underlying lactic acidosis and its possible significance as a prognostic marker in critical care patients, including breast cancer.

  7. Rumen microbial and fermentation characteristics are affected differently by bacterial probiotic supplementation during induced lactic and subacute acidosis in sheep

    Lettat Abderzak; Nozière Pierre; Silberberg Mathieu; Morgavi Diego P; Berger Claudette; Martin Cécile

    2012-01-01

    Abstract Background Ruminal disbiosis induced by feeding is the cause of ruminal acidosis, a digestive disorder prevalent in high-producing ruminants. Because probiotic microorganisms can modulate the gastrointestinal microbiota, propionibacteria- and lactobacilli-based probiotics were tested for their effectiveness in preventing different forms of acidosis. Results Lactic acidosis, butyric and propionic subacute ruminal acidosis (SARA) were induced by feed chalenges in three groups of four w...

  8. Atypical presentation of distal renal tubular acidosis in two siblings.

    Tasic, Velibor; Korneti, Petar; Gucev, Zoran; Hoppe, Bernd; Blau, Nenad; Cheong, Hae Il

    2008-07-01

    Primary distal renal tubular acidosis (dRTA) is an inherited disease characterized by the inability of the distal tubule to lower urine pH hypokalemic paralysis. Laboratory investigations revealed proximal tubular dysfunction (low molecular weight proteinuria, generalized hyperaminoaciduria, hypophosphatemia with hyperphosphaturia, and hypouricemia with hyperuricosuria). There was significant hyperoxaluria and laboratory evidence for mild rhabdomyolysis. Under potassium and alkali therapy, proximal tubular abnormalities, muscular enzymes, and oxaluria normalized. A homozygous mutation in the ATP6V1B1 gene, which is responsible for dRTA with early hearing loss, was detected in both siblings. In conclusion, proximal tubular dysfunction and hyperoxaluria may be found in children with dRTA and are reversible under appropriate therapy. PMID:18386070

  9. Screening renal stone formers for distal renal tubular acidosis

    Osther, P J; Hansen, A B; Røhl, H F

    1989-01-01

    A group of 110 consecutive renal stone formers were screened for distal renal tubular acidosis (RTA) using morning fasting urinary pH (mfUpH) levels followed by a short ammonium chloride loading test in patients with levels above 6.0. In 14 patients (12.7%) a renal acidification defect was noted......; 13 had incomplete and 1 had complete distal RTA. Distal RTA was found particularly in recurrent stone formers (17%), and especially in those with bilateral stone disease, where a distal renal tubular acidification defect was found in 50%. We have been unable to differentiate primary from secondary...... RTA in renal stone formers. Regardless of whether the acidification defect is primary or secondary to stone formation, however, all renal stone formers with distal RTA can expect to benefit from prophylactic alkaline therapy and it is recommended that the screening procedure, which is easy to use in...

  10. Markers of acidosis and stress in a sprint versus a conducted electrical weapon.

    Ho, Jeffrey D; Dawes, Donald M; Nystrom, Paul C; Collins, Donal P; Nelson, Rebecca S; Moore, Johanna C; Miner, James R

    2013-12-10

    Both profound acidosis and catecholamine excess have been proposed as underlying physiologic derangements in subjects at high risk for arrest related death (ARD). In this study, the objective was to determine a level of physical exertion that is "equivalent" in terms of levels of acidosis and catecholamines to a "standard" TASER X26 exposure. Data were collected on subjects who underwent a 5-s TASER X26 exposure or a sprint of variable distances during a law enforcement training exercise. Our results show that levels of acidosis and catecholamines are less among subjects exposed to the TASER X26 than among subjects who sprinted 20 yards or more. PMID:24314505

  11. Lactic acidosis, potassium, and the heart rate deflection point in professional road cyclists

    Lucia, A.; Hoyos, J; Santalla, A; Perez, M; Carvajal, A.; Chicharro, J.

    2002-01-01

    Objective: To determine the influence of lactic acidosis, the Bohr effect, and exercise induced hyperkalaemia on the occurrence of the heart rate deflection point (HRDP) in elite (professional) cyclists.

  12. Improving the welfare of dairy goats: Feeding behaviour identifies goats at risk of subacute rumen acidosis

    Giger-Reverdin, Sylvie; Sauvant, Daniel; Duvaux-Ponter, Christine

    2013-01-01

    Main messages: Feeding behaviour is highly variable between animals. Feeding behaviour modifies rumen pH pattern and occurrence of subacute ruminal acidosis (SARA). Avoiding SARA increases animal welfare, milk production and therefore farm profit - ability.

  13. Renal tubular acidosis presenting as respiratory paralysis: Report of a case and review of literature

    Kalita J; Nair P; Kumar G; Misra U

    2010-01-01

    Respiratory paralysis due to renal tubular acidosis (RTA) is rare. We report a 22-year-old lady who developed severe bulbar, respiratory and limb paralysis following respiratory infection. She had hypokalemia (1.6 meq/L) and hyperchloremic (110 meq/l) acidosis (pH 7.1). She was diagnosed as distal RTA by ammonium chloride test. She improved following sodium bicarbonate and potassium supplementation. RTA should be differentiated from familial periodic paralysis (FPP) because acetazolamide used...

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

    Parvaiz Ahmad Koul; Wahid, A.

    2011-01-01

    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 auto...

  15. Osteomalacia complicating renal tubular acidosis in association with Sjogren's syndrome.

    El Ati, Zohra; Fatma, Lilia Ben; Boulahya, Ghada; Rais, Lamia; Krid, Madiha; Smaoui, Wided; Maiz, Hedi Ben; Beji, Soumaya; Zouaghi, Karim; Moussa, Fatma Ben

    2014-09-01

    Renal involvement in Sjogren's syndrome (SS) is not uncommon and may precede other complaints. Tubulointerstitial nephritis is the most common renal disease in SS and may lead to renal tubular acidosis (RTA), which in turn may cause osteomalacia. Nevertheless, osteomalacia rarely occurs as the first manifestation of a renal tubule disorder due to SS. We herewith describe a 43-year-old woman who was admitted to our hospital for weakness, lumbago and inability to walk. X-ray of the long bones showed extensive demineralization of the bones. Laboratory investigations revealed chronic kidney disease with serum creatinine of 2.3 mg/dL and creatinine clearance of 40 mL/min, hypokalemia (3.2 mmol/L), hypophosphatemia (0.4 mmol/L), hypocalcemia (2.14 mmol/L) and hyperchloremic metabolic acidosis (chlorine: 114 mmol/L; alkaline reserve: 14 mmol/L). The serum alkaline phosphatase levels were elevated. The serum levels of 25-hydroxyvitamin D and 1,25-dihydroxy vitamin D were low and borderline low, respectively, and the parathyroid hormone level was 70 pg/L. Urinalysis showed inappropriate alkaline urine (urinary PH: 7), glycosuria with normal blood glucose, phosphaturia and uricosuria. These values indicated the presence of both distal and proximal RTA. Our patient reported dryness of the mouth and eyes and Schirmer's test showed xerophthalmia. An accessory salivary gland biopsy showed changes corresponding to stage IV of Chisholm and Masson score. Kidney biopsy showed diffuse and severe tubulo-interstitial nephritis with dense lymphoplasmocyte infiltrates. Sicca syndrome and renal interstitial infiltrates indicated SS as the underlying cause of the RTA and osteomalacia. The patient received alkalinization, vitamin D (Sterogyl ®), calcium supplements and steroids in an initial dose of 1 mg/kg/day, tapered to 10 mg daily. The prognosis was favorable and the serum creatinine level was 1.7 mg/dL, calcium was 2.2 mmol/L and serum phosphate was 0.9 mmol/L. PMID:25193912

  16. Distal renal tubular acidosis with multiorgan autoimmunity: a case report.

    van den Wildenberg, Maria J; Hoorn, Ewout J; Mohebbi, Nilufar; Wagner, Carsten A; Woittiez, Arend-Jan; de Vries, Peter A M; Laverman, Gozewijn D

    2015-04-01

    A 61-year-old woman with a history of pernicious anemia presented with progressive muscle weakness and dysarthria. Hypokalemic paralysis (serum potassium, 1.4 mEq/L) due to distal renal tubular acidosis (dRTA) was diagnosed. After excluding several possible causes, dRTA was considered autoimmune. However, the patient did not meet criteria for any of the autoimmune disorders classically associated with dRTA. She had very high antibody titers against parietal cells, intrinsic factor, and thyroid peroxidase (despite normal thyroid function). The patient consented to a kidney biopsy, and acid-base transporters, anion exchanger type 1 (AE1), and pendrin were undetectable by immunofluorescence. Indirect immunofluorescence detected diminished abundance of AE1- and pendrin-expressing intercalated cells in the kidney, as well as staining by the patient's serum of normal human intercalated cells and parietal cells expressing the adenosine triphosphatase hydrogen/potassium pump (H(+)/K(+)-ATPase) in normal human gastric mucosa. The dRTA likely is caused by circulating autoantibodies against intercalated cells, with possible cross-reactivity against structures containing gastric H(+)/K(+)-ATPase. This case demonstrates that in patients with dRTA without a classic autoimmune disorder, autoimmunity may still be the underlying cause. The mechanisms involved in autoantibody development and how dRTA can be caused by highly specific autoantibodies against intercalated cells have yet to be determined. PMID:25533600

  17. Pyruvate carboxylase deficiency: An underestimated cause of lactic acidosis

    F. Habarou

    2015-03-01

    Full Text Available Pyruvate carboxylase (PC is a biotin-containing mitochondrial enzyme that catalyzes the conversion of pyruvate to oxaloacetate, thereby being involved in gluconeogenesis and in energy production through replenishment of the tricarboxylic acid (TCA cycle with oxaloacetate. PC deficiency is a very rare metabolic disorder. We report on a new patient affected by the moderate form (the American type A. Diagnosis was nearly fortuitous, resulting from the revision of an initial diagnosis of mitochondrial complex IV (C IV defect. The patient presented with severe lactic acidosis and pronounced ketonuria, associated with lethargy at age 23 months. Intellectual disability was noted at this time. Amino acids in plasma and organic acids in urine did not show patterns of interest for the diagnostic work-up. In skin fibroblasts PC showed no detectable activity whereas biotinidase activity was normal. We had previously reported another patient with the severe form of PC deficiency and we show that she also had secondary C IV deficiency in fibroblasts. Different anaplerotic treatments in vivo and in vitro were tested using fibroblasts of both patients with 2 different types of PC deficiency, type A (patient 1 and type B (patient 2. Neither clinical nor biological effects in vivo and in vitro were observed using citrate, aspartate, oxoglutarate and bezafibrate. In conclusion, this case report suggests that the moderate form of PC deficiency may be underdiagnosed and illustrates the challenges raised by energetic disorders in terms of diagnostic work-up and therapeutical strategy even in a moderate form.

  18. Acidosis environment promotes osteoclast formation by acting on the last phase of preosteoclast differentiation: a study to elucidate the action points of acidosis and search for putative target molecules.

    Kato, Kohtaro; Morita, Ikuo

    2011-08-01

    Acidosis promoted tartaric acid-resistant acid phosphatase-positive multinuclear cell (TRAP+MNC) or osteoclast formation. Large osteoclast or TRAP+LMNC formation was observed far more in an acidosis environment than in a physiologically neutral environment. One of the major action points of acidosis was determined to be located in the last phase of preosteoclast differentiation using a co-culture system and a soluble RANKL-dependent bone marrow cell culture system. On-going osteoclast formation in an acidosis environment markedly deteriorated when the medium was replaced with physiologically neutral medium within the first 6h; however, bone marrow cells previously stimulated in an acidosis environment for 9h differentiated into TRAP+LMNC in pH 7.4 medium. Messenger RNA (mRNA) expression levels of DC-STAMP, a key molecule in cell fusion, and NFATc1 did not increase in the acidosis environment compared with those under physiologically neutral conditions. Ruthenium red, a general TRP antagonist, deteriorated acidosis-promoted TRAP+LMNC formation. 4-Alpha-PDD, a TRPV4-specific agonist, added in the last 21 h of preosteoclast differentiation, potentiated TRAP+LMNC formation in a mild acidosis environment, showing synergism between TRPV4 activation and acidosis. RN1734, a TRPV4-specific antagonist, partly inhibited acidosis-promoted TRAP+LMNC formation. We thus narrowed down the major action points of acidosis in osteoclast formation and elucidated the characteristics of this system in detail. Our results show that acidosis effectively uses TRPV4 to drive large-scale cell fusion and also utilizes systems independently of TRPV4. PMID:21575626

  19. A Rare Case of Type I RenalTubular Acidosis with Membranous Nephropathy Presenting as Hypokalemic Paralysis

    Sunder, Sham; Sathi, Satyanand; K Venkataramanan; Verma, Himanshu; Bhardwaj, Minakshi; Rajesh, J.; Mahapatra, Himanshu

    2013-01-01

    Type 1 renal tubular acidosis (RTA), or distal RTA (dRTA), is a disorder of renal tubular acidification, which is generally asymptomatic but may rarely present as hypokalemic paralysis. Here, we report the case of a young male who presented with sudden onset weakness of all 4 limbs and a 2-month history of swelling of the legs. An investigation revealed hypokalemia, metabolic acidosis, and nephrotic syndrome. Additional analyses revealed normal anion gap metabolic acidosis with a positive uri...

  20. Effect of sodium bicarbonate administration on mortality in patients with lactic acidosis: a retrospective analysis.

    Hyun Jeong Kim

    Full Text Available BACKGROUND: Lactic acidosis is a common cause of high anion gap metabolic acidosis. Sodium bicarbonate may be considered for an arterial pH <7.15 but paradoxically depresses cardiac performance and exacerbates acidosis by enhancing lactate production. This study aimed to evaluate the cause and mortality rate of lactic acidosis and to investigate the effect of factors, including sodium bicarbonate use, on death. METHODS: We conducted a single center analysis from May 2011 through April 2012. We retrospectively analyzed 103 patients with lactic acidosis among 207 patients with metabolic acidosis. We used SOFA and APACHE II as severity scores to estimate illness severity. Multivariate logistic regression analysis and Cox regression analysis models were used to identify factors that affect mortality. RESULTS: Of the 103 patients with a mean age of 66.1±11.4 years, eighty-three patients (80.6% died from sepsis (61.4%, hepatic failure, cardiogenic shock and other causes. The percentage of sodium bicarbonate administration (p = 0.006, catecholamine use, ventilator care and male gender were higher in the non-survival group than the survival group. The non-survival group had significantly higher initial and follow-up lactic acid levels, lower initial albumin, higher SOFA scores and APACHE II scores than the survival group. The mortality rate was significantly higher in patients who received sodium bicarbonate. Sodium bicarbonate administration (p = 0.016 was associated with higher mortality. Independent factors that affected mortality were SOFA score (Exp (B = 1.72, 95% CI = 1.12-2.63, p = 0.013 and sodium bicarbonate administration (Exp (B = 6.27, 95% CI = 1.10-35.78, p = 0.039. CONCLUSIONS: Lactic acidosis, which has a high mortality rate, should be evaluated in patients with metabolic acidosis. In addition, sodium bicarbonate should be prescribed with caution in the case of lactic acidosis because sodium bicarbonate

  1. Haptoglobin and serum amyloid a in subacute ruminal acidosis in goats

    F.H.D. González

    2010-12-01

    Full Text Available Ruminal acidosis is a frequent disorder that occurs in goats as a consequence of feedingmistakes in animals not adapted to a diet of easily fermentable carbohydrates. The subacuteform of the disease is difficult to diagnose because no apparent signs are shownand the acid-base parameters may remain within the normal range. The present studyaimed at testing the hypothesis that haptoglobin (Hp and serum amyloid A (SAA,the two major acute phase proteins in ruminants, may be useful as markers of subacuteacidosis in goats.A subacute acidosis was induced in six Murciano-Granadina goats through a diet of60% mixed feed-40% alfalfa hay offered during 5 days to goats not adapted to eatmixed feed. Two goats were rumen-fistulated to investigate the effect of feeding onruminal pH. Sampling of blood and urine of all animals was done before the inductionof the acidosis, during 5 days after the onset of induction and for 18 days after theinduction (recovery period.Ruminal pH in the fistulated goats dropped to less than 5.5 during the inductionperiod, and half of the goats had diarrhea on the third day after the induction of acidosis.Acid-base parameters showed that the acid-base compensatory mechanisms wereefficient in maintaining the equilibrium. Serum Hp had a moderate increase duringthe induction period, while SAA did not change. These results suggest that Hp mightbe a potential marker for ruminal acidosis in goats.

  2. Acidosis láctica por metformina desencadenada por una insuficiencia renal aguda Metformin-induced lactic acidosis due to acute renal failure

    M.D. Macías-Robles

    2011-04-01

    Full Text Available La acidosis láctica es una complicación grave pero infrecuente asociada al empleo de metformina. Se discuten los mecanismos fisiopatológicos implicados en la acidosis láctica, con especial atención al papel potencial del fármaco. Presentamos un caso severo de este efecto secundario de la metformina en una paciente con diabetes tipo 2 que ingresó en el Servicio de Urgencias Hospitalario por un cuadro de insuficiencia renal aguda. El diagnóstico quedó apoyado por unos niveles séricos elevados de la biguanida, procedimiento escasamente utilizado en la práctica clínica. El tratamiento consiste en suspender la administración del fármaco e iniciar de forma inmediata la hemodiálisis con bicarbonato, lo cual proporciona un tratamiento sintomático y etiológico al eliminar del suero tanto el lactato como el antidiabético oral. Los síntomas de la acidosis láctica por metformina son inespecíficos y el comienzo es sutil, lo que hace necesario un alto nivel de sospecha para establecer un diagnostico precoz.Lactic acidosis is a serious but uncommon side effect of metformin use. We discuss the pathophysiological mechanisms of lactic acidosis with particular regard to the role played by the drug as a potential cause of the entity. We report on a severe case of this kind of drug toxicity in a patient with type 2 diabetes mellitus, admitted to the emergency department with acute renal failure symptoms. The diagnosis was supported by elevated serum levels of the biguanide, a procedure scarcely used in clinical practice. The management of this complication consists in drug discontinuation and hemodialysis with bicarbonate that provides symptomatic and ethiological treatment by removing both the lactate and the hypoglycemic agent from the serum. Since the symptoms of metformin-associated lactic acidosis are unspecific and its onset is subtle, a high level of suspicion is needed to establish an early diagnosis.

  3. Hypokalemic periodic paralysis in Sjogren's syndrome secondary to distal renal tubular acidosis.

    Yılmaz, Hakkı; Kaya, Mustafa; Özbek, Mustafa; ÜUreten, Kemal; Safa Yıldırım, İ

    2013-07-01

    We report a 53-year-old Turkish female presented with progressive weakness and mild dyspnea. Laboratory results demonstrated severe hypokalemia with hyperchloremic metabolic acidosis. The urinary anion gap was positive in the presence of acidemia, thus she was diagnosed with hypokalemic paralysis from a severe distal renal tubular acidosis (RTA). Immunologic work-up showed a strongly positive ANA of 1:3,200 and positive antibodies to SSA and SSB. Schirmer's test was abnormal. Autoimmune and other tests revealed Sjögren syndrome as the underlying cause of the distal renal tubular acidosis. Renal involvement in Sjogren's syndrome (SS) is not uncommon and may precede sicca complaints. The pathology in most cases is a tubulointerstitial nephritis causing among other things, distal RTA, and, rarely, hypokalemic paralysis. Treatment consists of potassium repletion, alkali therapy, and corticosteroids. Primary SS could be a differential in women with acute weakness and hypokalemia. PMID:22212410

  4. Trimethoprim/Sulfamethoxazole-Induced Severe Lactic Acidosis: A Case Report and Review of the Literature.

    Bulathsinghala, Marie; Keefer, Kimberly; Van de Louw, Andry

    2016-04-01

    Propylene glycol (PG) is used as a solvent in numerous medications, including trimethoprim/sulfamethoxazole (TMP/SMX) and lorazepam, and is metabolized in the liver to lactic acid. Cases of lactic acidosis related to PG toxicity have been described and always involved large doses of benzodiazepines and PG. We present the first case of severe lactic acidosis after a 3-day course of TMP/SMX alone, involving allegedly safe amounts of PG.A 31-year-old female with neurofibromatosis and pilocytic astrocytoma, receiving temozolomide and steroids, was admitted to the intensive care unit for pneumonia and acute respiratory failure requiring intubation. Her initial hemodynamic and acid-base statuses were normal. She was treated with intravenous TMP/SMX for possible Pneumocystis jirovecii pneumonia and was successfully extubated on day 2. On day 3, she developed tachypnea and arterial blood gas analysis revealed a severe metabolic acidosis (pH 7.2, PCO2 19 mm Hg, bicarbonates 8 mEq/L) with anion gap of 25 mEq/L and lactate of 12.1 mmol/L. TMP/SMX was discontinued and the lactate decreased to 2.9 mmol/L within 24 hours while her plasma bicarbonates normalized, without additional intervention. The patient never developed hypotension or severe hypoxia, and her renal and liver functions were normal. No other cause for lactic acidosis was identified and it resolved after TMP/SMX cessation alone, suggesting PG toxicity.Although PG-related lactic acidosis is well recognized after large doses of lorazepam, clinicians should bear in mind that TMP/SMX contains PG as well and should suspect PG toxicity in patients developing unexplained metabolic acidosis while receiving TMP/SMX. PMID:27124045

  5. Renal Tubular Acidosis after Jejunoileal Bypass for Morbid Obesity: role of secondary hyperparathyroidism

    Andersen, NN; Ladefoged, NN

    1991-01-01

    The effect of calcium infusion was studied in patients with renal tubular acidosis (RTA) and secondary hyperparathyroidism. Both developed after jejunoileal bypass operation (JIB) for morbid obesity. In three of four cases the acidification defect was abolished, probably due to a decrease of serum...... parathyroid hormone. As we found RTA in 9% (95% confidence limits 2-21%) of our patients, screening for acidosis is recommended in obesity patients after malabsorptive operations. RTA can be verified through an ammonium loading test. Before deciding on re-establishing bowel continuity due to RTA, we suggest...

  6. Indomethacin abolishes cerebral blood flow increase in response to acetazolamide-induced extracellular acidosis

    Wang, Qian; Paulson, O B; Lassen, N A

    1993-01-01

    by acetazolamide (Az), a drug that induces brain extracellular acidosis, which triggers its effect on CBF. We compared the results to the inhibitory effect of indomethacin on the CBF increase during hypercapnia. Indomethacin but not diclofenac, another potent cyclooxygenase inhibitor, was found to...... block almost completely the CBF increase caused by Az-induced extracellular acidosis or by CO2, but it did not influence the CBF increase produced by sodium nitroprusside or papaverine. The results suggest that indomethacin exerts its action on CO2 reactivity by a nonprostaglandin-mediated mechanism...

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

    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.

  8. Renal tubular acidosis presenting as respiratory paralysis: Report of a case and review of literature

    Kalita J

    2010-01-01

    Full Text Available Respiratory paralysis due to renal tubular acidosis (RTA is rare. We report a 22-year-old lady who developed severe bulbar, respiratory and limb paralysis following respiratory infection. She had hypokalemia (1.6 meq/L and hyperchloremic (110 meq/l acidosis (pH 7.1. She was diagnosed as distal RTA by ammonium chloride test. She improved following sodium bicarbonate and potassium supplementation. RTA should be differentiated from familial periodic paralysis (FPP because acetazolamide used in FPP aggravates RTA and sodium bicarbonate used in RTA aggravates hypokalemic periodic paralysis.

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

    Koul, Parvaiz Ahmad; Wahid, A

    2011-09-01

    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. PMID:21912036

  10. Identification of neonatal near miss by systematic screening for metabolic acidosis at birth

    Bonnaerens, A.; Thaens, A.; Mesens, T.; Van Holsbeke, C; E. T. M. de Jonge; Gyselaers, Wilfried

    2011-01-01

    Aims: To evaluate the relevance of systematic screening for neonatal metabolic acidosis at birth as part of perinatal audit. Methods: For every baby, born in Ziekenhuis Oost Limburg, Genk Belgium between 1/1/2010 and 31/12/2010, cord blood was analysed to diagnose metabolic acidosis, defined as arterial or venous pH ≤ 7.05 or 7.17 respectively, in association with base excess of ≤ -10 mmol/L. Three observers identified indicators for suboptimal peripartal care with likely contribution to ...

  11. Calcium citrate improves the epithelial-to-mesenchymal transition induced by acidosis in proximal tubular cells

    Maria José Rodriguez Cabalgante; Liliana Gadola; Leonella Luzardo; María Márquez; José Boggia; Mirian Aparecida Boim

    2012-01-01

    INTRODUCTION: Epithelial-to-mesenchymal transition (EMT) is a key event in renal fibrosis. The aims of the study were to evaluate acidosis induced EMT, transforming-growth-factor (TGF) β1 role and citrate effect on it. METHODS: HK2 cells (ATCC 2290) were cultured in DMEM/HAM F12 medium, pH 7.4. At 80% confluence, after 24 hr under serum free conditions, cells were distributed in three groups (24 hours): A) Control: pH 7.4, B) Acidosis: pH 7.0 and C) Calcium citrate (0.2 mmol/L) + pH 7.0. Chan...

  12. [Gastric emptying and metabolic acidosis. III. Study of gastric retention of a sodium citrate solution using an experimental model of metabolic acidosis in rats].

    Baracat, E C; Collares, E F

    1992-01-01

    The gastric emptying of sodium citrate solution 0.25 mEq/ml was studied in rats with metabolic acidosis induced by orogastric infusion of 0.5 M ammonium chloride solution. Two control groups were used: one infused with 0.5 M sodium chloride and the other with water. The 3 solutions content was 2 ml/100 g weight of the animal. Six hours after the infusion, there was a moderate metabolic acidosis in the group with ammonium citrate. This 6 hour interval marked the beginning of the gastric emptying study. The test meal (sodium citrate 0.25 mEq/ml) was utilized containing 6 mg% red fenol as a marker. The gastric emptying of sodium citrate was studied at 5, 10, 20 and 30 minutes after the infusion, and the results showed no differences between the 3 groups. The data suggest that the duodenal receptors to pH were more effective do determine the pattern of gastric response than the acidosis. PMID:1339143

  13. Scalp blood lactate for intra-partum assessment of fetal metabolic acidosis

    Heinis, A.M.; Spaanderman, M.E.A.; Gunnewiek, J.M.; Lotgering, F.K.

    2011-01-01

    Objective. To study to what extent the fetal scalp blood lactate concentration during labor correlates with fetal scalp pH and base deficit, and metabolic acidosis at birth, and to suggest lactate cut-off values to serve as indicators for either reassurance or immediate intervention. Design. A retro

  14. Tumour-specific metabolic adaptation to acidosis is coupled to epigenetic stability in osteosarcoma cells.

    Chano, Tokuhiro; Avnet, Sofia; Kusuzaki, Katsuyuki; Bonuccelli, Gloria; Sonveaux, Pierre; Rotili, Dante; Mai, Antonello; Baldini, Nicola

    2016-01-01

    The glycolytic-based metabolism of cancers promotes an acidic microenvironment that is responsible for increased aggressiveness. However, the effects of acidosis on tumour metabolism have been almost unexplored. By using capillary electrophoresis with time-of-flight mass spectrometry, we observed a significant metabolic difference associated with glycolysis repression (dihydroxyacetone phosphate), increase of amino acid catabolism (phosphocreatine and glutamate) and urea cycle enhancement (arginino succinic acid) in osteosarcoma (OS) cells compared with normal fibroblasts. Noteworthy, metabolites associated with chromatin modification, like UDP-glucose and N(8)-acetylspermidine, decreased more in OS cells than in fibroblasts. COBRA assay and acetyl-H3 immunoblotting indicated an epigenetic stability in OS cells than in normal cells, and OS cells were more sensitive to an HDAC inhibitor under acidosis than under neutral pH. Since our data suggest that acidosis promotes a metabolic reprogramming that can contribute to the epigenetic maintenance under acidosis only in tumour cells, the acidic microenvironment should be considered for future therapies. PMID:27186436

  15. Severity and Nature of Acidosis in Diarrheic Calves Over and Under One Week of Age

    Naylor, Jonathan M.

    1987-01-01

    A prospective study of the severity of dehydration and acidosis was carried out in 42 calves under 35 days of age presented for treatment of neonatal diarrhea. Clinically the mean level of dehydration was 8 to 10%. The plasma volume was 65% of that in the hydrated calf but the calves only gained 6.5% in weight during therapy.

  16. Tumour-specific metabolic adaptation to acidosis is coupled to epigenetic stability in osteosarcoma cells

    Chano, Tokuhiro; Avnet, Sofia; Kusuzaki, Katsuyuki; Bonuccelli, Gloria; Sonveaux, Pierre; Rotili, Dante; Mai, Antonello; Baldini, Nicola

    2016-01-01

    The glycolytic-based metabolism of cancers promotes an acidic microenvironment that is responsible for increased aggressiveness. However, the effects of acidosis on tumour metabolism have been almost unexplored. By using capillary electrophoresis with time-of-flight mass spectrometry, we observed a significant metabolic difference associated with glycolysis repression (dihydroxyacetone phosphate), increase of amino acid catabolism (phosphocreatine and glutamate) and urea cycle enhancement (arginino succinic acid) in osteosarcoma (OS) cells compared with normal fibroblasts. Noteworthy, metabolites associated with chromatin modification, like UDP-glucose and N8-acetylspermidine, decreased more in OS cells than in fibroblasts. COBRA assay and acetyl-H3 immunoblotting indicated an epigenetic stability in OS cells than in normal cells, and OS cells were more sensitive to an HDAC inhibitor under acidosis than under neutral pH. Since our data suggest that acidosis promotes a metabolic reprogramming that can contribute to the epigenetic maintenance under acidosis only in tumour cells, the acidic microenvironment should be considered for future therapies. PMID:27186436

  17. Lactic acidosis occurrence during exercises in the smoke chamber in a 53-year-old firefighter with no significant medical history

    Agata Bronisz

    2014-04-01

    Full Text Available Lactic acidosis is a form of metabolic acidosis with a high anion gap, reduced rate of arterial blood pH under 7.35 mmol/l, and lactic acid concentration over 7 mmol/l. In the literature we can find some descriptions of the cases of lactic acidosis in patients with severe systemic diseases (cancer, acquired immunodeficiency syndrome, sepsis, diabetes with cardiovascular disease and after organ transplantations. We present the case of lactic acidosis in a patient with no chronic disease - a firefighter in whom lactic acidosis has developed during standard exercises in the smoke chamber.

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

    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

  19. The acidosis-induced right shift of the HbO2 dissociation curve is maintained during erythrocyte storage

    Opdahl, Helge; Strømme, Tæwje A; Jørgensen, Lise; Bajelan, Livia; Heier, Hans E

    2011-01-01

    Background and objectives . In fresh blood, tissue hypoxia increases microcirculatory acidosis, which enhances erythrocyte O2 unloading and increases the amount of available O2. Storage of eryfhrocytes increases the HbO2 affinity and reduces O2 unloading. We examined the development of the affinity change during a period of 5 weeks of storage by present blood bank standards, and investigated to what extent acidosis offsets the affinity change. Materials and methods . Blood from volunteer dono...

  20. Rumen microbial and fermentation characteristics are affected differently by bacterial probiotic supplementation during induced lactic and subacute acidosis in sheep

    Lettat Abderzak

    2012-07-01

    Full Text Available Abstract Background Ruminal disbiosis induced by feeding is the cause of ruminal acidosis, a digestive disorder prevalent in high-producing ruminants. Because probiotic microorganisms can modulate the gastrointestinal microbiota, propionibacteria- and lactobacilli-based probiotics were tested for their effectiveness in preventing different forms of acidosis. Results Lactic acidosis, butyric and propionic subacute ruminal acidosis (SARA were induced by feed chalenges in three groups of four wethers intraruminally dosed with wheat, corn or beet pulp. In each group, wethers were either not supplemented (C or supplemented with Propionibacterium P63 alone (P or combined with L. plantarum (Lp + P or L. rhamnosus (Lr + P. Compared with C, all the probiotics stimulated lactobacilli proliferation, which reached up to 25% of total bacteria during wheat-induced lactic acidosis. This induced a large increase in lactate concentration, which decreased ruminal pH. During the corn-induced butyric SARA, Lp + P decreased Prevotella spp. proportion with a concomitant decrease in microbial amylase activity and total volatile fatty acids concentration, and an increase in xylanase activity and pH. Relative to the beet pulp-induced propionic SARA, P and Lr + P improved ruminal pH without affecting the microbial or fermentation characteristics. Regardless of acidosis type, denaturing gradient gel electrophoresis revealed that probiotic supplementations modified the bacterial community structure. Conclusion This work showed that the effectiveness of the bacterial probiotics tested depended on the acidosis type. Although these probiotics were ineffective in lactic acidosis because of a deeply disturbed rumen microbiota, some of the probiotics tested may be useful to minimize the occurrence of butyric and propionic SARA in sheep. However, their modes of action need to be further investigated.

  1. A Rare Cause of Metabolic Acidosis: Fatal Transdermal Methanol Intoxication in an Infant.

    Sahbudak Bal, Zumrut; Can, Fulya Kamit; Anil, Ayse Berna; Bal, Alkan; Anil, Murat; Gokalp, Gamze; Yavascan, Onder; Aksu, Nejat

    2016-08-01

    Oral methanol intoxication is common, but dermal intoxication is rare. We report a previously healthy 19-month-old female infant admitted to the emergency department (ED) with vomiting and tonic-clonic seizure. On physical examination, she was comatose and presented signs of decompensated shock with Kussmaul breathing. Her left thigh was edematous, with purple coloration. Methanol intoxication was suspected due to high anion gap metabolic acidosis (pH, 6.89; HCO3, occipital lobe were detected by computed tomography of the brain. The patient died after 7 days.Although methanol intoxication occurs predominantly in adults, it must be considered in children with high-anion gap metabolic acidosis. This case report demonstrates that fatal transdermal methanol intoxication can occur in children, and it is the second report in the English literature of transdermal methanol intoxication in an infant. PMID:26196361

  2. Alteration in Fecal Microbiota Associated with Grain-induced Subacute Ruminal Acidosis Challenge in Dairy Cows

    Danscher, Anne Mette; Derakshani, Hooman; Li, Shucong;

    2014-01-01

    Introduction: High prevalence of subacute rumen acidosis (SARA) in dairy herds has been reported with large impact on production and welfare. The field diagnosis of SARA is currently unclear and primarily based on point measurements of rumen pH, which are inaccurate. Consequently, SARA cases in t...... markers of the disease. bovine, subacute ruminal acidosis, fecal microbiome, biological marker Host publication information...... field are often not detected. Thus, other and better markers of SARA are needed. The purpose of this research was to study the feces microbiome during SARA and assess the possibilities of using feces microbial markers as indicators of SARA. Methods: Six lactating, rumen cannulated, Danish Holstein cows...... predictive value was estimated to R2: 87.0 and Q2: 73.2, respectively. Conclusion: Results confirm that intensive grain feeding changes the feces microbiome. The identification of specific taxa characteristic of SARA could provide new knowledge of the pathogenesis and might be useful as future biological...

  3. Rapid Revival of a Patient after very Severe Metabolic Acidosis: A Case Report

    Sajad Ahmadi

    2013-01-01

    Full Text Available Background: Metabolic acidosis is a fatal finding in trauma patients thatcomplicates the process of resuscitation.Case: The case was a 37-year-old man with open fracture in both legs and fracturein second lumbar vertebral (L2. The serial arterial blood gas (ABG test resultsshowed a pH value of 6.7 indicating a very severe and special case of metabolicacidosis. The rate of mortality for such a case was very high. The patient wastreated with sodium bicarbonate and successfully revived after four hours posttreatment and metabolic acidosis was resolved.Conclusion: This indicated that bicarbonate administration is useful for verysevere cases. The good condition of the patient after survival from the severeacademia allowed for extubation.

  4. Hyperchloremic Metabolic Acidosis due to Cholestyramine: A Case Report and Literature Review.

    Kamar, Fareed B; McQuillan, Rory F

    2015-01-01

    Cholestyramine is a bile acid sequestrant that has been used in the treatment of hypercholesterolemia, pruritus due to elevated bile acid levels, and diarrhea due to bile acid malabsorption. This medication can rarely cause hyperchloremic nonanion gap metabolic acidosis, a complication featured in this report of an adult male with concomitant acute kidney injury. This case emphasizes the caution that must be taken in prescribing cholestyramine to patients who may also be volume depleted, in renal failure, or taking spironolactone. PMID:26425378

  5. Muscle oxidative metabolism accelerates with mild acidosis during incremental intermittent isometric plantar flexion exercise

    Homma, Toshiyuki; Hamaoka, Takafumi; Sako, Takayuki; Murakami, Motohide; Esaki, Kazuki; Kime, Ryotaro; Katsumura, Toshihito

    2005-01-01

    Background It has been thought that intramuscular ADP and phosphocreatine (PCr) concentrations are important regulators of mitochondorial respiration. There is a threshold work rate or metabolic rate for cellular acidosis, and the decrease in muscle PCr is accelerated with drop in pH during incremental exercise. We tested the hypothesis that increase in muscle oxygen consumption (o2mus) is accelerated with rapid decrease in PCr (concomitant increase in ADP) in muscles with drop in pH occurs d...

  6. Cleistanthus collinus induces type I distal renal tubular acidosis and type II respiratory failure in rats

    Maneksh, Delinda; Sidharthan, Anita; Kettimuthu, Kavithapriya; Kanthakumar, Praghalathan; Lourthuraj, Amala A.; Ramachandran, Anup; Subramani, Sathya

    2010-01-01

    Background and Purpose: A water decoction of the poisonous shrub Cleistanthus collinus is used for suicidal purposes. The mortality rate is 28%. The clinical profile includes distal renal tubular acidosis (DRTA) and respiratory failure. The mechanism of toxicity is unclear. Objectives: To demonstrate features of C. collinus toxicity in a rat model and to identify its mechanism(s) of action. Materials and Methods: Rats were anesthetized and the carotid artery was cannulated. Electrocardiogram ...

  7. Dermal bone in early tetrapods: a palaeophysiological hypothesis of adaptation for terrestrial acidosis

    Janis, Christine M.; Devlin, Kelly; Warren, Daniel E.; Witzmann, Florian

    2012-01-01

    The dermal bone sculpture of early, basal tetrapods of the Permo-Carboniferous is unlike the bone surface of any living vertebrate, and its function has long been obscure. Drawing from physiological studies of extant tetrapods, where dermal bone or other calcified tissues aid in regulating acid–base balance relating to hypercapnia (excess blood carbon dioxide) and/or lactate acidosis, we propose a similar function for these sculptured dermal bones in early tetrapods. Unlike the condition in m...

  8. Sjögren’s, Renal Tubular Acidosis And Osteomalacia - An Asian Indian Series

    Sandhya, Pulukool; Danda, Debashish; Rajaratnam, Simon; Thomas, Nihal

    2014-01-01

    Objective: To study the profile of Renal Tubular Acidosis (RTA) in Asian Indian patients with Primary Sjögren's Syndrome (pSS). Methods: The Electronic medical records of patients with a diagnosis of pSS seen between 2003 and 2010 at our tertiary care teaching hospital were screened for RTA. Clinical features, immunological profile, acid-base balance and electrolyte status, 25-hydroxyvitamin D (25(OH) D3) levels, histopathological changes in minor salivary gland biopsy samples and radiologica...

  9. Management of Metformin-Associated Lactic Acidosis by Continuous Renal Replacement Therapy

    Keller, Geoffray; Cour, Martin; Hernu, Romain; Illinger, Julien; Robert, Dominique; Argaud, Laurent

    2011-01-01

    Background Metformin-associated lactic acidosis (MALA) is a severe metabolic failure with high related mortality. Although its use is controversial, intermittent hemodialysis is reported to be the most frequently used treatment in conjunction with nonspecific supportive measures. Our aim was to report the evolution and outcome of cases managed by continuous renal replacement therapy (CRRT). Methodology and Principal Findings Over a 3-year period, we retrospectively identified patients admitte...

  10. Multiplexed Microneedle-based Biosensor Array for Characterization of Metabolic Acidosis

    Miller, Philip R; Skoog, Shelby A.; Edwards, Thayne L.; Lopez, DeAnna M.; David R. Wheeler; Dulce C Arango; Xiao, Xiaoyin; Brozik, Susan M.; Wang, Joseph; Polsky, Ronen; Roger J. Narayan

    2011-01-01

    The development of a microneedle-based biosensor array for multiplexed in situ detection of exercise-induced metabolic acidosis, tumor microenvironment, and other variations in tissue chemistry is described. Simultaneous and selective amperometric detection of pH, glucose, and lactate over a range of physiologically-relevant concentrations in complex media is demonstrated. Furthermore, materials modified with a cell-resistant (Lipidure®) coating were shown to inhibit macrophage adhesion; no s...

  11. Fluoxetine Treatment Abolishes the In Vitro Respiratory Response to Acidosis in Neonatal Mice

    Voituron, Nicolas; Shvarev, Yuri; Menuet, Clément; Bevengut, Michelle; Fasano, Caroline; Vigneault, Erika; Mestikawy, Salah El; Hilaire, Gérard

    2010-01-01

    Background To secure pH homeostasis, the central respiratory network must permanently adapt its rhythmic motor drive to environment and behaviour. In neonates, it is commonly admitted that the retrotrapezoid/parafacial respiratory group of neurons of the ventral medulla plays the primary role in the respiratory response to acidosis, although the serotonergic system may also contribute to this response. Methodology/Principal Findings Using en bloc medullary preparations from neonatal mice, we ...

  12. Hearing impairment in association with distal renal tubular acidosis among Saudi children.

    Zakzouk, S M; Sobki, S H; Mansour, F; al Anazy, F H

    1995-10-01

    A follow-up of seven patients with the autosomal recessive inherited syndrome of distal renal tubular acidosis (RTA) and sensorineural hearing loss is described. Five patients were diagnosed as having primary distal renal tubular acidosis and rickets, four were found to have severe sensorineural hearing loss of over 80 dB: two of which are brothers. Two patients were diagnosed as having secondary distal renal acidosis due to a genetic disorder called osteopetrosis; they are brothers and their audiograms showed a mild conductive hearing loss of an average 35 dB bilaterally. All patients had growth retardation with improvement due to alkaline therapy but their hearing loss was not affected by the medication. The pedigrees of two families with half sibs showed the familial incidence for consanguineous marriage. Consanguinity was found to be positive in five out of the seven patients. The tribal tradition in Saudi Arabia fosters consanguineous marriages for cultural and social reasons and pre-arranged marriages are still seen. PMID:7499943

  13. High anion gap refractory metabolic acidosis as a critical presentation of endosulfan poisoning

    Raj Kumar Sharma

    2011-01-01

    Full Text Available Organochloride insecticides are chlorinated cyclic hydrocarbons. One of such insecticides is endosulfan (6,7,8,9,10-10 hexachloro 1,5,5a,6,9,9a-hexahydro-6-methano-2,4,3-hexadithioxanthiep in 3-oxide and it has been widely used in agriculture since 1960. The uncontrolled use of these compounds in developing countries has resulted in the deaths of animals and humans. Characteristic clinical signs following acute exposure are indicative of CNS disturbances or overstimulation. Mortality and morbidity rates are high and there is no specific antidote. We present an uncommon presentation of endosulfan poisoning in a 32-year-old male with high anion gap severe refractory metabolic acidosis. The patient was treated with continuous renal replacement therapy and was salvaged. Till date, there is no case report from India for endosulfan poisoning with severe metabolic acidosis and hypotension. Through this case report, we emphasize the role of continuous renal replacement therapy as a rescue therapy for endosulfan poisoning with severe refractory metabolic acidosis and hypotension, even though it is a non dialyzable poison.

  14. Branched-chain amino acid metabolism in rat muscle: abnormal regulation in acidosis

    May, R.C.; Hara, Y.; Kelly, R.A.; Block, K.P.; Buse, M.G.; Mitch, W.E.

    1987-06-01

    Branched-chain amino acid (BCAA) metabolism is frequently abnormal in pathological conditions accompanied by chronic metabolic acidosis. To study how metabolic acidosis affects BCAA metabolism in muscle, rats were gavage fed a 14% protein diet with or without 4 mmol NH/sub 4/Cl x 100 g body wt/sup -1/ x day/sup -1/. Epitrochlearis muscles were incubated with L-(1-/sup 14/C)-valine and L-(1-/sup 14/C)leucine, and rates of decarboxylation, net transamination, and incorporation into muscle protein were measured. Plasma and muscle BCAA levels were lower in acidotic rats. Rates of valine and leucine decarboxylation and net transamination were higher in muscles from acidotic rats; these differences were associated with a 79% increase in the total activity of branched-chain ..cap alpha..-keto acid dehydrogenase and a 146% increase in the activated form of the enzyme. They conclude that acidosis affects the regulation of BCAA metabolism by enhancing flux through the transaminase and by directly stimulating oxidative catabolism through activation of branched-chain ..cap alpha..-keto acid dehydrogenase.

  15. Lentiform fork sign: a magnetic resonance finding in a case of acute metabolic acidosis.

    Grasso, Daniela; Borreggine, Carmela; Perfetto, Francesco; Bertozzi, Vincenzo; Trivisano, Marina; Specchio, Luigi Maria; Grilli, Gianpaolo; Macarini, Luca

    2014-06-01

    We report a 33 year-old woman addicted to chronic unspecified solvents abuse with stupor, respiratory disorders, tetraplegia and severe metabolic acidosis. On admission an unenhanced cranial CT scan showed symmetrical hypodensities of both lentiform nuclei. MR imaging performed 12 hours after stupor demonstrates bilateral putaminal hemorrhagic necrosis, bilateral external capsule, corona radiata and deep cerebellar hyperintensities with right cingulate cortex involvement. DWI reflected bilateral putaminal hyperintensities with restricted water diffusion as to citotoxic edema and development of vasogenic edema in the external capsule recalling a fork. On day twenty, after specific treatments MRI demonstrated a bilateral putaminal marginal enhancement. Bilateral putaminal necrosis is a characteristic but non-specific radiological finding of methanol poisoning. Lentiform Fork sign is a rare MRI finding reported in literature in 22 patients with various conditions characterized by metabolic acidosis. Vasogenic edema may be due to the differences in metabolic vulnerability between neurons and astrocytes. We postulate that metabolic acidosis could have an important role to generate this sign. PMID:24976195

  16. Lentiform Fork Sign: a Magnetic Resonance Finding in a Case of Acute Metabolic Acidosis

    Grasso, Daniela; Borreggine, Carmela; Perfetto, Francesco; Bertozzi, Vincenzo; Trivisano, Marina; Specchio, Luigi Maria; Grilli, Gianpaolo; Macarini, Luca

    2014-01-01

    Summary We report a 33 year-old woman addicted to chronic unspecified solvents abuse with stupor, respiratory disorders, tetraplegia and severe metabolic acidosis. On admission an unenhanced cranial CT scan showed symmetrical hypodensities of both lentiform nuclei. MR imaging performed 12 hours after stupor demonstrates bilateral putaminal hemorrhagic necrosis, bilateral external capsule, corona radiata and deep cerebellar hyperintensities with right cingulate cortex involvement. DWI reflected bilateral putaminal hyperintensities with restricted water diffusion as to citotoxic edema and development of vasogenic edema in the external capsule recalling a fork. On day twenty, after specific treatments MRI demonstrated a bilateral putaminal marginal enhancement. Bilateral putaminal necrosis is a characteristic but non-specific radiological finding of methanol poisoning. Lentiform Fork sign is a rare MRI finding reported in literature in 22 patients with various conditions characterized by metabolic acidosis. Vasogenic edema may be due to the differences in metabolic vulnerability between neurons and astrocytes. We postulate that metabolic acidosis could have an important role to generate this sign. PMID:24976195

  17. Acidosis Decreases c-Myc Oncogene Expression in Human Lymphoma Cells: A Role for the Proton-Sensing G Protein-Coupled Receptor TDAG8

    Zhigang Li; Lixue Dong; Eric Dean; Yang, Li V.

    2013-01-01

    Acidosis is a biochemical hallmark of the tumor microenvironment. Here, we report that acute acidosis decreases c-Myc oncogene expression in U937 human lymphoma cells. The level of c-Myc transcripts, but not mRNA or protein stability, contributes to c-Myc protein reduction under acidosis. The pH-sensing receptor TDAG8 (GPR65) is involved in acidosis-induced c-Myc downregulation. TDAG8 is expressed in U937 lymphoma cells, and the overexpression or knockdown of TDAG8 further decreases or partia...

  18. Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis.

    Kraut, Jeffrey A; Xing, Shelly Xiaolei

    2011-09-01

    An increase in serum osmolality and serum osmolal gap with or without high-anion-gap metabolic acidosis is an important clue to exposure to one of the toxic alcohols, which include methanol, ethylene glycol, diethylene glycol, propylene glycol, or isopropanol. However, the increase in serum osmolal gap and metabolic acidosis can occur either together or alone depending on several factors, including baseline serum osmolal gap, molecular weight of the alcohol, and stage of metabolism of the alcohol. In addition, other disorders, including diabetic or alcoholic ketoacidosis, acute kidney injury, chronic kidney disease, and lactic acidosis, can cause high-anion-gap metabolic acidosis associated with an increased serum osmolal gap and therefore should be explored in the differential diagnosis. It is essential for clinicians to understand the value and limitations of osmolal gap to assist in reaching the correct diagnosis and initiating appropriate treatment. In this teaching case, we present a systematic approach to diagnosing high serum osmolality and increased serum osmolal gap with or without high-anion-gap metabolic acidosis. PMID:21794966

  19. Distal renal tubular acidosis as a cause of osteomalacia in a patient with primary Sjögren's syndrome

    Jovelić Aleksandra

    2005-01-01

    Full Text Available Background. One half of the patients with primary Sjögren’s syndrome has extraglandular manifestations, including renal involvement. The most frequent renal lesion is tubulo-interstitial nephritis, which manifests clinically as distal tubular acidosis and may result in the development of osteomalacia. Case report. In a 29 - year-old female patient, with bilateral nephrolithiasis, the diagnosis of primary Sjögren’s syndrome, tubulo-interstitial nephritis, distal renal tubular acidosis, and hypokalemia were established. She was treated for hypokalemia. Two years later she developed bone pains and muscle weakness, she wasn’t able to walk, her proximal muscles and pelvic bones were painful, with radiological signs of pelvic bones osteopenia and pubic bones fractures. The diagnosis of osteomalacia was established and the treatment started with Schol’s solution, vitamin D and calcium. In the following two months, acidosis was corrected, and the patient started walking. Conclusion. In our patient with primary Sjögren’s syndrome and interstitial nephritis, osteomalacia was a result of the long time decompensate acidosis, so the correction of acidosis, and the supplementation of vitamin D and calcium were the integral part of the therapy.

  20. Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance

    Menegon L.F.

    1998-01-01

    Full Text Available Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in male Wistar-Hannover rats (200-250 g. Chronic acidosis (pH 7.16 ± 0.13 caused a sustained increase in renal fractional Na+ excretion (267.9 ± 36.4%, accompanied by an increase in fractional proximal (113.3 ± 3.6% and post-proximal (179.7 ± 20.2% Na+ and urinary K+ (163.4 ± 5.6% excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. A lower final body weight was observed in the acidotic (232 ± 4.6 g and pair-fed (225 ± 3.6 g rats compared to the controls (258 ± 3.7 g. In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 ± 0.05 g compared to the other experimental groups (control, 1.46 ± 0.05 g; pair-fed, 1.4 ± 0.05 g. We suggest that altered renal Na+ and K+ handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transport.

  1. Effect of chronic metabolic acidosis on bone density and bone architecture in vivo in rats.

    Gasser, Jürg A; Hulter, Henry N; Imboden, Peter; Krapf, Reto

    2014-03-01

    Chronic metabolic acidosis (CMA) might result in a decrease in vivo in bone mass based on its reported in vitro inhibition of bone mineralization, bone formation, or stimulation of bone resorption, but such data, in the absence of other disorders, have not been reported. CMA also results in negative nitrogen balance, which might decrease skeletal muscle mass. This study analyzed the net in vivo effects of CMA's cellular and physicochemical processes on bone turnover, trabecular and cortical bone density, and bone microarchitecture using both peripheral quantitative computed tomography and μCT. CMA induced by NH4Cl administration (15 mEq/kg body wt/day) in intact and ovariectomized (OVX) rats resulted in stable CMA (mean Δ[HCO3(-)]p = 10 mmol/l). CMA decreased plasma osteocalcin and increased TRAP5b in intact and OVX animals. CMA decreased total volumetric bone mineral density (vBMD) after 6 and 10 wk (week 10: intact normal +2.1 ± 0.9% vs. intact acidosis -3.6 ± 1.2%, P effect attributable to a decrease in cortical thickness and, thus, cortical bone mass (no significant effect on cancellous vBMD, week 10) attributed to an increase in endosteal bone resorption (nominally increased endosteal circumference). Trabecular bone volume (BV/TV) decreased significantly in both CMA groups at 6 and 10 wk, associated with a decrease in trabecular number. CMA significantly decreased muscle cross-sectional area in the proximal hindlimb at 6 and 10 wk. In conclusion, chronic metabolic acidosis induces a large decrease in cortical bone mass (a prime determinant of bone fragility) in intact and OVX rats and impairs bone microarchitecture characterized by a decrease in trabecular number. PMID:24352505

  2. Sjögren’s, Renal Tubular Acidosis And Osteomalacia - An Asian Indian Series

    Sandhya, Pulukool; Danda, Debashish; Rajaratnam, Simon; Thomas, Nihal

    2014-01-01

    Objective: To study the profile of Renal Tubular Acidosis (RTA) in Asian Indian patients with Primary Sjögren's Syndrome (pSS). Methods: The Electronic medical records of patients with a diagnosis of pSS seen between 2003 and 2010 at our tertiary care teaching hospital were screened for RTA. Clinical features, immunological profile, acid-base balance and electrolyte status, 25-hydroxyvitamin D (25(OH) D3) levels, histopathological changes in minor salivary gland biopsy samples and radiological findings were retrieved. RTA was diagnosed in cases of hyperchloremic metabolic acidosis with urinary pH values higher than 5.5. Those with known features suggestive of RTA including hypokalemic paralysis, hyperchloremia and nephrocalcinosis without acidosis were defined as incomplete RTA. Results: Of the 380 patients with clinically suspected pSS, 25 had RTA. The median age was 32 (18-60) years. Nineteen patients had complete RTA. Six had incomplete RTA. Only 10 patients (40%) had symptoms related to RTA at presentation. Sixteen patients (64%) had present or past history of hypokalemic paralysis. Pseudofractures were seen in 7 patients and an additional 2 had subclinical radiological osteomalacia. Majority of the patients (61.2%) had a normal 25(OH) D3 level. Those with osteomalacia had significantly lower serum phosphate, blood ph and higher alkaline phosphatase. Serum calcium and 25(OH) D3 levels were not significantly different between patients with osteomalacia and those without. Conclusion: Most patients were asymptomatic for RTA inspite of clinically overt and elicitable features. Skeletal manifestation was a common finding in patients with Sjögren and RTA, despite normal levels of 25 (OH) D3 in a majority. PMID:25584094

  3. SYSTEMIC LUPUS ERYTHEMATOSUS PRESENTING AS HYPOKALEMIC PERIODIC PARALYSIS SECONDARY TO DISTAL RENAL TUBULAR ACIDOSIS

    Ranjeet; Gurinder

    2014-01-01

    Systemic lupus erythematosus, referred to as SLE or lupus, is sometimes called the “great imitator.” Why? Because of its wide range of symptoms, people often confuse lupus with other health problems. We report the case of a 22-year-old woman who presented with a flaccid paralysis of limbs due to severe hypokalemia as a consequence of distal renal tubular acidosis (dRTA). A search for the cause of dRTA revealed latent Systemic Lupus Erythematosus (SLE). SLE presenting as dRTA ...

  4. SYSTEMIC LUPUS ERYTHEMATOSUS PRESENTING AS HYPOKALEMIC PERIODIC PARALYSIS SECONDARY TO DISTAL RENAL TUBULAR ACIDOSIS

    Ranjeet

    2014-05-01

    Full Text Available Systemic lupus erythematosus, referred to as SLE or lupus, is sometimes called the “great imitator.” Why? Because of its wide range of symptoms, people often confuse lupus with other health problems. We report the case of a 22-year-old woman who presented with a flaccid paralysis of limbs due to severe hypokalemia as a consequence of distal renal tubular acidosis (dRTA. A search for the cause of dRTA revealed latent Systemic Lupus Erythematosus (SLE. SLE presenting as dRTA is uncommon

  5. Primary Sjö-gren's syndrome presenting with distal, renal tubular acidosis and rhabdomyolysis.

    Prakash, E B S; Fernando, M E; Sathiyasekaran, Malathi; Bhoopathy, R M; Jayanth, J J; Samuel, J

    2006-12-01

    Primary Sjögren's syndrome (PSS) is rare in India. Clinically manifest renal disease in PSS is uncommon and is usually an autoimmune tubulointerstitial nephritis presenting with distal renal tubular acidosis (dRTA) or a urinary concentrating defect. Hypokalemic paralysis due to dRTA in PSS is rare but well documented in medical literature. Rhabdomyolysis as a consequence of hypokalemia in PSS is exceptional. We report a case of PSS with dRTA and rhabdomyolysis causing prolonged respiratory failure and quadriparesis. PMID:17334013

  6. Serum acute phase proteins in cows with SARA (Subacute Ruminal Acidosis) suspect

    C. Cannizzo; Gianesella, M.; Giudice, E.; Messina, V; G. Piccione; M. Morgante

    2012-01-01

    The aim of this study was to evaluate the variations of Acute Phase Proteins (APPs) and other blood constituents during the onset of the sub-acute ruminal acidosis (SARA) pathological status. A total of 108 cows from 12 dairy herds were randomly selected and divided into three Groups of 36 animals each. All animals were subjected to a rumenocentesis. Group A was composed by subjects with a rumen pH>5.8, Group B was composed by subjects with a rumen pH ≤5.5≤5.8 and Group C was composed by subj...

  7. Metabolic acidosis in late pregnancy due to 5-oxoproline (pyroglutamic acid)—A case report

    K. Jeyanthan; Sahathevan Sathiyathasan; Hamid, R.

    2012-01-01

    Introduction: Accumulation of 5-oxoproline (pyroglutamic acid) is a rare cause of severe, high anion gap metabolic acidosis in adults. Case: A 21 year old lady presented at 39 weeks gestation in her first pregnancy with 2 weeks history of shortness of breath. She suffered from ear ache and had been taking Paracetamol on regular basis for a year. She was admitted to having regular alcohol intake until the pregnancy when she stopped. She was not in acute distress and all her observations were s...

  8. D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome

    N. Gurukripa Kowlgi; Lovely Chhabra

    2015-01-01

    D-lactic acidosis or D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. The unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid among other organic acids. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium...

  9. Linfoma marginal del bazo asociado a acidosis láctica tipo B: Caso clínico Type B lactic acidosis associated with marginal lymphoma of the spleen: Report of one case

    Jorge Vega; María de los Ángeles Rodríguez; Armando Peña; Alejadro Vásquez

    2012-01-01

    Lactic acidosis in the absence of hypoxia or tissue hypoperfusion (type B) is very rare and is associated with the use of some drugs or malignancy. We report a 79-year-old woman, with a marginal non-Hodgkin's lymphoma of the spleen that was subjected to a splenectomy one year ago. She presented with unexplained tachypnea associated with pancytopenia and elevation of IgM to 10 times over the higher normal limit. Laboratory tests showed the presence of metabolic acidosis and high lactic acid le...

  10. Draft Genome Sequence of Lactobacillus delbrueckii Strain #22 Isolated from a Patient with Short Bowel Syndrome and Previous d-Lactic Acidosis and Encephalopathy.

    Domann, Eugen; Fischer, Florence; Glowatzki, Fabian; Fritzenwanker, Moritz; Hain, Torsten; Zechel-Gran, Silke; Giffhorn-Katz, Susanne; Neubauer, Bernd A

    2016-01-01

    d-Lactic acidosis with associated encephalopathy caused by overgrowth of intestinal lactic acid bacteria is a rarely diagnosed neurological complication of patients with short bowel syndrome. Here, we report the draft genome sequence of Lactobacillus delbrueckii strain #22 isolated from a patient with short bowel syndrome and previous d-lactic acidosis/encephalopathy. PMID:27469967

  11. Recurrent Anion Gap Acidosis: An Unusual Presentation of X-Linked Adrenoleukodystrophy in a Five-year-old Male

    Schwab, Joel; Pena, Loren; Sigman, Laura; Waggoner, Darrel

    2010-01-01

    We are presenting a five-year-old male with recurrent anion gap acidosis. During his last admission, it was detected that he had elevated VLCFA and the evaluation discovered that he had X-linked Adrenooleukodystrophy. He had the Addisonian only phenotype without any clinical or radiographic CNS findings. We were unable to find any other reports of this presentation of ALD. If the work-up of recurrent anion gap acidosis does not uncover an etiology, X-linked ALD should be considered in the dif...

  12. [Higher Brain Dysfunction in Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis and Stroke-Like Episodes (MELAS)].

    Ichikawa, Hiroo

    2016-02-01

    Stroke-like episodes are one of the cardinal features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), and occur in 84-99% of the patients. The affected areas detected on neuroimaging do not have classical vascular distribution, and involve predominantly the temporal, parietal and occipital lobes. Thus, the neurological symptoms including higher brain dysfunction correlate with this topographical distribution. In association with the occipital lobe involvement, the most frequent symptom is cortical blindness. Other symptoms have been occasionally reported in case reports: visual agnosia, prosopagnosia, cortical deafness, auditory agnosia, topographical disorientation, various types of aphasia, hemispatial neglect, and so on. On the other hand, cognitive decline associated with more diffuse brain impairment rather than with focal stroke-like lesions has been postulated. This condition is also known as mitochondrial dementia. Domains of cognitive dysfunction include abstract reasoning, verbal memory, visual memory, language (naming and fluency), executive or constructive functions, attention, and visuospatial function. Cognitive functions and intellectual abilities may decline from initially minimal cognitive impairment to dementia. To date, the neuropsychological and neurologic impairment has been reported to be associated with cerebral lactic acidosis as estimated by ventricular spectroscopic lactate levels. PMID:26873235

  13. Magnetic resonance imaging detects placental hypoxia and acidosis in mouse models of perturbed pregnancies.

    Gabriele Bobek

    Full Text Available Endothelial dysfunction as a result of dysregulation of anti-angiogenic molecules secreted by the placenta leads to the maternal hypertensive response characteristic of the pregnancy complication of preeclampsia. Structural abnormalities in the placenta have been proposed to result in altered placental perfusion, placental oxidative stress, cellular damage and inflammation and the release of anti-angiogenic compounds into the maternal circulation. The exact link between these factors is unclear. Here we show, using Magnetic Resonance Imaging as a tool to examine placental changes in mouse models of perturbed pregnancies, that T 2 contrast between distinct regions of the placenta is abolished at complete loss of blood flow. Alterations in T 2 (spin-spin or transverse relaxation times are explained as a consequence of hypoxia and acidosis within the tissue. Similar changes are observed in perturbed pregnancies, indicating that acidosis as well as hypoxia may be a feature of pregnancy complications such as preeclampsia and may play a prominent role in the signalling pathways that lead to the increased secretion of anti-angiogenic compounds.

  14. Lipoyltransferase 1 Gene Defect Resulting in Fatal Lactic Acidosis in Two Siblings

    Taché, Véronique; Bivina, Liga; White, Sophie; Gregg, Jeffrey; Deignan, Joshua; Boyadjievd, Simeon A.; Poulain, Francis R.

    2016-01-01

    A term male neonate developed severe intractable lactic acidosis on day of life 1 and died the same day at our institution. The family previously lost another term, female newborn on day of life 1 from suspected sepsis at an outside hospital. After performing an autopsy on the neonate who died at our institution, extensive and lengthy neonatal and parental genetic testing, as well as biochemical analyses, and whole exome sequencing analysis identified compound heterozygous mutations in the lipoyltransferase 1 (LIPT1) gene responsible for the lipoylation of the 2-keto dehydrogenase complexes in the proband. These mutations were also identified in the deceased sibling. The clinical manifestations of these two siblings are consistent with those recently described in two unrelated families with lactic acidosis due to LIPT1 mutations, an underrecognized and underreported cause of neonatal death. Conclusions. Our observations contribute to the delineation of a new autosomal recessive metabolic disorder, leading to neonatal death. Our case report also highlights the importance of an interdisciplinary team in solving challenging cases. PMID:27247813

  15. Lipoyltransferase 1 Gene Defect Resulting in Fatal Lactic Acidosis in Two Siblings.

    Taché, Véronique; Bivina, Liga; White, Sophie; Gregg, Jeffrey; Deignan, Joshua; Boyadjievd, Simeon A; Poulain, Francis R

    2016-01-01

    A term male neonate developed severe intractable lactic acidosis on day of life 1 and died the same day at our institution. The family previously lost another term, female newborn on day of life 1 from suspected sepsis at an outside hospital. After performing an autopsy on the neonate who died at our institution, extensive and lengthy neonatal and parental genetic testing, as well as biochemical analyses, and whole exome sequencing analysis identified compound heterozygous mutations in the lipoyltransferase 1 (LIPT1) gene responsible for the lipoylation of the 2-keto dehydrogenase complexes in the proband. These mutations were also identified in the deceased sibling. The clinical manifestations of these two siblings are consistent with those recently described in two unrelated families with lactic acidosis due to LIPT1 mutations, an underrecognized and underreported cause of neonatal death. Conclusions. Our observations contribute to the delineation of a new autosomal recessive metabolic disorder, leading to neonatal death. Our case report also highlights the importance of an interdisciplinary team in solving challenging cases. PMID:27247813

  16. Lipoyltransferase 1 Gene Defect Resulting in Fatal Lactic Acidosis in Two Siblings

    Véronique Taché

    2016-01-01

    Full Text Available A term male neonate developed severe intractable lactic acidosis on day of life 1 and died the same day at our institution. The family previously lost another term, female newborn on day of life 1 from suspected sepsis at an outside hospital. After performing an autopsy on the neonate who died at our institution, extensive and lengthy neonatal and parental genetic testing, as well as biochemical analyses, and whole exome sequencing analysis identified compound heterozygous mutations in the lipoyltransferase 1 (LIPT1 gene responsible for the lipoylation of the 2-keto dehydrogenase complexes in the proband. These mutations were also identified in the deceased sibling. The clinical manifestations of these two siblings are consistent with those recently described in two unrelated families with lactic acidosis due to LIPT1 mutations, an underrecognized and underreported cause of neonatal death. Conclusions. Our observations contribute to the delineation of a new autosomal recessive metabolic disorder, leading to neonatal death. Our case report also highlights the importance of an interdisciplinary team in solving challenging cases.

  17. Mechanism of potassium depletion during chronic metabolic acidosis in the rat

    Pair-fed rats on a normal K diet were given either 1.5% NH4Cl or water for 4 days. The acid-fed animals developed metabolic acidosis, negative K balance, and K depletion. Urinary Na excretion and urinary flow were not different between the groups beyond the first day. After the 4 days, isolated kidneys from animals in each of these groups were perfused at normal pH and bicarbonate concentrations. Urinary K excretion was similar between the groups despite the potassium depletion in the acid-fed animals. In contrast, isolated kidneys from animals with comparable K depletion induced by dietary K restriction readily conserved K. Sodium excretion and urinary flow were similar among the three groups of isolated kidneys. Plasma aldosterone concentrations were greater in the acid-fed rats after the 4 days of NH4Cl ingestion than in the control animals. Adrenalectomized rats were treated with either normal (4 μg/day) or high (22 μg/day) aldosterone replacement while ingesting NH4Cl for 4 days. Only in the presence of high aldosterone replacement did the acid-fed adrenalectomized animals develop K depletion. The authors conclude that chronic metabolic acidosis stimulates aldosterone secretion, and that aldosterone maintains the inappropriately high urinary potassium excretion and K depletion seen in this acid-base disorder

  18. Metabolic acidosis mimicking diabetic ketoacidosis after use of calorie-free mineral water.

    Dahl, Gry T; Woldseth, Berit; Lindemann, Rolf

    2012-09-01

    A previously healthy boy was admitted with fever, tachycardia, dyspnea, and was vomiting. A blood test showed a severe metabolic acidosis with pH 7.08 and an anion gap of 36 mmol/L. His urine had an odor of acetone. The serum glucose was 5.6 mmol/L, and no glucosuria was found. Diabetic ketoacidosis could therefore be eliminated. Lactate level was normal. Tests for the most common metabolic diseases were negative. Because of herpes stomatitis, the boy had lost appetite and only been drinking Diet Coke and water the last days. Diet Coke or Coca-Cola Light is sweetened with a blend containing cyclamates, aspartame, and acesulfame potassium, all free of calories. The etiology of the metabolic acidosis appeared to be a catabolic situation exaggerated by fasting with no intake of calories. The elevated anion gap was due to a severe starvation ketoacidosis, mimicking a diabetic ketoacidosis. Pediatricians should recommend carbohydrate/calorie-containing fluids for rehydration of children with acute fever, diarrhea, or illness. PMID:22457081

  19. D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome

    N. Gurukripa Kowlgi

    2015-01-01

    Full Text Available D-lactic acidosis or D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. The unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid among other organic acids. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium, ataxia, and slurred speech. Diagnosis is made by a combination of clinical and laboratory data including special assays for D-lactate. Treatment includes correcting the acidosis and decreasing substrate for D-lactate such as carbohydrates in meals. In addition, antibiotics can be used to clear colonic flora. Although newer techniques for diagnosis and treatment are being developed, clinical diagnosis still holds paramount importance, as there can be many confounders in the diagnosis as will be discussed subsequently.

  20. Tumor environmental factors glucose deprivation and lactic acidosis induce mitotic chromosomal instability--an implication in aneuploid human tumors.

    Chunyan Dai

    Full Text Available Mitotic chromosomal instability (CIN plays important roles in tumor progression, but what causes CIN is incompletely understood. In general, tumor CIN arises from abnormal mitosis, which is caused by either intrinsic or extrinsic factors. While intrinsic factors such as mitotic checkpoint genes have been intensively studied, the impact of tumor microenvironmental factors on tumor CIN is largely unknown. We investigate if glucose deprivation and lactic acidosis--two tumor microenvironmental factors--could induce cancer cell CIN. We show that glucose deprivation with lactic acidosis significantly increases CIN in 4T1, MCF-7 and HCT116 scored by micronuclei, or aneuploidy, or abnormal mitosis, potentially via damaging DNA, up-regulating mitotic checkpoint genes, and/or amplifying centrosome. Of note, the feature of CIN induced by glucose deprivation with lactic acidosis is similar to that of aneuploid human tumors. We conclude that tumor environmental factors glucose deprivation and lactic acidosis can induce tumor CIN and propose that they are potentially responsible for human tumor aneuploidy.

  1. Episodic, transient systemic acidosis delays evolution of the malignant phenotype: Possible mechanism for cancer prevention by increased physical activity

    Maini Philip K

    2010-04-01

    Full Text Available Abstract Background The transition from premalignant to invasive tumour growth is a prolonged multistep process governed by phenotypic adaptation to changing microenvironmental selection pressures. Cancer prevention strategies are required to interrupt or delay somatic evolution of the malignant invasive phenotype. Empirical studies have consistently demonstrated that increased physical activity is highly effective in reducing the risk of breast cancer but the mechanism is unknown. Results Here we propose the hypothesis that exercise-induced transient systemic acidosis will alter the in situ tumour microenvironment and delay tumour adaptation to regional hypoxia and acidosis in the later stages of carcinogenesis. We test this hypothesis using a hybrid cellular automaton approach. This model has been previously applied to somatic evolution on epithelial surfaces and demonstrated three phases of somatic evolution, with cancer cells escaping in turn from the constraints of limited space, nutrient supply and waste removal. In this paper we extend the model to test our hypothesis that transient systemic acidosis is sufficient to arrest, or at least delay, transition from in situ to invasive cancer. Conclusions Model simulations demonstrate that repeated episodes of transient systemic acidosis will interrupt critical evolutionary steps in the later stages of carcinogenesis resulting in substantial delay in the evolution to the invasive phenotype. Our results suggest transient systemic acidosis may mediate the observed reduction in cancer risk associated with increased physical activity. Reviewers This article was reviewed by Natalia Komarova (nominated by Marek Kimmel, Heiko Enderling (nominated by Marek Kimmel, Mark Little (nominated by Marek Kimmel and Yang Kuang.

  2. Endocrine and metabolic emergencies in children: hypocalcemia, hypoglycemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis.

    Kim, Se Young

    2015-12-01

    It is important to fast diagnosis and management of the pediatric patients of the endocrine metabolic emergencies because the signs and symptoms of these disorders are nonspecific. Delayed diagnosis and treatment may lead to serious consequences of the pediatric patients, for example, cerebral dysfunction leading to coma or death of the patients with hypoglycemia, hypocalcemia, adrenal insufficiency, or diabetic ketoacidosis. The index of suspicion of the endocrine metabolic emergencies should be preceded prior to the starting nonspecific treatment. Importantly, proper diagnosis depends on the collection of blood and urine specimen before nonspecific therapy (intravenous hydration, electrolytes, glucose or calcium injection). At the same time, the taking of precise history and searching for pathognomonic physical findings should be performed. This review was described for fast diagnosis and proper management of hypoglycemic emergencies, hypocalcemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis. PMID:26817004

  3. An unusual case of refractory metabolic acidosis after homeopathic medicinal treatment

    Sameer Saraf

    2014-01-01

    Full Text Available Homeopathy is one of the most frequently used and controversial systems of complementary and alternative medicine (CAM. It is based on the ′principle of similars′, whereby highly diluted preparations of substances that cause symptoms in healthy individuals are used to stimulate healing in patients who have similar symptoms when ill 1. General trends show a rise in the number of individuals utilising naturopathic and homeopathic therapeutic methods 2. The patients who seek homeopathic treatment are primarily those suffering from long-standing, chronic disease 1. Certainly, the CAM can show clinical benefits. However, some of these also involve a considerable risk of sometimes severe side-effects. We here are reporting an unusual case of refractory metabolic acidosis after homeopathic medicinal treatment.

  4. Dermal bone in early tetrapods: a palaeophysiological hypothesis of adaptation for terrestrial acidosis.

    Janis, Christine M; Devlin, Kelly; Warren, Daniel E; Witzmann, Florian

    2012-08-01

    The dermal bone sculpture of early, basal tetrapods of the Permo-Carboniferous is unlike the bone surface of any living vertebrate, and its function has long been obscure. Drawing from physiological studies of extant tetrapods, where dermal bone or other calcified tissues aid in regulating acid-base balance relating to hypercapnia (excess blood carbon dioxide) and/or lactate acidosis, we propose a similar function for these sculptured dermal bones in early tetrapods. Unlike the condition in modern reptiles, which experience hypercapnia when submerged in water, these animals would have experienced hypercapnia on land, owing to likely inefficient means of eliminating carbon dioxide. The different patterns of dermal bone sculpture in these tetrapods largely correlates with levels of terrestriality: sculpture is reduced or lost in stem amniotes that likely had the more efficient lung ventilation mode of costal aspiration, and in small-sized stem amphibians that would have been able to use the skin for gas exchange. PMID:22535781

  5. Systemic lupus erythematosus with distal renal tubular acidosis presenting as hypokalemic paralysis with respiratory failure.

    Koul, Parvaiz Ahmad; Wahid, Abdul; Shah, Bashir Ahmad

    2003-01-01

    An eighteen-year-old woman presented with hypokalemic respiratory failure. She was found to have distal renal tubular acidosis (dRTA) as the underlying cause for hypokalemia. This was treated successfully, and no apparent etiology for the dRTA was discovered. Three years later she presented with full-blown picture of systemic lupus erythematosus (SLE) together with features of persistent dRTA complicated, this time, with bilateral renal calculi and nephrocalcinosis. It is very likely that the dRTA was an early feature that preceded the other markers of SLE. The moral of this case is that patients with dRTA should be followed-up carefully as a primary cause for the dRTA may show up in-due-course and to monitor the treatment so as to prevent long-term complications of the RTA. PMID:18209445

  6. Serum acute phase proteins in cows with SARA (Subacute Ruminal Acidosis suspect

    C. Cannizzo

    2012-02-01

    Full Text Available The aim of this study was to evaluate the variations of Acute Phase Proteins (APPs and other blood constituents during the onset of the sub-acute ruminal acidosis (SARA pathological status. A total of 108 cows from 12 dairy herds were randomly selected and divided into three Groups of 36 animals each. All animals were subjected to a rumenocentesis. Group A was composed by subjects with a rumen pH>5.8, Group B was composed by subjects with a rumen pH ≤5.5≤5.8 and Group C was composed by subjects with a rumen pH<5.5. Blood samples were collected by jugular venipuncture and Haptoglobin (Hp, Serum Amyloid A (SAA, Total Proteins, Albumin and White Blood Cells (WBC were determined. One-way ANOVA showed a statistical significance on Rumen pH, Hp, SAA. SARA seems not stimulate the APPs production from liver.

  7. Profound Intraoperative Metabolic Acidosis and Hypotension in a Child Undergoing Multilevel Spinal Fusion

    Mohanad Shukry

    2009-01-01

    Full Text Available The prone position may cause cardiovascular system depression. Yet, the mechanisms involved and preemptive measures are not well understood (Edgcombe et al. (2008. During spinal surgery in the prone position, hypotension may occur. Implicated factors include prolonged abdominal compression impeding venous return resulting in increased blood loss, decreased cardiovascular reserve, and the use of total intravenous anesthesia (TIVA which has been shown to blunt the sympathetic response more than inhalation anesthesia. We present a case of hypotension during spinal surgery with all its challenges. Hypotension and acidosis persisted despite all supporting measures, and only to improve with supine positioning. Differential diagnosis for such an event are discussed. Although abdominal compression may not be obvious before the start of surgery, compressing the spine during surgery may lead to abdominal compression and hypoperfusion to abdominal organs.

  8. Esubacute acidosis in rumen of high-yield dairy cows: Prevalence and prevention

    Petrujkić Branko T.

    2008-01-01

    Full Text Available The objective of the investigations presented in this paper was to establish the frequency of the incidence of subacute acidosis in the rumen of cows (SARA in the first three months of lactation and the possibilities for its prevention using a mineral mix based on bentonite, zeolite, magnesium oxide, and sodium bicarbonate (Mix plus. The values obtained for the rumen pH content show that subacute rumen acidosis occurs in in 20 percent of the examined cows in the early stage of lactation. For these investigations, cows in early stages of lactation were chosen and divided into 2 groups. Cows of the experimental group were administered a fodder mix which contained the mineral mix for a buffer effect (Mix plus. The average values of the rumen pH content in the control and the experimental group of cows at the beginning and on the 30th day of the experiment were approximately the same and did not differ significantly (p>0.05. On the 60th day of the experiment, the values for the electrochemical reaction of the rumen content for the control group amounted to an average of 6.219±0.18, and for the experimental group of cows it was 6.772±0.23. The obtained difference was statistically very significant (p<0.001. At the end of the experiment, on the 90th day, the average pH value of the rumen content of cows of the control group was 6.308±0.16, while this value in the experimental group of cows was significantly higher and amounted to 6.676±0.29 (p<0.01.

  9. Diagnostic Challenge in a Patient with Severe Anion Gap Metabolic Acidosis

    Eugene M. Tan

    2015-01-01

    Full Text Available The approach to the patient with acute renal failure and elevated anion and osmolal gap is difficult. Differential diagnoses include toxic alcohol ingestion, diabetic or starvation ketoacidosis, or 5-oxoproline acidosis. We present a 76-year-old female with type 2 diabetes mellitus, who was found at home in a confused state. Laboratory analysis revealed serum pH 6.84, bicarbonate 5.8 mmol/L, pCO2 29 mmHg, anion gap 22.2 mmol/L, osmolal gap 17.4 mOsm/kg, elevated beta-hydroxybutyrate (4.2 mmol/L, random blood sugar 213 mg/dL, creatinine 2.1 mg/dL, and potassium 7.5 mmol/L with no electrocardiogram (EKG changes. Fomepizole and hemodialysis were initiated for presumed ethylene glycol or methanol ingestion. Drug screens returned negative for ethylene glycol, alcohols, and acetaminophen, but there were elevated urine levels of acetone (11 mg/dL. The acetaminophen level was negative, and 5-oxoproline was not analyzed. After 5 days in the intensive care unit (ICU, her mental status improved with supportive care. She was discharged to a nursing facility. Though a diagnosis was not established, our patient’s presentation was likely due to starvation ketosis combined with chronic acetaminophen ingestion. Acetone ingestion is less likely. Overall, our case illustrates the importance of systematically approaching an elevated osmolal and anion gap metabolic acidosis.

  10. Successful recovery from iatrogenic severe hypernatremia and severe metabolic acidosis resulting from accidental use of inappropriate bicarbonate concentrate for hemodialysis treatment

    Guruprasad P Bhosale

    2015-01-01

    Full Text Available Bicarbonate dialysis is the treatment modality of choice for correction of metabolic acidosis in chronic renal failure. However, improper selection of dialysate concentrate can result in life-threatening human errors. We report a case of iatrogenic severe hypernatremia (sodium 207 mEq/L and severe metabolic acidosis (pH 6.65 that resulted due to accidental use of inappropriate bicarbonate concentrate for hemodialysis treatment. There was successful recovery in this patient with no neurological sequelae. To the best of our knowledge, this is the first case report in adults of severe hypernatremia along with severe metabolic acidosis due to error in the preparation of dialysis fluid.

  11. Linfoma marginal del bazo asociado a acidosis láctica tipo B: Caso clínico Type B lactic acidosis associated with marginal lymphoma of the spleen: Report of one case

    Jorge Vega

    2012-02-01

    Full Text Available Lactic acidosis in the absence of hypoxia or tissue hypoperfusion (type B is very rare and is associated with the use of some drugs or malignancy. We report a 79-year-old woman, with a marginal non-Hodgkin's lymphoma of the spleen that was subjected to a splenectomy one year ago. She presented with unexplained tachypnea associated with pancytopenia and elevation of IgM to 10 times over the higher normal limit. Laboratory tests showed the presence of metabolic acidosis and high lactic acid levels in the absence of infection, tissue hypoxia or hypoperfusion. She was treated with sodium bicarbonate and steroids without obtaining a reduction in lactate levels. Twelve days after admission, a single dose of Rituximab quickly normalized lactate concentrations and platelet count. After the fourth dose of Rituximab, pancytopenia disappeared and IgM fell to 25% of its baseline concentration.

  12. Non-Specific Inhibition of Ischemia- and Acidosis-Induced Intracellular Calcium Elevations and Membrane Currents by α-Phenyl-N-tert-butylnitrone, Butylated Hydroxytoluene and Trolox

    Christopher Katnik; Javier Cuevas

    2014-01-01

    Ischemia, and subsequent acidosis, induces neuronal death following brain injury. Oxidative stress is believed to be a key component of this neuronal degeneration. Acute chemical ischemia (azide in the absence of external glucose) and acidosis (external media buffered to pH 6.0) produce increases in intracellular calcium concentration ([Ca2+] i ) and inward membrane currents in cultured rat cortical neurons. Two α-tocopherol analogues, trolox and butylated hydroxytoluene (BHT), and the spin t...

  13. Successful recovery from iatrogenic severe hypernatremia and severe metabolic acidosis resulting from accidental use of inappropriate bicarbonate concentrate for hemodialysis treatment

    Bhosale, Guruprasad P; Veena R Shah

    2015-01-01

    Bicarbonate dialysis is the treatment modality of choice for correction of metabolic acidosis in chronic renal failure. However, improper selection of dialysate concentrate can result in life-threatening human errors. We report a case of iatrogenic severe hypernatremia (sodium 207 mEq/L) and severe metabolic acidosis (pH 6.65) that resulted due to accidental use of inappropriate bicarbonate concentrate for hemodialysis treatment. There was successful recovery in this patient with no neurologi...

  14. Pathophysiology of incomplete renal tubular acidosis in recurrent renal stone formers: evidence of disturbed calcium, bone and citrate metabolism

    Osther, P J; Bollerslev, Jens; Hansen, A B;

    1993-01-01

    Urinary acidification, bone metabolism and urinary excretion of calcium and citrate were evaluated in 10 recurrent stone formers with incomplete renal tubular acidosis (iRTA), 10 recurrent stone formers with normal urinary acidification (NUA) and 10 normal controls (NC). Patients with iRTA had......-carbonic acidosis during fasting may be a pathophysilogical factor of both nephrolithiasis and disturbed bone metabolism in stone formers with iRTA....... significantly increased in iRTA compared with NUA and NC (P <0.01), indicating increased bone turnover in stone formers with iRTA. Stone formers with iRTA thus presented with disturbed calcium, bone and citrate metabolism--the same metabolic abnormalities which characterize classic type 1 RTA. Mild non...

  15. Hypokalemic paralysis and osteomalacia secondary to renal tubular acidosis in a case with primary Sjögren's syndrome.

    Kawashima, Masanori; Amano, Tetsuki; Morita, Yoshitaka; Yamamura, Masahiro; Makino, Hirofumi

    2006-01-01

    A 39-year-old Japanese woman was admitted to our hospital for severe weakness owing to potassium deficiency caused by type 1 renal tubular acidosis (RTA1). Sicca complex, serological tests, and lip biopsy revealed that she had Sjögren's syndrome (SS). Acidosis was corrected by alkali supplement treatment. She also had an impaired renal function with proteinuria, and high absorbance on Ga scintigram was recognized in both kidneys. She was taking warfarin potassium after aortic valve substitution due to aortic regurgitation, therefore renal biopsy was not performed. Prednisone (20 mg/day) was administered for renal inflammation. One month later, she suffered severe chest wall pains with some local tender points over the costae of both sides, which was presumed to be due to pseudo-fractures based on osteomalacia. Hypokalemic paralysis and osteomalacia should be taken into consideration in the diagnosis of SS with RTA1. PMID:16622725

  16. Osteomalacia complicating renal tubular acidosis in association with Sjogren′s syndrome

    Zohra El Ati

    2014-01-01

    Full Text Available Renal involvement in Sjogren′s syndrome (SS is not uncommon and may precede other complaints. Tubulointerstitial nephritis is the most common renal disease in SS and may lead to renal tubular acidosis (RTA, which in turn may cause osteomalacia. Nevertheless, osteomalacia rarely occurs as the first manifestation of a renal tubule disorder due to SS. We herewith describe a 43-year-old woman who was admitted to our hospital for weakness, lumbago and inability to walk. X-ray of the long bones showed extensive demineralization of the bones. Laboratory investigations revealed chronic kidney disease with serum creatinine of 2.3 mg/dL and creatinine clearance of 40 mL/min, hypokalemia (3.2 mmol/L, hypophosphatemia (0.4 mmol/L, hypocalcemia (2.14 mmol/L and hyperchloremic metabolic acidosis (chlorine: 114 mmol/L; alkaline reserve: 14 mmol/L. The serum alkaline phosphatase levels were elevated. The serum levels of 25-hydroxyvitamin D and 1,25-dihydroxy vitamin D were low and borderline low, respectively, and the parathyroid hormone level was 70 pg/L. Urinalysis showed inappropriate alkaline urine (urinary PH: 7, glycosuria with normal blood glucose, phosphaturia and uricosuria. These values indicated the presence of both distal and proximal RTA. Our patient reported dryness of the mouth and eyes and Schirmer′s test showed xerophthalmia. An accessory salivary gland biopsy showed changes corresponding to stage IV of Chisholm and Masson score. Kidney biopsy showed diffuse and severe tubulo-interstitial nephritis with dense lymphoplasmocyte infiltrates. Sicca syndrome and renal interstitial infiltrates indicated SS as the underlying cause of the RTA and osteomalacia. The patient received alkalinization, vitamin D (Sterogyl ®, calcium supplements and steroids in an initial dose of 1 mg/kg/day, tapered to 10 mg daily. The prognosis was favorable and the serum creatinine level was 1.7 mg/dL, calcium was 2.2 mmol/L and serum phosphate was 0.9 mmol/L.

  17. Oral rehydration therapy: efficacy of sodium citrate equals to sodium bicarbonate for correction of acidosis in diarrhoea.

    Islam, M. R.; Samadi, A R; Ahmed, S. M. [وسمية محمد أحمد; Bardhan, P K; Ali, A.

    1984-01-01

    Forty patients with moderate degrees of dehydration and acidosis because of acute watery diarrhoea were successfully treated randomly with either WHO recommended oral rehydration solution containing 2.5 g sodium bicarbonate or an oral solution containing 2.94 g sodium citrate in place of sodium bicarbonate per litre of oral rehydration rehydration solution. Efficacies were compared by measuring oral fluid intake, stool and vomitus output, change in body weight, hydration status, and rate of c...

  18. Sympathetic activation in exercise is not dependent on muscle acidosis. Direct evidence from studies in metabolic myopathies

    Vissing, J.; Vissing, S. F.; MacLean, D. A.; Saltin, B.; Quistorff, B.; Haller, R. G.; Blomqvist, C. G. (Principal Investigator)

    1998-01-01

    Muscle acidosis has been implicated as a major determinant of reflex sympathetic activation during exercise. To test this hypothesis we studied sympathetic exercise responses in metabolic myopathies in which muscle acidosis is impaired or augmented during exercise. As an index of reflex sympathetic activation to muscle, microneurographic measurements of muscle sympathetic nerve activity (MSNA) were obtained from the peroneal nerve. MSNA was measured during static handgrip exercise at 30% of maximal voluntary contraction force to exhaustion in patients in whom exercise-induced muscle acidosis is absent (seven myophosphorylase deficient patients; MD [McArdle's disease], and one patient with muscle phosphofructokinase deficiency [PFKD]), augmented (one patient with mitochondrial myopathy [MM]), or normal (five healthy controls). Muscle pH was monitored by 31P-magnetic resonance spectroscopy during handgrip exercise in the five control subjects, four MD patients, and the MM and PFKD patients. With handgrip to exhaustion, the increase in MSNA over baseline (bursts per minute [bpm] and total activity [%]) was not impaired in patients with MD (17+/-2 bpm, 124+/-42%) or PFKD (65 bpm, 307%), and was not enhanced in the MM patient (24 bpm, 131%) compared with controls (17+/-4 bpm, 115+/-17%). Post-handgrip ischemia studied in one McArdle patient, caused sustained elevation of MSNA above basal suggesting a chemoreflex activation of MSNA. Handgrip exercise elicited an enhanced drop in muscle pH of 0.51 U in the MM patient compared with the decrease in controls of 0.13+/-0.02 U. In contrast, muscle pH increased with exercise in MD by 0.12+/-0.05 U and in PFKD by 0.01 U. In conclusion, patients with glycogenolytic, glycolytic, and oxidative phosphorylation defects show normal muscle sympathetic nerve responses to static exercise. These findings indicate that muscle acidosis is not a prerequisite for sympathetic activation in exercise.

  19. Thiamine Deficiency in a Developed Country: Acute Lactic Acidosis in Two Neonates Due to Unsupplemented Parenteral Nutrition.

    Salvatori, Guglielmo; Mondì, Vito; Piersigilli, Fiammetta; Capolupo, Irma; Pannone, Veronica; Vici, Carlo Dionisi; Rizzo, Cristiano; Dotta, Andrea

    2016-08-01

    Thiamine is a water-soluble vitamin implicated in several metabolic processes. Its deficiency, due to prolonged parenteral nutrition without adequate vitamin supplementation, can lead to multiorgan failure characterized by cardiovascular impairment and metabolic acidosis refractory to bicarbonate administration. Only thiamine administration allows the remission of symptoms. We report 2 preterm infants with acute thiamine deficiency due to prolonged parenteral nutrition without adequate vitamin supplementation. PMID:25591974

  20. An Uncommon Presentation of HDR Syndrome: Distal Renal Tubular Acidosis in a Patient with Sjögren's Syndrome

    Ebru Sevinç OK

    2015-12-01

    Full Text Available HDR syndrome is an autosomal dominant disorder characterized by hypoparathyroidism, sensorineural deafness and renal dysplasia. Haploinsufficiency of GATA3 on chromosome 10p15 is implicated in the pathogenesis of the syndrome. It may manifest itself with clinical features other than the classical triad. Here we report a case of HDR syndrome with concomitant Sjögren’s syndrome in a 33-year-old who female presented with distal renal tubular acidosis (dRTA.

  1. Acidosis decreases c-Myc oncogene expression in human lymphoma cells: a role for the proton-sensing G protein-coupled receptor TDAG8.

    Li, Zhigang; Dong, Lixue; Dean, Eric; Yang, Li V

    2013-01-01

    Acidosis is a biochemical hallmark of the tumor microenvironment. Here, we report that acute acidosis decreases c-Myc oncogene expression in U937 human lymphoma cells. The level of c-Myc transcripts, but not mRNA or protein stability, contributes to c-Myc protein reduction under acidosis. The pH-sensing receptor TDAG8 (GPR65) is involved in acidosis-induced c-Myc downregulation. TDAG8 is expressed in U937 lymphoma cells, and the overexpression or knockdown of TDAG8 further decreases or partially rescues c-Myc expression, respectively. Acidic pH alone is insufficient to reduce c-Myc expression, as it does not decrease c-Myc in H1299 lung cancer cells expressing very low levels of pH-sensing G protein-coupled receptors (GPCRs). Instead, c-Myc is slightly increased by acidosis in H1299 cells, but this increase is completely inhibited by ectopic overexpression of TDAG8. Interestingly, TDAG8 expression is decreased by more than 50% in human lymphoma samples in comparison to non-tumorous lymph nodes and spleens, suggesting a potential tumor suppressor function of TDAG8 in lymphoma. Collectively, our results identify a novel mechanism of c-Myc regulation by acidosis in the tumor microenvironment and indicate that modulation of TDAG8 and related pH-sensing receptor pathways may be exploited as a new approach to inhibit Myc expression. PMID:24152439

  2. Acidosis Decreases c-Myc Oncogene Expression in Human Lymphoma Cells: A Role for the Proton-Sensing G Protein-Coupled Receptor TDAG8

    Zhigang Li

    2013-10-01

    Full Text Available Acidosis is a biochemical hallmark of the tumor microenvironment. Here, we report that acute acidosis decreases c-Myc oncogene expression in U937 human lymphoma cells. The level of c-Myc transcripts, but not mRNA or protein stability, contributes to c-Myc protein reduction under acidosis. The pH-sensing receptor TDAG8 (GPR65 is involved in acidosis-induced c-Myc downregulation. TDAG8 is expressed in U937 lymphoma cells, and the overexpression or knockdown of TDAG8 further decreases or partially rescues c-Myc expression, respectively. Acidic pH alone is insufficient to reduce c-Myc expression, as it does not decrease c-Myc in H1299 lung cancer cells expressing very low levels of pH-sensing G protein-coupled receptors (GPCRs. Instead, c-Myc is slightly increased by acidosis in H1299 cells, but this increase is completely inhibited by ectopic overexpression of TDAG8. Interestingly, TDAG8 expression is decreased by more than 50% in human lymphoma samples in comparison to non-tumorous lymph nodes and spleens, suggesting a potential tumor suppressor function of TDAG8 in lymphoma. Collectively, our results identify a novel mechanism of c-Myc regulation by acidosis in the tumor microenvironment and indicate that modulation of TDAG8 and related pH-sensing receptor pathways may be exploited as a new approach to inhibit Myc expression.

  3. Topiramate and severe metabolic acidosis: case report Acidose metabólica grave por topiramato: relato de caso

    Jayme E. Burmeister

    2005-06-01

    Full Text Available Topiramate infrequently induces anion gap metabolic acidosis through carbonic anhydrase inhibition on the distal tubule of the nephron - a type 2 renal tubular acidosis. We report on a 40 years old woman previously healthy that developed significant asymptomatic metabolic acidosis during topiramate therapy at a dosage of 100mg/day for three months. Stopping medication was followed by normalization of the acid-base status within five weeks. This infrequent side effect appears unpredictable and should be given careful attention.Topiramato pode produzir raramente uma acidose metabólica através da inibição da anidrase carbônica no túbulo distal do néfron - acidose tubular renal do tipo 2. Relatamos o caso de mulher de 40 anos previamente saudável que desenvolveu quadro de acidose metabólica assintomática grave, sem outra etiologia identificável, durante uso de topiramato na dose de 100mg/dia por três meses. Este efeito colateral, embora infrequente, parece ser imprevisível e requer atenção cuidadosa.

  4. Tolerance of acute hypercapnic acidosis by the European eel ( Anguilla anguilla)

    McKenzie, D J; Taylor, E W; Dalla Valle, A Z;

    2002-01-01

    throughout, as a consequence of a significant increase in stroke volume at PwCO(2)s of 40, 60 and 80 mm Hg. The eels maintained O(2) uptake at routine normocapnic levels throughout hypercapnic exposure. A comparison of the rates of blood O(2) delivery (calculated from CO and caO(2)) against O(2) consumption...... at PwCO(2)s of 60 mm Hg and 80 mm Hg indicated that a portion of O(2) uptake was due to cutaneous respiration. Thus, the European eel's exceptional tolerance of acute hypercapnia is probably a consequence of the tolerance of its heart to acidosis and hypoxia, and a contribution to O(2) uptake from......European eels ( Anguilla anguilla) were exposed sequentially to partial pressures of CO(2) in the water ( PwCO(2)) of 5, 10, 20, 40, 60 then 80 mm Hg (equivalent to 0.66-10.5 kPa), for 30 min at each level. This caused a profound drop in arterial plasma pH, from 7.9 to below 7.2, an increase...

  5. Lactic acidosis and diastolic hypotension after intermittent albuterol nebulization in a pediatric patient

    Tehila A. Saadia

    2015-01-01

    Full Text Available We describe a case of 13-year-old female with intermittent asthma who developed lactic acidosis and diastolic hypotension after receiving intermittent albuterol nebulizer treatment. She presented to the emergency department (ED with sudden onset of shortness of breath and chest pain. She received two albuterol nebulizer treatments at home without symptomatic relief. She was treated in the ED with intermittent albuterol nebulization for a total of 22.5 mg over the next 5 hours. A decrease in diastolic blood pressure from 60 mmHg to 40 mmHg was noted after the treatment. Blood lactate level was 5.9 mmol/L. She recovered from it and was discharged to home but she had recurrence of shortness of breath and presented to the ED two days later. She was treated with albuterol nebulization for a total of 17.5 mg over the next two and half hours and developed diastolic hypotension again, as low as 30 mm Hg. After discontinuation of albuterol nebulization, her BP normalized. Cardiopulmonary and metabolic side effects of continuous albuterol therapy have been reported in the recent medical literature. Our patient, however, developed these adverse effects on intermittent albuterol nebulizer treatment. It is important for the pediatrician to recognize the adverse effects of β2-agonist therapy to avoid carrying out extensive workup for hypotension and hyperlactatemia prolonging hospital stay.

  6. Metabolic Acidosis and Strong Ion Gap in Critically Ill Patients with Acute Kidney Injury

    Cai-Mei Zheng

    2014-01-01

    Full Text Available Purpose. To determine the influence of physicochemical parameters on survival in metabolic acidosis (MA and acute kidney injury (AKI patients. Materials and Methods. Seventy-eight MA patients were collected and assigned to AKI or non-AKI group. We analyzed the physiochemical parameters on survival at 24 h, 72 h, 1 week, 1 month, and 3 months after AKI. Results. Mortality rate was higher in the AKI group. AKI group had higher anion gap (AG, strong ion gap (SIG, and apparent strong ion difference (SIDa values than non-AKI group. SIG value was higher in the AKI survivors than nonsurvivors and this value was correlated serum creatinine, phosphate, albumin, and chloride levels. SIG and serum albumin are negatively correlated with Acute Physiology and Chronic Health Evaluation IV scores. AG was associated with mortality at 1 and 3 months post-AKI, whereas SIG value was associated with mortality at 24 h, 72 h, 1 week, 1 month, and 3 months post-AKI. Conclusions. Whether high or low SIG values correlate with mortality in MA patients with AKI depends on its correlation with serum creatinine, chloride, albumin, and phosphate (P levels. AG predicts short-term mortality and SIG value predicts both short- and long-term mortality among MA patients with AKI.

  7. Differential effects of acidosis, high potassium concentrations, and metabolic inhibition on noradrenaline release and its presynaptic muscarinic regulation.

    Haunstetter, Armin; Schulze Icking, Babette; Backs, Johannes; Krüger, Carsten; Haass, Markus

    2002-03-01

    It was the aim of the present study to characterize the effect of single components of ischaemia, such as inhibition of aerobic and anaerobic energy production by combined anoxic and glucose-free perfusion (metabolic inhibition), high extracellular potassium concentrations (hyperkalaemia), and acidosis, on (1). the stimulated release of noradrenaline from the in situ perfused guinea-pig heart and (2). its presynaptic modulation by the muscarinic agonist carbachol. The release of endogenous noradrenaline from efferent cardiac sympathetic nerve endings was induced by electrical stimulation of the left stellate ganglion (1 min, 5 V, 12 Hz) and quantified in the coronary venous effluent by high-performance liquid chromatography. Under control conditions, two consecutive electrical stimulations (S1, S2) elicited a similar noradrenaline overflow (S2/S1: 0.98 plus minus 0.05). After 10 min of global myocardial ischaemia overflow of endogenous noradrenaline was significantly reduced (S2/S1: 0.18 plus minus 0.03; P< 0.05). When studied separately, metabolic inhibition, hyperkalaemia (16 mM), and acidosis (pH 6.0) each markedly attenuated stimulated noradrenaline overflow (S2/S1: 0.65 plus minus 0.05, 0.43 plus minus 0.14, and 0.37 plus minus 0.09, respectively; P< 0.05). The muscarinic agonist carbachol (10 microM) inhibited stimulated noradrenaline release under normoxic conditions (S2/S1: 0.41 plus minus 0.07; P< 0.05). However, after 10 min of global myocardial ischaemia the inhibitory effect of carbachol on noradrenaline overflow was completely lost. Single components of ischaemia had a differential effect on presynaptic muscarinic modulation. Whereas hyperkalaemia (8-16 mM) did not affect muscarinic inhibition of noradrenaline release, carbachol lost its inhibitory effect during acidosis and metabolic inhibition. In conclusion, hyperkalaemia, metabolic inhibition, and severe acidosis each contribute to reduced overflow of noradrenaline after 10 min of myocardial

  8. Incidence of lactic acidosis toxicity among patients on stavudine or zidovudine containing antiretroviral therapy at Lighthouse clinics

    W Ng'ambi

    2012-11-01

    Full Text Available Although stavudine and zidovudine remain frequently used in low-income countries in Africa, they are associated with long-term toxicities. Lactic acidosis is one of the most serious toxicities in antiretroviral treatment (ART and occurs predominantly in regimens containing stavudine (D4T or zidovudine (AZT. We conducted this study to determine the incidence and risk factors for lactic acidosis among HIV-positive patients that have been on ART for at least 6 months. This study will bridge the gap that exists due to scarcity of data on the extent of toxicities due to long-term use of D4T and AZT. We conducted a retrospective cohort study using routine clinic data from the Lighthouse and Martin Preuss Centre electronic data systems. We used the clinic data collected between 1st January 2004 and 31st December 2011. We included into the analysis all patients that have been on D4T- or AZT-containing ARV drugs for at least 6 months. We analysed the data using Poisson regression of the number of cases of lactic acidosis (LA on gender, age at ART initiation, baseline BMI, and lipodystrophy in order to determine the incidence and risk factors for lactic acidosis. All statistical analyses were done at 5% significance level. We identified 14,854 patients that have ever been on D4T- or AZT-containing ARV drugs for longer than 5 months. Of these, 43% were male and median age was 34 years. The total number of cases of confirmed LA was 342 with observed mortality rate 40% more than the patients without confirmed LA. There were 23.02 cases of LA for every 1000 patient-years on D4T- or AZT-containing ART regimens. The strongest risk factor identified for developing LA was having a baseline BMI >25 with incidence rate ratio (IRR 3.11 (95% CI: 2.49, 3.88. The IRR for patients with a diagnosis of lipodystrophy was 1.77 (95% CI: 1.35, 2.32. Patients aged <30 years at ART initiation had 31% reduced risk of developing LA as compared to patients aged>39 years at ART

  9. Risk factors for mortality in children with diabetic keto acidosis from developing countries

    Varadarajan; Poovazhagi

    2014-01-01

    Diabetic keto acidosis(DKA) is the major cause for mortality in children with Diabetes mellitus(DM). With increasing incidence of type 1 DM worldwide, there is an absolute increase of DM among children between 0-14 year age group and overall incidence among less than 30 years remain the same. This shift towards younger age group is more of concern especially in developing countries where mortality in DKA is alarmingly high. Prior to the era of insulin, DKA was associated with 100% mortality and subsequently mortality rates have come down and is now, 0.15%-0.31% in developed countries. However the scenario in developing countries like India, Pakistan, and Bangladesh are very different and mortality is still high in children with DKA. Prospective studies on DKA in children are lacking in developing countries. Literature on DKA related mortality are based on retrospective studies and are very recent from countries like India, Pakistan and Bangladesh. There exists an urgent need to understand the differences between developed and developing countries with respect to mortality rates and factors associated with increased mortality in children with DKA. Higher mortality rates, increased incidence of cerebral edema, sepsis, shock and renal failure have been identified among DKA in children from developing countries.Root cause for all these complications and increased mortality in DKA could be delayed diagnosis in children from developing countries. This necessitates creating awareness among parents, public and physicians by health education to identify symptoms of DM/DKA in children, in order to decrease mortality in DKA. Based on past experience in Parma, Italy it is possible to prevent occurrence of DKA both in new onset DM and in children with established DM, by simple interventions to increase awareness among public and physicians.

  10. Progress in Diagnosing Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like Episodes

    Ying-Xin Wang; Wei-Dong Le

    2015-01-01

    Objective:Mitochondrial myopathy,encephalopathy,lactic acidosis,and stroke-like episodes (MELAS) is a progressive,multisystem affected mitochondrial disease associated with a number of disease-related defective genes.MELAS has unpredictable presentations and clinical course,and it can be commonly misdiagnosed as encephalitis,cerebral infarction,or brain neoplasms.This review aimed to update the diagnosis progress in MELAS,which may provide better understanding of the disease nature and help make the right diagnosis as well.Data Sources:The data used in this review came from published peer review articles from October 1984 to October 2014,which were obtained from PubMed.The search term is "MELAS".Study Selection:Information selected from those reported studies is mainly based on the progress on clinical features,blood biochemistry,neuroimaging,muscle biopsy,and genetics in diagnosing MELAS.Results:MELAS has a wide heterogeneity in genetics and clinical manifestations.The relationship between mutations and phenotypes remains unclear.Advanced serial functional magnetic resonance imaging (MRI) can provide directional information on this disease.Muscle biopsy has meaningful value in diagnosing MELAS,which shows the presence of ragged red fibers and mosaic appearance of cytochrome oxidase negative fibers.Genetic studies have reported that approximately 80% of MELAS cases are caused by the mutation m.3243A>G of the mitochondrial transfer RNA (Leu (UUR)) gene (MT-TL1).Conclusions:MELAS involves multiple systems with variable clinical symptoms and recurrent episodes.The prognosis of MELAS patients depends on timely diagnosis.Therefore,overall diagnosis of MELAS should be based on the maternal inheritance family history,clinical manifestation,and findings from serial MRI,muscle biopsy,and genetics.

  11. Fatores de risco maternos associados à acidose fetal Maternal risk factors associated with fetal acidosis

    José Mauro Madi

    2010-09-01

    Full Text Available OBJETIVOS: avaliar os fatores de risco maternos associados à acidose fetal. MÉTODOS: estudo tipo caso-controle composto por 188 recém-nascidos, sendo que 47 compuseram o grupo casos (pH de artéria umbilical OBJECTIVES: to assess maternal risk factors associated with fetal acidosis. METHODS: a case-control type study was conducted of 188 neonates, of whom 47 comprised the case group (umbilical arterial pH <7.0 and 141 the control (umbilical arterial pH E7.1 <7.3. The study included only single-gestation neonates without congenital malformations. Both maternal and fetal variables were taken into consideration. Statistical analysis involved the calculation of the raw and adjusted Odds Ratio, Student's t-test, the chi-squared test and multivariate analysis using Enter-method non-conditional logistic regression. The level of statistical significance was set at p<0.05. RESULTS: in the case group higher percentages of caesarian sections and pre-term births were observed, involving almost five times as much intensive care and twenty-five times more likelihood of Apgar in the 5th minute <7. No association was observed between the groups and fetal presentation, mother's age, history of miscarriage, years of schooling of mother or attendance at prenatal sessions. After multivariate analysis, the only risk factors that remained significant were complications relating to the placenta or the umbilical cord. Deliveries involving complications relating to the placenta or the umbilical cord were three times more likely to involve fetal acidemia. CONCLUSIONS: acidemia among neonates was associated with a higher percentage of caesarians, premature births, a need for intensive care and treatment and an Apgar index of <7 in the 5th minute. After multivariate analysis, complications relating to premature displacement of the placenta and the umbilical cord were the only remaining risk factors associated with fetal acidemia.

  12. Reversible lactic acidosis in a newborn with thiamine transporter-2 deficiency.

    Pérez-Dueñas, Belén; Serrano, Mercedes; Rebollo, Mónica; Muchart, Jordi; Gargallo, Eva; Dupuits, Celine; Artuch, Rafael

    2013-05-01

    Thiamine transporter-2 deficiency is a recessive disease caused by mutations in the SLC19A3 gene. Patients manifest acute episodes of encephalopathy; symmetric lesions in the cortex, basal ganglia, thalami or periaqueductal gray matter, and a dramatic response to biotin or thiamine. We report a 30-day-old patient with mutations in the SLC19A3 gene who presented with acute encephalopathy and increased level of lactate in the blood (8.6 mmol/L) and cerebrospinal fluid (7.12 mmol/L), a high excretion of α-ketoglutarate in the urine, and increased concentrations of the branched-chain amino acids leucine and isoleucine in the plasma. MRI detected bilateral and symmetric cortico-subcortical lesions involving the perirolandic area, bilateral putamina, and medial thalami. Some lesions showed low apparent diffusion coefficient values suggesting an acute evolution; others had high values likely to be subacute or chronic, most likely related to the perinatal period. After treatment with thiamine and biotin, irritability and opisthotonus disappeared, and the patient recovered consciousness. Biochemical disturbances also disappeared within 48 hours. After discontinuing biotin, the patient remained stable for 6 months on thiamine supplementation (20 mg/kg/day). The examination revealed subtle signs of neurologic sequelae, and MRI showed necrotic changes and volume loss in some affected areas. Our observations suggest that patients with thiamine transporter 2 deficiency may be vulnerable to metabolic decompensation during the perinatal period, when energy demands are high. Thiamine defects should be excluded in newborns and infants with lactic acidosis because prognosis largely depends on the time from diagnosis to thiamine supplementation. PMID:23589815

  13. Non-Specific Inhibition of Ischemia- and Acidosis-Induced Intracellular Calcium Elevations and Membrane Currents by α-Phenyl-N-tert-butylnitrone, Butylated Hydroxytoluene and Trolox

    Christopher Katnik

    2014-02-01

    Full Text Available Ischemia, and subsequent acidosis, induces neuronal death following brain injury. Oxidative stress is believed to be a key component of this neuronal degeneration. Acute chemical ischemia (azide in the absence of external glucose and acidosis (external media buffered to pH 6.0 produce increases in intracellular calcium concentration ([Ca2+]i and inward membrane currents in cultured rat cortical neurons. Two α-tocopherol analogues, trolox and butylated hydroxytoluene (BHT, and the spin trapping molecule α-Phenyl-N-tert-butylnitrone (PBN were used to determine the role of free radicals in these responses. PBN and BHT inhibited the initial transient increases in [Ca2+]i, produced by ischemia, acidosis and acidic ischemia and increased steady state levels in response to acidosis and the acidic ischemia. BHT and PBN also potentiated the rate at which [Ca2+]i increased after the initial transients during acidic ischemia. Trolox inhibited peak and sustained increases in [Ca2+]i during ischemia. BHT inhibited ischemia induced initial inward currents and trolox inhibited initial inward currents activated by acidosis and acidic ischemia. Given the inconsistent results obtained using these antioxidants, it is unlikely their effects were due to elimination of free radicals. Instead, it appears these compounds have non-specific effects on the ion channels and exchangers responsible for these responses.

  14. Acidosis promotes Bcl-2 family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor Gpr65 signaling to Mek/Erk.

    Ryder, Christopher; McColl, Karen; Zhong, Fei; Distelhorst, Clark W

    2012-08-10

    Acidosis arises in solid and lymphoid malignancies secondary to altered nutrient supply and utilization. Tumor acidosis correlates with therapeutic resistance, although the mechanism behind this effect is not fully understood. Here we show that incubation of lymphoma cell lines in acidic conditions (pH 6.5) blocks apoptosis induced by multiple cytotoxic metabolic stresses, including deprivation of glucose or glutamine and treatment with dexamethasone. We sought to examine the role of the Bcl-2 family of apoptosis regulators in this process. Interestingly, we found that acidic culture causes elevation of both Bcl-2 and Bcl-xL, while also attenuating glutamine starvation-induced elevation of p53-up-regulated modulator of apoptosis (PUMA) and Bim. We confirmed with knockdown studies that these shifts direct survival decisions during starvation and acidosis. Importantly, the promotion of a high anti- to pro-apoptotic Bcl-2 family member ratio by acidosis renders cells exquisitely sensitive to the Bcl-2/Bcl-xL antagonist ABT-737, suggesting that acidosis causes Bcl-2 family dependence. This dependence appears to be mediated, in part, by the acid-sensing G protein-coupled receptor, GPR65, via a MEK/ERK pathway. PMID:22685289

  15. Acidosis láctica fatal en paciente con síndrome de inmunodeficiencia adquirido y tratamiento antiretroviral de alto grado de actividad: comunicación de un caso Fatal lactic acidosis in a patient with acquired immunodeficiency syndrome treated with highly active antiretroviral therapy: Report of one case

    Martín Lasso B; Jorge Pérez G; L. Miguel Noriega R; Rebeca Northland A

    2000-01-01

    Type B lactic acidosis occurs without any evidence of cellular hypoxia and is associated with the use of drugs or toxins. We report a 36 years old woman with acquired immunodeficiency syndrome that was admitted to the hospital with a severe lactic acidosis. She had been treated with didanosine, stavudine and efavirenz for four months prior to admission. Despite the use of high bicarbonate doses and vasoactive drugs, the patient had a catastrophic evolution and died in shock and multiple organ...

  16. Effects of tight versus non tight control of metabolic acidosis on early renal function after kidney transplantation

    Etezadi Farhad

    2012-09-01

    Full Text Available Abstract Background Recently, several studies have been conducted to determine the optimal strategy for intra-operative fluid replacement therapy in renal transplantation surgery. Since infusion of sodium bicarbonate as a buffer seems to be safer than other buffer compounds (lactate, gluconate, acetatethat indirectly convert into it within the liver, We hypothesized tight control of metabolic acidosis by infusion of sodium bicarbonate may improve early post-operative renal function in renal transplant recipients. Methods 120 patients were randomly divided into two equal groups. In group A, bicarbonate was infused intra-operatively according to Base Excess (BE measurements to achieve the normal values of BE (−5 to +5 mEq/L. In group B, infusion of bicarbonate was allowed only in case of severe metabolic acidosis (BE ≤ −15 mEq/L or bicarbonate ≤ 10 mEq/L or PH ≤ 7.15. Minute ventilation was adjusted to keep PaCO2 within the normal range. Primary end-point was sampling of serum creatinine level in first, second, third and seventh post-operative days for statistical comparison between groups. Secondary objectives were comparison of cumulative urine volumes in the first 24 h of post-operative period and serum BUN levels which were obtained in first, second, third and seventh post-operative days. Results In group A, all of consecutive serum creatinine levels were significantly lower in comparison with group B. With regard to secondary outcomes, no significant difference between groups was observed. Conclusion Intra-operative tight control of metabolic acidosis by infusion of Sodium Bicarbonate in renal transplant recipients may improve early post-operative renal function.

  17. A Comparison of Treating Metabolic Acidosis in CKD Stage 4 Hypertensive Kidney Disease with Fruits and Vegetables or Sodium Bicarbonate

    Goraya, Nimrit; Simoni, Jan; Jo, Chan-Hee

    2013-01-01

    Summary Background and objectives Current guidelines recommend Na+-based alkali for CKD with metabolic acidosis and plasma total CO2 (PTCO2) < 22 mM. Because diets in industrialized societies are typically acid-producing, we compared base-producing fruits and vegetables with oral NaHCO3 (HCO3) regarding the primary outcome of follow-up estimated GFR (eGFR) and secondary outcomes of improved metabolic acidosis and reduced urine indices of kidney injury. Design, setting, participants, & measurements Individuals with stage 4 (eGFR, 15–29 ml/min per 1.73 m2) CKD due to hypertensive nephropathy, had a PTCO2 level < 22 mM, and were receiving angiotensin-converting enzyme inhibition were randomly assigned to 1 year of daily oral NaHCO3 at 1.0 mEq/kg per day (n=35) or fruits and vegetables dosed to reduce dietary acid by half (n=36). Results Plasma cystatin C–calculated eGFR did not differ at baseline and 1 year between groups. One-year PTCO2 was higher than baseline in the HCO3 group (21.2±1.3 versus 19.5±1.5 mM; P<0.01) and the fruits and vegetables group (19.9±1.7 versus 19.3±1.9 mM; P<0.01), consistent with improved metabolic acidosis, and was higher in the HCO3 than the fruits and vegetable group (P<0.001). One-year urine indices of kidney injury were lower than baseline in both groups. Plasma [K+] did not increase in either group. Conclusions One year of fruits and vegetables or NaHCO3 in individuals with stage 4 CKD yielded eGFR that was not different, was associated with higher-than-baseline PTCO2, and was associated with lower-than-baseline urine indices of kidney injury. The data indicate that fruits and vegetables improve metabolic acidosis and reduce kidney injury in stage 4 CKD without producing hyperkalemia. PMID:23393104

  18. Endolymphatic Sac Enlargement in a Girl with a Novel Mutation for Distal Renal Tubular Acidosis and Severe Deafness

    Rink Nikki; Bitzan Martin; O'Gorman Gus; Nagel Mato; Torban Elena; Goodyer Paul

    2012-01-01

    Hereditary distal renal tubular acidosis (dRTA) is caused by mutations of genes encoding subunits of the H+-ATPase (ATP6V0A4 and ATP6V1B1) expressed in α -intercalated cells of the distal renal tubule and in the cochlea. We report on a 2-year-old girl with distal RTA and profound speech delay which was initially misdiagnosed as autism. Genetic analysis showed compound heterozygous mutations with one known and one novel mutation of the ATP6V1B1 gene; cerebral magnetic resonance imaging (MRI) r...

  19. Survival after cardiopulmonary arrest with extreme hyperkalaemia and hypothermia in a patient with metformin-associated lactic acidosis

    Tay, Stan; Lee, I-Lynn

    2012-01-01

    Potassium levels are regularly used as a prognostic factor to cease resuscitation in significant hypothermia. In this case report, we highlight how survival is still possible with extreme hyperkalaemia in severe hypothermia. We present a case of a 65-year-old Caucasian man who presented with metformin associated lactic acidosis. On presentation he had potassium of 9.1 mmol/l and a temperature of 31.5°C. Cardiopulmonary resuscitation was commenced when he went into asystolic arrest. This prese...

  20. An Unusual Initial Presentation of Sjögren’s Syndrome: Severe Hypokalemic Paralysis Secondary to Distal Renal Tubular Acidosis

    Sengul, Erkan; Bunul, Fatih; Yazici, Ayten; Sengul, Aysun; Dindar, Sevim; Halhalli, Gökçen Selma Kilic; Binnetoglu, Emine

    2013-01-01

    Sjögren’s syndrome is mainly affects the exocrine glands. Patients usually complain of persistent dryness of the mouth and eyes. However, nonexocrine organs such as the kidneys are often affected in these patients. Distal renal tubular acidosis (dRTA) and interstitiel nephritis are common in Sjögren’s syndrome. Nonetheless, severe hypokalemia and paralysis secondary to dRTA are unusual initial manifestation of Sjögren’s syndrome. Here, we describe a case of a 48 year old women admitted to the...

  1. Successfully Treated Calcific Uremic Arteriolopathy: Two Cases of a High Anion Gap Metabolic Acidosis with Intravenous Sodium Thiosulfate

    Joshua L. Rein

    2014-01-01

    Full Text Available Calcific uremic arteriolopathy (CUA is a rare and potentially fatal disorder of calcification involving subcutaneous small vessels and fat in patients with renal insufficiency. We describe the successful use of intravenous sodium thiosulfate (STS for the treatment of CUA in two patients. The first case was complicated by the development of a severe anion gap metabolic acidosis, which was accompanied by a seizure. Both patients had complete wound healing within five months. Although STS should be considered in the treatment of CUA, little is known about pharmacokinetics and additional studies are required to determine dosing strategies to minimize severe potential side effects.

  2. Effects of acidosis and NO on nicorandil-activated KATP channels in guinea-pig ventricular myocytes

    Moncada, Gustavo A; Kishi, Yukio; Numano, Fujio; Hiraoka, Masayasu; Sawanobori, Tohru

    2000-01-01

    Nicorandil is a hybrid compound of K+ channel opener and nitrate. We investigated a possible interaction of acidosis and nitric oxide (NO)-donors on the nicorandil-activated ATP-sensitive K+ channel (KATP) in guinea-pig ventricular myocytes using the patch-clamp technique.In whole-cell recordings, external application of 300 μM nicorandil activated KATP in the presence of 2 mM intracellular ATP concentration ([ATP]i) at external pH (pHo) 7.4, but the activated current was decreased by reducin...

  3. Persistent lactic acidosis after chronic topical application of silver sulfadiazine in a pediatric burn patient: a review of the literature

    Willis, Monte S.; Cairns, Bruce A; Purdy, Ashley; Bortsov, Andrey V; Jones, Samuel W.; Ortiz-Pujols, Shiara M; Willis, Tina M Schade; Jr, Benny L Joyner

    2013-01-01

    A 3-year old male who sustained 2nd and 3rd degree burns that covered approximately 60% TBSA presented to a large adult and pediatric verified burn center. On hospital day (HD) 26 of his stay, Candida fungemia was identified by blood culture, delaying operative management until HD 47. On HD 47, after his first operative intervention, the patient developed a persistent metabolic and lactic acidosis. On HD 66, a search for a cause of his osmol gap of 56 mOsm/kg revealed a potential source-propy...

  4.  Distal Renal Tubular Acidosis, Hypokalemic Paralysis, Nephrocalcinosis, Primary Hypothyroidism, Growth Retardation, Osteomalacia and Osteoporosis Leading to Pathological Fracture: A Case Report

    Mayada Mohammad Swar

    2011-07-01

    Full Text Available  Renal tubular acidosis (RTA is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acidosis (dRTA, hypokalemic paralysis, primary hypothyroidism, growth retardation, osteomalacia and osteopenia leading to stress fracture. All these features presenting in a single case (as in our case is a rare occurrence, so far other cases of distal renal tubular acidosis (dRTA have been reported.

  5. Distal renal tubular acidosis, hypokalemic paralysis, nephrocalcinosis, primary hypothyroidism, growth retardation, osteomalacia and osteoporosis leading to pathological fracture: a case report.

    Basak, Ramen C; Sharkawi, Khairy Mostafa; Rahman, Mohammad Mizanur; Swar, Mayada Mohammad

    2011-07-01

    Renal tubular acidosis (RTA) is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acidosis (dRTA), hypokalemic paralysis, primary hypothyroidism, growth retardation, osteomalacia and osteopenia leading to stress fracture. All these features presenting in a single case (as in our case) is a rare occurrence, so far other cases of distal renal tubular acidosis (dRTA) have been reported. PMID:22043434

  6. Ácidosis D-láctica secundaria a síndrome de intestino corto D-Lactic acidosis secondary to short bowel syndrome

    M. J. Tapia Guerrero

    2010-10-01

    Full Text Available El síndrome de intestino corto aparece por la reducción de la superficie absortiva intestinal efectiva por pérdida funcional o anatómica de una parte de intestino delgado. Se presenta el caso de una mujer de 35 años con síndrome de intestino corto severo secundario a isquemia intestinal aguda en la edad adulta, que presenta a los 5 años de evolución episodios de mareos con inestabilidad en la marcha y pérdida de fuerza en las manos, llegándose al diagnóstico de acidosis D-láctica. La acidosis D-láctica representa una complicación infrecuente, pero importante por su sintomatología, de este síndrome. Se debe a un cambio en la flora intestinal debido a un sobrecrecimiento de bacterias acidolácticas, que producen D-lactato. Debe sospecharse en aquellos casos de acidosis sin causa aparente y manifestaciones neurológicas sin focalidad en pacientes con síndrome de intestino corto o intervenidos de by-pass yeyuno-ileal. El tratamiento apropiado resuelve con frecuencia los síntomas neurológicos y previene o reduce las recurrencias.The short bowel syndrome appears for the reduction of intestinal absorptive surface due to functional or anatomical loss of part of the small bowel. We present the case of a 35-year-old woman with severe short bowel syndrome secondary to acute intestinal ischemia in adults, who presented at 5 years of evolution episodes of dizziness with gait instability and loss of strength in hands. The diagnosis was D-lactic acidosis. D-lactic acidosis is a rare complication, but important for their symptoms, of this syndrome. It is due to a change in intestinal flora secondary to an overgrowth of lactic acid bacteria that produce D-lactate. D-lactic acidosis should be looked for in cases of metabolic acidosis in which the identity of acidosis is not apparent, neurological manifestations without focality and the patient has short bowel syndrome or patients who have had jejunoileal bypass surgery. Appropiate treatment

  7. Endolymphatic Sac Enlargement in a Girl with a Novel Mutation for Distal Renal Tubular Acidosis and Severe Deafness

    Rink Nikki

    2012-01-01

    Full Text Available Hereditary distal renal tubular acidosis (dRTA is caused by mutations of genes encoding subunits of the H+-ATPase (ATP6V0A4 and ATP6V1B1 expressed in α-intercalated cells of the distal renal tubule and in the cochlea. We report on a 2-year-old girl with distal RTA and profound speech delay which was initially misdiagnosed as autism. Genetic analysis showed compound heterozygous mutations with one known and one novel mutation of the ATP6V1B1 gene; cerebral magnetic resonance imaging (MRI revealed bilateral enlargement of the endolymphatic sacs of the inner ear. With improved cooperation, audiometric testing showed that hearing loss was most profound on the right, where endolymphatic sac enlargement was greatest, demonstrating a clear link between the degree of deafness and the degree of inner ear abnormality. This case indicates the value of MRI for diagnosis of inner ear involvement in very young children with distal RTA. Although citrate therapy quickly corrects the acidosis and restores growth, early diagnosis of deafness is crucial so that hearing aids can be used to assist acquisition of speech and to provide enough auditory nerve stimulation to assure the affected infants remain candidates for cochlear implantation.

  8. Endolymphatic sac enlargement in a girl with a novel mutation for distal renal tubular acidosis and severe deafness.

    Nikki, Rink; Martin, Bitzan; Gus, O'Gorman; Mato, Nagel; Elena, Torban; Paul, Goodyer

    2012-01-01

    Hereditary distal renal tubular acidosis (dRTA) is caused by mutations of genes encoding subunits of the H(+)-ATPase (ATP6V0A4 and ATP6V1B1) expressed in α-intercalated cells of the distal renal tubule and in the cochlea. We report on a 2-year-old girl with distal RTA and profound speech delay which was initially misdiagnosed as autism. Genetic analysis showed compound heterozygous mutations with one known and one novel mutation of the ATP6V1B1 gene; cerebral magnetic resonance imaging (MRI) revealed bilateral enlargement of the endolymphatic sacs of the inner ear. With improved cooperation, audiometric testing showed that hearing loss was most profound on the right, where endolymphatic sac enlargement was greatest, demonstrating a clear link between the degree of deafness and the degree of inner ear abnormality. This case indicates the value of MRI for diagnosis of inner ear involvement in very young children with distal RTA. Although citrate therapy quickly corrects the acidosis and restores growth, early diagnosis of deafness is crucial so that hearing aids can be used to assist acquisition of speech and to provide enough auditory nerve stimulation to assure the affected infants remain candidates for cochlear implantation. PMID:22966473

  9. Short Review of Our Work - “Chronic Metabolic Acidosis Destroys Pancreas” with Focus on the Functional Exocrine Pancreatic Disorders

    linic of San Fran

    2015-07-01

    Full Text Available We deeply appreciate your publishing of our work - “Chronic metabolic acidosis destroys pancreas” in JOP (2014 [1]. We feel that our work can give the food for thought to many young researchers and health practitioners. A short review of our work may generate various questions and ideas for further investigations. In our work, we have focused on negative affects of the chronic metabolic acidosis on pancreatic function including: • Premature activation of the proteases within the pancreas • Diminishing the antimicrobial activity of the pancreatic juice • Suppressing of the flushing out zymogens from the pancreas • Precipitation of the aggressive bile acids • Calcification Authors believe that further research may provide more details of how the acidification destroys the pancreas and causes chronic pancreatitis. We would like to share some of our thoughts on this subject as follows: Descriptions of symptoms of chronic pancreatitis such as pain, malabsorption syndrome, steatorrhea, and weight loss are found in almost all medical books, textbooks, and articles. The medical literature refers to these conditions as “pancreatic insufficiency”. It is known that these symptoms occur when only 10 % of the exocrine pancreatic function is left intact. This is not an “insufficiency.” It is a pancreatic “failure” when the therapeutic opportunities are very limited.

  10. Lactate production retards, not causes, acidosis: a theoretical approach for physical education students.

    R. Hohl

    2005-07-01

    increased blood  lactate detection  is the  effect  not  the  cause  of acidosis.   The  students  must  understand that if muscles do not  produce  lactate, acidoses and fatigue  would accour faster,  impairing  high intensity exercise performance.  This information must be considered  in their  training schedules.

  11. Subacute ruminal acidosis challenge changed in situ degradability of feedstuffs in dairy goats.

    Li, Fei; Cao, Yangchun; Liu, Nannan; Yang, Xinjian; Yao, Junhu; Yan, Dabing

    2014-01-01

    This study investigated the effects of wheat-induced subacute ruminal acidosis (SARA) on rumen bacterial populations and in situ degradabilities of NDF, starch, and crude protein of feeds. Four multiparous dairy goats (BW=60±3.3kg) fitted with ruminal cannulas were assigned to a 2×2 crossover design (28-d treatment periods separated by a 7-d washout interval). The treatment diets consisted of 2 levels of cracked wheat: 0 (control, corn based concentrate) and 35% (diet-induced SARA, wheat-based concentrate), with a constant forage- (45% alfalfa hay and 5% corn silage of DM) to-concentrate (50% of DM) ratio. Results indicate that diets with a 35% wheat decreased ruminal pH (6.21 vs. 5.98) and increased the duration (1.13 vs. 4.72h/d) and area (0.12 vs. 0.78 pH × h/d) of ruminal pH below 5.6 and induced SARA. The SARA increased ruminal total volatile fatty acid concentration, from 105.0 to 123.8mM, and decreased the acetate molar proportion (62.8 vs. 56.6mol/100mol) and the acetate-to-propionate ratio (3.5 vs. 2.8). Compared with the control group, SARA decreases the relative abundance of Fibrobacter succinogenes (-59.3%) and Ruminococcus flavefaciens (-68.4%), whereas it increased Succinimonas amylolytica (198.1%) and Ruminobacter amylophilus (125.2%). The SARA decreased 24- and 48-h dry matter (DM) and neutral detergent fiber (NDF) degradabilities of corn silage. The 48-h degradabilities of DM (51.0 vs. 48.2%) and NDF (40.3 vs. 36.0%) in alfalfa hay were not affected by SARA, but the SARA tended to reduce the 24-h DM (49.6 vs. 46.3%) and NDF (37.8 vs. 33.2%) degradabilities. The effective ruminal degradabilities of DM and NDF in alfalfa hay and corn silage were reduced during SARA. In situ degradability parameters of DM and starch of wheat were not affected by SARA, but starch degradability of corn (9.5 vs. 13.3%/h) increased. The SARA reduced in situ 12-h degradabilities of DM and crude protein of soybean meal and extruded soybean without affecting the

  12. Ibuprofen-Induced Hypokalemia and Distal Renal Tubular Acidosis: A Patient’s Perceptions of Over-the-Counter Medications and Their Adverse Effects

    Mark D. Salter

    2013-01-01

    Full Text Available We highlight a case of distal renal tubular acidosis secondary to ibuprofen and codeine use. Of particular interest in this case are the patient’s perception of over-the-counter (OTC medication use, her own OTC use prior to admission, and her knowledge of adverse reactions or side effects of these medications prior to taking them.

  13. Mucosal necrosis of the small intestine in myopathy,encephalopathy, lactic acidosis, and stroke-like episodes syndrome

    Keita Fukuyama; Yasuhide Ishikawa; Tetsuro Ogino; Hidenobu Inoue; Ryoya Yamaoka; Tetsuro Hirose; Tomohiko Nishihira

    2012-01-01

    This report presents a case of massive mucosal necrosis of the small intestine in a patient with mitochondrial myopathy,encephalopathy,lactic acidosis,and stroke-like episodes (MELAS),which particularly affects the brain,nervous system and muscles.A 45-year-old Japanese female,with an established diagnosis of MELAS,presented with vomiting.Computed tomography showed portomesenteric venous gas and pneumatosis intestinalis.She underwent a resection of the small intestine.A microscopic study showed necrosis of the mucosa and vacuolar degeneration of smooth muscle cells in the arterial wall.Immunohistochemistry showed anti-mitochondrial antibody to be highly expressed in the crypts adjacent the necrotic mucosa.The microscopic and immunohistochemical findings suggested the presence of a large number of abnormal mitochondria in MELAS to be closely linked to mucosal necrosis of the small intestine.

  14. Knock-down of hypoxia-induced carbonic anhydrases IX and XII radiosensitizes tumor cells by increasing intracellular acidosis

    Jérôme eDoyen

    2013-01-01

    Full Text Available The relationship between acidosis within the tumor microenvironment and radioresistance of hypoxic tumor cells remains unclear. Previously we reported that hypoxia-induced carbonic anhydrases CAIX and CAXII constitute a robust pHi-regulating system that confers a survival advantage on hypoxic human colon carcinoma LS174Tr cells in acidic microenvironments. Here we investigate the role of acidosis, CAIX and CAXII knock-down in combination with ionizing radiation. Fibroblasts cells (-/+ CAIX and LS174Tr cells (inducible knock-down for ca9/ca12 were analyzed for cell cycle phase distribution and survival after irradiation in extracellular pHo manipulations and hypoxia (1% O2 exposure. Radiotherapy was used to target ca9/ca12-silenced LS174Tr tumors grown in nude mice. We found that diminishing the pHi-regulating capacity of fibroblasts through inhibition of NHE-1 sensitize cells to radiation-induced cell death. Secondly, the pHi-regulating function of CAIX plays a key protective role in irradiated fibroblasts in an acidic environment as accompanied by a reduced number of cells in the radiosensitive phases of the cell cycle. Thirdly, we demonstrate that irradiation of LS174Tr spheroids, silenced for either ca9 or both ca9/ca12, showed a respective 50% and 75% increase in cell death as a result of a decrease in cell number in the radioresistant S phase and a disruption of CA-mediated pHi regulation. Finally, LS174Tr tumor progression was strongly decreased when ca9/ca12 silencing was combined with irradiation in vivo. These findings highlight the combinatory use of radiotherapy with targeting of the pHi-regulating carbonic anhydrases as an anti-cancer strategy.

  15. Effects of grain, fructose, and histidine on ruminal pH and fermentation products during an induced subacute acidosis protocol.

    Golder, H M; Celi, P; Rabiee, A R; Heuer, C; Bramley, E; Miller, D W; King, R; Lean, I J

    2012-04-01

    The effects of grain, fructose, and histidine on ruminal pH and fermentation products were studied in dairy cattle during an induced subacute acidosis protocol. Thirty Holstein heifers were randomly allocated to 5 treatment groups: (1) control (no grain); (2) grain [fed at a crushed triticale dry matter intake (DMI) of 1.2% of body weight (BW)]; (3) grain (0.8% of BW DMI)+fructose (0.4% of BW DMI); (4) grain (1.2% of BW DMI)+histidine (6 g/head); and (5) grain (0.8% of BW DMI)+fructose (0.4% of BW DMI)+histidine (6 g/head) in a partial factorial arrangement. Heifers were fed 1 kg of grain daily with ad libitum access to ryegrass silage and alfalfa hay for 10 d. Feed was withheld for 14 h before challenge day, on which heifers were fed 200 g of alfalfa hay and then the treatment diets immediately thereafter. Rumen samples were collected 5 min after diet ingestion, 60 min later, and at 3 subsequent 50-min intervals. Grain decreased ruminal pH and increased ammonia, total volatile fatty acid (VFA), acetate, butyrate, propionate, and valerate concentrations compared with controls. The addition of grain had no effect on ruminal D- and L-lactate concentrations. Fructose markedly decreased ruminal pH and markedly increased D- and L-lactate concentrations. Fructose increased total VFA and butyrate and decreased valerate concentrations. Although histidine did not have a marked effect on ruminal fermentation, increased concentrations of histamine were observed following feeding. This study demonstrates that the substitution of some grain for fructose can lower ruminal pH and increase VFA and lactate concentrations, warranting further investigation into the role of sugars on the risk of acidosis in dairy cattle. PMID:22459843

  16. Acidosis láctica fatal en paciente con síndrome de inmunodeficiencia adquirido y tratamiento antiretroviral de alto grado de actividad: comunicación de un caso Fatal lactic acidosis in a patient with acquired immunodeficiency syndrome treated with highly active antiretroviral therapy: Report of one case

    Martín Lasso B

    2000-10-01

    Full Text Available Type B lactic acidosis occurs without any evidence of cellular hypoxia and is associated with the use of drugs or toxins. We report a 36 years old woman with acquired immunodeficiency syndrome that was admitted to the hospital with a severe lactic acidosis. She had been treated with didanosine, stavudine and efavirenz for four months prior to admission. Despite the use of high bicarbonate doses and vasoactive drugs, the patient had a catastrophic evolution and died in shock and multiple organ failure, 68 hours after admission. (Rev Méd Chile 2000; 128: 1139-43.

  17. Ácidosis D-láctica secundaria a síndrome de intestino corto D-Lactic acidosis secondary to short bowel syndrome

    M. J. Tapia Guerrero; Olveira Fuster, G.; M. Bravo Utrera; N. Colomo Rodríguez; Fernández García, J. C.

    2010-01-01

    El síndrome de intestino corto aparece por la reducción de la superficie absortiva intestinal efectiva por pérdida funcional o anatómica de una parte de intestino delgado. Se presenta el caso de una mujer de 35 años con síndrome de intestino corto severo secundario a isquemia intestinal aguda en la edad adulta, que presenta a los 5 años de evolución episodios de mareos con inestabilidad en la marcha y pérdida de fuerza en las manos, llegándose al diagnóstico de acidosis D-láctica. La acidosis...

  18. Arrhythmogenic Biophysical Phenotype for SCN5A Mutation S1787N Depends upon Splice Variant Background and Intracellular Acidosis.

    Rou-Mu Hu

    Full Text Available SCN5A is a susceptibility gene for type 3 long QT syndrome, Brugada syndrome, and sudden infant death syndrome. INa dysfunction from mutated SCN5A can depend upon the splice variant background in which it is expressed and also upon environmental factors such as acidosis. S1787N was reported previously as a LQT3-associated mutation and has also been observed in 1 of 295 healthy white controls. Here, we determined the in vitro biophysical phenotype of SCN5A-S1787N in an effort to further assess its possible pathogenicity.We engineered S1787N in the two most common alternatively spliced SCN5A isoforms, the major isoform lacking a glutamine at position 1077 (Q1077del and the minor isoform containing Q1077, and expressed these two engineered constructs in HEK293 cells for electrophysiological study. Macroscopic voltage-gated INa was measured 24 hours after transfection with standard whole-cell patch clamp techniques. We applied intracellular solutions with pH7.4 or pH6.7. S1787N in the Q1077 background had WT-like INa including peak INa density, activation and inactivation parameters, and late INa amplitude in both pH 7.4 and pH 6.7. However, with S1787N in the Q1077del background, the percentages of INa late/peak were increased by 2.1 fold in pH 7.4 and by 2.9 fold in pH 6.7 when compared to WT.The LQT3-like biophysical phenotype for S1787N depends on both the SCN5A splice variant and on the intracellular pH. These findings provide further evidence that the splice variant and environmental factors affect the molecular phenotype of cardiac SCN5A-encoded sodium channel (Nav1.5, has implications for the clinical phenotype, and may provide insight into acidosis-induced arrhythmia mechanisms.

  19. Persistent lactic acidosis in neonatal hypoxic-ischaemic encephalopathy correlates with EEG grade and electrographic seizure burden.

    Murray, D M

    2012-02-03

    BACKGROUND: Predicting at birth which infants with perinatal hypoxic-ischaemic injury will progress to significant encephalopathy remains a challenge. OBJECTIVE: To determine whether lactic acidosis at birth in asphyxiated neonates could predict the grade of EEG encephalopathy by examining the relationship between time taken for the normalisation of lactate, severity of encephalopathy and seizure burden. METHODS: Continuous early video-EEG monitoring was performed in babies at risk for hypoxic-ischaemic encephalopathy. Encephalopathy was graded from the EEG data. Total seizure burden (seconds) was calculated for each baby. Initial blood gas measurements of pH, base deficit and lactate were taken within 30 minutes of delivery. Time to normal serum lactate was determined in hours from birth for each infant. RESULTS: All 50 term infants had raised initial serum lactate (median (lower, upper quartiles) 11.7 (10.2, 14.9)). There were no significant differences between the initial serum lactate, pH and base deficit in infants with normal\\/mildly abnormal (n = 24), moderately abnormal (n = 14), severely abnormal (n = 5) and inactive EEGs (n = 7). Time to normal lactate varied significantly with EEG grade (median (lower, upper quartile) 6.0 (4.1, 9.5) for mild\\/normal EEG, 13.5 (6.8, 23.5) moderate EEG, 41.5 (30.0, 55.5) severe group, 12.0 (8.1, 21.5) inactive group; p<0.001). Time to normal lactate correlated significantly with EEG seizure burden (seconds; R = 0.446, p = 0.002). Mean (SD) time to normal lactate was 10.0 (7.2) hours in infants who did not have seizures and 27.3 (19.0) hours in the 13 infants with electrographic seizures (p = 0.002). CONCLUSIONS: Serum lactate levels in the first 30 minutes of life do not predict the severity of the ensuing encephalopathy. In contrast, sustained lactic acidosis is associated with severe encephalopathy on EEG and correlates with seizure burden.

  20. Deficiency of the iron-sulfur clusters of mitochondrial reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase (complex I) in an infant with congenital lactic acidosis.

    Moreadith, R W; Batshaw, M L; Ohnishi, T.; Kerr, D.; Knox, B; Jackson, D; Hruban, R; Olson, J; Reynafarje, B; Lehninger, A L

    1984-01-01

    We report the case of an infant with hypoglycemia, progressive lactic acidosis, an increased serum lactate/pyruvate ratio, and elevated plasma alanine, who had a moderate to profound decrease in the ability of mitochondria from four organs to oxidize pyruvate, malate plus glutamate, citrate, and other NAD+-linked respiratory substrates. The capacity to oxidize the flavin adenine dinucleotide-linked substrate, succinate, was normal. The most pronounced deficiency was in skeletal muscle, the le...

  1. Acidosis Sensing Receptor GPR65 Correlates with Anti-Apoptotic Bcl-2 Family Member Expression in CLL Cells: Potential Implications for the CLL Microenvironment

    Rosko, Ashley E.; McColl, Karen S.; Zhong, Fei; Ryder, Christopher B; Chang, Ming-Jin; Sattar, Abdus; Caimi, Paolo F.; Hill, Brian T; Al-harbi, Sayer; Almasan, Alexandru; Distelhorst, Clark W.

    2014-01-01

    The tumor microenvironment is generally an acidic environment, yet the effect of extracellular acidosis on chronic lymphocytic leukemia (CLL) is not well established. Here we are the first to report that the extracellular acid sensing G-protein coupled receptor, GPR65, is expressed in primary CLL cells where its level correlate strongly with anti-apoptotic Bcl-2 family member levels. GPR65 expression is found normally within the lymphoid lineage and has not been previously reported in CLL. We...

  2. Distal Renal Tubular Acidosis, Hypokalemic Paralysis, Nephrocalcinosis, Primary Hypothyroidism, Growth Retardation, Osteomalacia and Osteoporosis Leading to Pathological Fracture: A Case Report

    Mayada Mohammad Swar; Mohammad Mizanur Rahman; Khairy Mostafa Sharkawi; Basak, Ramen C.

    2011-01-01

     Renal tubular acidosis (RTA) is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acido...

  3. The diversity of the fecal bacterial community and its relationship with the concentration of volatile fatty acids in the feces during subacute rumen acidosis in dairy cows

    Mao Shengyong; Zhang Ruiyang; Wang Dongsheng; Zhu Weiyun

    2012-01-01

    Abstract Background Sub-acute ruminal acidosis (SARA) is a well-recognized digestive disorder found in particular in well-managed dairy herds. SARA can result in increased flow of fermentable substrates to the hindgut, which can increase the production of volatile fatty acids, alter the structure of the microbial community, and have a negative effect on animal health and productivity. However, little is known about changes in the structure of the microbial community and its relationship with ...

  4. 奶牛瘤胃酸中毒的发病机制和防治措施%The Mechanism and Prevention of Dairy Cow Rumen Acidosis

    杨艳玲; 沈赞明

    2015-01-01

    The cow rumen acidosis is caused by the high concentrated feed used .It has improved ruminal pH ,microbial flora ,eventually led to a decline in milk production and milk quality ,triggering a series of nutritional and metabolic disease ,great harm to dairy production .This pa‐per reviews several aspects of acute acidosis and subacute ruminal acidosis in the etiology ,pathogenesis and prevention measures to provide sci‐entific and theoretical basis for actual production .%奶牛瘤胃酸中毒是由于大量饲喂易发酵的碳水化合物日粮引起的,造成奶牛瘤胃酸度增加,微生物菌群失调,最终导致奶牛产奶量和乳品质下降,进而引发一系列的营养代谢病,对奶牛生产危害极大。文章就急性瘤胃酸中毒和亚急性瘤胃酸中毒的发病病因、发病机理及防治措施等几方面进行综述,为实际生产提供科学的理论依据。

  5. Hyperlactatemia and metabolic acidosis in critically ill patient%重症患者的高乳酸血症与代谢性酸中毒

    杜微; 刘大为

    2011-01-01

    高乳酸血症和代谢性酸中毒的关系一直是讨论的热点,涉及到休克复苏、机体内环境稳定及营养支持等方面.一方面重症患者组织低灌注时无氧酵解增加带来的乳酸生成增多会加重代谢性酸中毒,而另一方面乳酸在器官水平和细胞水平被利用会引起血乳酸水平降低进而减轻代谢性酸中毒,最终血乳酸水平取决于两者的平衡.%The relationship between hyperlactatemia and metabolic acidosis, which may involve shock resuscitation,homoiostasis, and nutritional support, remains a hot topic. On one hand, increased production of lac-tate due to anaerobic glycolysis during tissue hypoperfusion can aggravate metabolic acidosis; on the other hand,the utilization of lactate at organ and cell levels may lower blood lactate level, and thus alleviate metabolic acidosis.The ultimate blood lactate level depends on the balance of these two action mechanisms.

  6. Diffusion and Perfusion Characteristics of MELAS (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-Like Episode) in Thirteen Patients

    We analyzed the diffusion and perfusion characteristics of acute MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode) lesions in a large series to investigate the controversial changes of the apparent diffusion coefficient (ADC) that were reported in prior studies. We analyzed 44 newly appearing lesions during 28 stroke-like episodes in 13 patients with MELAS. We performed a visual assessment of the MR images including the ADC and perfusion maps, comparison of the ADC between the normal and abnormal areas, comparison of % ADC between the 44 MELAS lesions and the 30 acute ischemic infarcts. In addition, the patterns of evolution on follow-up MR images were analyzed. Decreased, increased, and normal ADCs were noted in 16 (36%), 16 (36%), and 12 (27%) lesions, respectively. The mean % ADC was 102 ± 40.9% in the MELAS and 64 ± 17.8% in the acute vascular infarcts (p < 0.001), while perfusion imaging demonstrated hyper-perfusion in six acute MELAS lesions. On follow-up images, resolution, progression, and tissue loss were noted in 10, 4, and 17 lesions, respectively. The cytotoxic edema gradually evolves following an acute stroke-like episode in patients with MELAS, and this may overlap with hyper-perfusion and vasogenic edema. The edematous swelling may be reversible or it may evolve to encephalomalacia, suggesting irreversible damage

  7. Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure – A case report

    Bagshaw Sean M

    2004-08-01

    Full Text Available Abstract Background Dialysis disequilibrium syndrome (DDS is the clinical phenomenon of acute neurologic symptoms attributed to cerebral edema that occurs during or following intermittent hemodialysis (HD. We describe a case of DDS-induced cerebral edema that resulted in irreversible brain injury and death following acute HD and review the relevant literature of the association of DDS and HD. Case Presentation A 22-year-old male with obstructive uropathy presented to hospital with severe sepsis syndrome secondary to pneumonia. Laboratory investigations included a pH of 6.95, PaCO2 10 mmHg, HCO3 2 mmol/L, serum sodium 132 mmol/L, serum osmolality 330 mosmol/kg, and urea 130 mg/dL (46.7 mmol/L. Diagnostic imaging demonstrated multifocal pneumonia, bilateral hydronephrosis and bladder wall thickening. During HD the patient became progressively obtunded. Repeat laboratory investigations showed pH 7.36, HCO3 19 mmol/L, potassium 1.8 mmol/L, and urea 38.4 mg/dL (13.7 mmol/L (urea-reduction-ratio 71%. Following HD, spontaneous movements were absent with no pupillary or brainstem reflexes. Head CT-scan showed diffuse cerebral edema with effacement of basal cisterns and generalized loss of gray-white differentiation. Brain death was declared. Conclusions Death is a rare consequence of DDS in adults following HD. Several features may have predisposed this patient to DDS including: central nervous system adaptations from chronic kidney disease with efficient serum urea removal and correction of serum hyperosmolality; severe cerebral intracellular acidosis; relative hypercapnea; and post-HD hemodynamic instability with compounded cerebral ischemia.

  8. Does high-dose metformin cause lactic acidosis in type 2 diabetic patients after CABG surgery? A double blind randomized clinical trial

    Rahman Ghafari

    2011-06-01

    Full Text Available Metformin is a dimethyl biguanide oral anti-hyperglycemic agent. Lactic acidosis due to metformin is a fatal metabolic condition that limits its use in patients in poor clinical condition, consequently reducing the number of patients who benefit from this medication. In a double blind randomized clinical trial, we investigated 200 type 2 diabetic patients after coronary artery bypass surgery in the open heart ICU of the Mazandaran Heart Center, and randomly assigned them to equal intervention and control groups. The intervention group received regular insulin infusion along with 2 metformin 500 mg tablets every twelve hours, while the control group received only intravenous insulin with 2 placebo tablets every twelve hours. Lactate level, pH, base excess, blood glucose and serum creatinine were measured over five 12 h periods, with data averaged for each period. The primary outcome in this study was high lactate levels. Comparison between the 2 groups was made by independent Student’s t-test. To compare changes in multiple measures in each group and analysis of group interaction, a repeated measurement ANOVA test was used. There was no significant difference between the 2 groups regarding pH, base excess, or bicarbonate intake (P>0.05. No patient showed lactic acidosis in either group. Lactate levels were 23.0 vs 23.4 in the insulin-metformin and insulin only groups when the study was started, respectively. At the end of the study, those levels were 18.7 vs 18.9, respectively. In addition, the ANOVA repeated measurement test did not show a significant difference in terms of changes in the amount of lactate level between the 2 groups during the five measurement tests of the study period (P>0.05. High-dose metformin (1,000 mg twice daily with insulin does not cause lactic acidosis in type 2 diabetic patients after coronary artery

  9. Evaluating in vitro dose-response effects of Lavandula officinalis essential oil on rumen fermentation characteristics, methane production and ruminal acidosis

    Yadeghari, Shahin; Malecky, Mostafa; Dehghan Banadaky, Mehdi; Navidshad, Bahman

    2015-01-01

    Four in vitro experiments (Exp.) were conducted to evaluate lavender essential oil (LEO) effects at 0 (control), 250 (low dose), 500 (medium dose), 750 and 1000 µL per L (high doses) of incubation medium on rumen gas production kinetics (Exp.1), ruminal digestibility and fermentation (Exp.2), methane production (Exp.3) and rumen acidosis (Exp.4). The asymptote of gas production (A) increased quadratically (p < 0.001), but the lag phase (L) increased (p = 0.003), and gas production rate (µ) de...

  10. Atp6v0a4 knockout mouse is a model of distal renal tubular acidosis with hearing loss, with additional extrarenal phenotype

    Elizabeth E. Norgett; Golder, Zoe J.; Lorente-Cánovas, Beatriz; Ingham, Neil; Steel, Karen P; Karet Frankl, Fiona E.

    2012-01-01

    Autosomal recessive distal renal tubular acidosis (dRTA) is a severe disorder of acid–base homeostasis, often accompanied by sensorineural deafness. We and others have previously shown that mutations in the tissue-restricted a4 and B1 subunits of the H+-ATPase underlie this syndrome. Here, we describe an Atp6v0a4 knockout mouse, which lacks the a4 subunit. Using β-galactosidase as a reporter for the null gene, developmental a4 expression was detected in developing bone, nose, eye, and skin, i...

  11. (Uncommon) Mechanisms of Branchial Ammonia Excretion in the Common Carp (Cyprinus carpio) in Response to Environmentally Induced Metabolic Acidosis.

    Wright, Patricia A; Wood, Chris M; Hiroi, Junya; Wilson, Jonathan M

    2016-01-01

    Freshwater fishes generally increase ammonia excretion in acidic waters. The new model of ammonia transport in freshwater fish involves an association between the Rhesus (Rh) protein Rhcg-b, the Na(+)/H(+) exchanger (NHE), and a suite of other membrane transporters. We tested the hypothesis that Rhcg-b and NHE3 together play a critical role in branchial ammonia excretion in common carp (Cyprinus carpio) chronically exposed to a low-pH environment. Carp were exposed to three sequential environmental treatments-control pH 7.6 water (24 h), pH 4.0 water (72 h), and recovery pH 7.6 water (24 h)-or in a separate series were simply exposed to either control (72 h) or pH 4.0 (72 h) water. Branchial ammonia excretion was increased by ∼2.5-fold in the acid compared with the control period, despite the absence of an increase in the plasma-to-water partial pressure NH3 gradient. Alanine aminotransferase activity was higher in the gills of fish exposed to pH 4 versus control water, suggesting that ammonia may be generated in gill tissue. Gill Rhcg-b and NHE3b messenger RNA levels were significantly elevated in acid-treated relative to control fish, but at the protein level Rhcg-b decreased (30%) and NHE3b increased (2-fold) in response to water of pH 4.0. Using immunofluorescence microscopy, NHE3b and Rhcg-b were found to be colocalized to ionocytes along the interlamellar space of the filament of control fish. After 72 h of acid exposure, Rhcg-b staining almost disappeared from this region, and NHE3b was more prominent along the lamellae. We propose that ammoniagenesis within the gill tissue itself is responsible for the higher rates of branchial ammonia excretion during chronic metabolic acidosis. Unexpectedly, gill Rhcg-b does not appear to be important in gill ammonia transport in low-pH water, but the strong induction of NHE3b suggests that some NH4(+) may be eliminated directly in exchange for Na(+). These findings contrast with previous studies in larval zebrafish

  12. Carnosine inhibits carbonic anhydrase IX-mediated extracellular acidosis and suppresses growth of HeLa tumor xenografts

    Carbonic anhydrase IX (CA IX) is a transmembrane enzyme that is present in many types of solid tumors. Expression of CA IX is driven predominantly by the hypoxia-inducible factor (HIF) pathway and helps to maintain intracellular pH homeostasis under hypoxic conditions, resulting in acidification of the tumor microenvironment. Carnosine (β-alanyl-L-histidine) is an anti-tumorigenic agent that inhibits the proliferation of cancer cells. In this study, we investigated the role of CA IX in carnosine-mediated antitumor activity and whether the underlying mechanism involves transcriptional and translational modulation of HIF-1α and CA IX and/or altered CA IX function. The effect of carnosine was studied using two-dimensional cell monolayers of several cell lines with endogenous CA IX expression as well as Madin Darby canine kidney transfectants, three-dimensional HeLa spheroids, and an in vivo model of HeLa xenografts in nude mice. mRNA and protein expression and protein localization were analyzed by real-time PCR, western blot analysis, and immunofluorescence staining, respectively. Cell viability was measured by a flow cytometric assay. Expression of HIF-1α and CA IX in tumors was assessed by immunohistochemical staining. Real-time measurement of pH was performed using a sensor dish reader. Binding of CA IX to specific antibodies and metabolon partners was investigated by competitive ELISA and proximity ligation assays, respectively. Carnosine increased the expression levels of HIF-1α and HIF targets and increased the extracellular pH, suggesting an inhibitory effect on CA IX-mediated acidosis. Moreover, carnosine significantly inhibited the growth of three-dimensional spheroids and tumor xenografts compared with untreated controls. Competitive ELISA showed that carnosine disrupted binding between CA IX and antibodies specific for its catalytic domain. This finding was supported by reduced formation of the functional metabolon of CA IX and anion exchanger 2 in the

  13. 儿童远端肾小管酸中毒1例%1 Case of Children With Distal Renal Tubular Acidosis

    王瑞彬

    2015-01-01

    在儿科临床工作中,如果小儿有烦渴,多饮,多尿,腹泻,乏力,低钾血症,不明原因的代谢性酸中毒,生长发育落后,佝偻病,要考虑到本病,进一步检查血离子,血气,肾功能,尿常规,双肾超声,腕骨 X 线片。注意酸碱度,有无高氯性酸中毒,电解质紊乱,活动性佝偻病,肾结石,肾钙化。%In pediatric clinical work if the child has thirst, polydipsia, polyuria, diarrhea, fatigue, hypokalemia, metabolic acidosis, unexplained, growth retardation, rickets, taking into account the disease, further examination of blood ions, blood gas, kidney function, urine routine, renal ultrasound, Carpale x-ray. Note that the pH is hyperchloremic acidosis, electrolyte disorder, activity of rickets, kidney stones, renal calcification.

  14. The Pathogenesis and Prevention of Ruminal Acidosis in Cattle%牛瘤胃酸中毒发病机制与防治的研究进展

    陈渊; 朱家增; 邓立新; 李小波; 贺丛; 贺秀媛

    2011-01-01

    With the development of intensive cultivation on cattle, the high-concentrated feed has been used more and more widely. It has improved the bovine performance trait and caused some nutrition metabolic diseases, especially ruminal acidosis's occurrence, which has resulted in enormously economic losses. The pathogenesis and prevention of ruminal acidosis are discussed systematically in this article in order to provide theoretical instruction for preventing the occurrence of this disease.%随着牛集约化养殖的发展,高精饲料的使用越来越广泛,这在不断提高牛生产性能的同时也引起了一些营养代谢病,特别是瘤胃酸中毒的发生,给养殖业造成了巨大的经济损失.作者就牛瘤胃酸中毒的发病机制与防治进行了较为系统地论述,以期为临床生产中更有效地预防和控制该病的发生和流行提供一定的理论参考.

  15. Deficiency of the iron-sulfur clusters of mitochondrial reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase (complex I) in an infant with congenital lactic acidosis.

    Moreadith, R W; Batshaw, M L; Ohnishi, T; Kerr, D; Knox, B; Jackson, D; Hruban, R; Olson, J; Reynafarje, B; Lehninger, A L

    1984-09-01

    We report the case of an infant with hypoglycemia, progressive lactic acidosis, an increased serum lactate/pyruvate ratio, and elevated plasma alanine, who had a moderate to profound decrease in the ability of mitochondria from four organs to oxidize pyruvate, malate plus glutamate, citrate, and other NAD+-linked respiratory substrates. The capacity to oxidize the flavin adenine dinucleotide-linked substrate, succinate, was normal. The most pronounced deficiency was in skeletal muscle, the least in kidney mitochondria. Enzymatic assays on isolated mitochondria ruled out defects in complexes II, III, and IV of the respiratory chain. Further studies showed that the defect was localized in the inner membrane mitochondrial NADH-ubiquinone oxidoreductase (complex I). When ferricyanide was used as an artificial electron acceptor, complex I activity was normal, indicating that electrons from NADH could reduce the flavin mononucleotide cofactor. However, electron paramagnetic resonance spectroscopy performed on liver submitochondrial particles showed an almost total loss of the iron-sulfur clusters characteristic of complex I, whereas normal signals were noted for other mitochondrial iron-sulfur clusters. This infant is presented as the first reported case of congenital lactic acidosis caused by a deficiency of the iron-sulfur clusters of complex I of the mitochondrial electron transport chain. PMID:6432847

  16. [Gastric emptying and metabolic acidosis. II. Study, in an experimental model in rats, of gastric retention of a sodium bicarbonate solution].

    Belangero, V M; Collares, E F

    1992-01-01

    The gastric emptying of a 0.25 M sodium bicarbonate solution was studied in rats with metabolic acidosis induced by a previous (6 hours) orogastric infusion of a 0.5 M ammonium chloride solution. Two control groups were used: one previously infused with 0.5 M sodium chloride and the other with water, in the same volume that further solutions. Every animal was fed with 2 ml/100 g of its weight of these solutions. The test meal (bicarbonate solution) was utilized containing 6 mg% red fenol as a marker. The gastric retentions were determined 6 hours after those first meals at 5, 10, 20 and 30 minutes. The results demonstrated that the gastric retentions of the bicarbonate solution were significantly lower in the acidotic group than that one of water group (at 20 minutes) and that one of the sodium chloride (at 10, 20 and 30 minutes). The data here presented suggest that metabolic acidosis accelerates the gastric emptying of a sodium bicarbonate solution. PMID:1339142

  17. Renal Tubular Acidosis

    ... is normal, but too much acid—acidosis—can disturb many bodily functions. Healthy kidneys help maintain acid- ... disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and ...

  18. Relationship of hyperlactatemia and metabolic acidosis%高乳酸血症与代谢性酸中毒的相互关系

    杜微; 刘大为; 石岩; 隆云; 芮曦; 王小亭

    2011-01-01

    目的 观察重症患者的高乳酸血症与代谢性酸中毒的相关性,以提供更为准确的反映组织灌注的指标.方法 回顾了2009年8月至2010年4月,9个月间所有重症医学科(ICU)患者的血气分析结果.入选标准为患者同时抽取的一份动脉血标本同时送检血气分析、血清电解质、血清白蛋白检查,其中血气分析结果中乳酸升高,满足高乳酸血症标准(Lac≥2 mmol/L)的结果.结果 在这一乳酸升高(Lac≥2)的人群中用传统方法判断代酸,代酸发生率33.9%,用Stewart's方法判断代酸,代酸发生率为56.0%.但该组人群血清pH值不具有典型酸血症的特点(7.42±0.07),存活组中乳酸占代酸的百分比为(33.6±17.9)%,死亡组中乳酸占代酸的百分比为(42.1±18.5)%,P=0.008;存活组中SIG占代酸百分比为(28.6±23.5)%,死亡组中SIG占代酸的百分比(44.9±23.0)%,P=0.000.结论 在ICU乳酸升高的人群中,乳酸并不是引起代酸的主要成分,乳酸和SIG共同组成代酸的主要组分,但乳酸占代酸的百分比和SIG占代酸的百分比升高可能提示预后不佳,这两个指标也许能为临床提供更准确的反映组织灌注的信息.%Objective To investigate the acid-base abnormalities of the patients with hyperlactatemia and explore the relationship of hyperlactatemia and metabolic acidosis so as to seek a more precise index of reflecting organ perfusion. Methods From August 2009 to April 2010, all consecutive patients admitted into intensive care unit received an analysis of blood gas. Those individuals with arterial lactate ≥2 mmol/L were selected. Results In the group of hyperlactatemic patients, the occurrence of metabolic acidosis as judged by the traditional method was less than that by the Stewart's method (33.9% vs 56. 0% ). No typical acidemia was found. And all components of metabolic acidosis were calculated. Lactate and SIG (strong ion gap ) contributed a certain percentage to metabolic acidosis in the

  19. Peripartal changes in reticuloruminal pH and temperature in dairy cows differing in the susceptibility to subacute rumen acidosis.

    Humer, E; Ghareeb, K; Harder, H; Mickdam, E; Khol-Parisini, A; Zebeli, Q

    2015-12-01

    The present study aimed to investigate changes in the reticuloruminal pH and temperature dynamics in periparturient dairy cows. Reticuloruminal pH and temperature measurements were conducted from 7 d before until 8 d after parturition using indwelling sensors. Nine Simmental and 4 Brown Swiss dairy cows were fed a close-up total mixed ration (52.5% neutral detergent fiber, 5.68MJ of net energy for lactation per kg of dry matter) with additional 1kg/cow per d concentrate mixture (29.5% neutral detergent fiber and 6.25MJ of net energy for lactation per kg of dry matter), starting from 2 wk before the estimated calving date. Postpartum, all cows had free access to the same close-up diet and were gradually fed increasing amounts of a concentrate-rich total mixed ration for early-lactation cows (32.7% neutral detergent fiber, 7.22MJ of net energy for lactation per kg of dry matter). Data showed depressed reticuloruminal pH early postpartum, but only in the group of cows defined as subacute ruminal acidosis (SARA) susceptible (n=8), which had a higher duration time of pH cows (n=5; 15±6min/d). Also, compared with SARA-tolerant cows (112±91min/d), the SARA-susceptible group showed longer (1,049±75min/d) duration time of pH cows (6.25±0.05), but no differences were observed in the duration of pH cows produced more milk (30.4±1.2kg/d) compared with Brown Swiss cows (27.9±1.3kg/d). Neither total dry matter intake nor milk yield were different between SARA-susceptible and SARA-tolerant groups. However, SARA-tolerant cows consumed greater amounts of the close-up total mixed ration than their SARA-susceptible counterparts, whereas no difference was observed in the intake of the early-lactating total mixed ration between the groups. Reticuloruminal temperature was not affected by breed or SARA susceptibility. Interestingly, the mean reticuloruminal temperature and the time duration of temperature >39.5°C abruptly dropped from d 2 to 1 before calving by 0.35°C and 430min

  20. Comparison of conventional and diffusion-weighted MRI and proton MR spectroscopy in patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like events

    Abe, K.; Hikita, T.; Sakoda, S. [Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, 565-0871, Osaka (Japan); Yoshimura, H.; Tanaka, H.; Fujita, N. [Department of Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, 565-0871, Osaka (Japan)

    2004-02-01

    The mechanism of neurological disturbances in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is controversial. We studied 12 patients with MELAS using conventional and diffusion weighted MRI (DWI) and MR spectroscopy (MRS), to look at the physiopathology of the stroke-like events. Although conventional MRI showed lesions in all patients, DWI was more sensitive. One patient did not show high signal on DWI 48 h after a from stroke-like episode, but MRS demonstrated a lactate peak in left occipital lobe; 2 weeks after the attack, high signal was demonstrated on the right frontal lobe where MRS had shown a lactate peak. Our findings suggest a possible predictive ability of {sup 1}H-MRS, in showing early MELAS lesions and supports the hypothesis that mitochondrial metabolic dysfunction may precedes abnormalities on DWI. (orig.)

  1. Predisposition to metabolic acidosis induced by topiramate Predisposição a acidose metabólica induzida por topiramato

    MARIA AUGUSTA MONTENEGRO

    2000-12-01

    Full Text Available RATIONALE: Metabolic acidosis induced by topiramate is a well documented but infrequent adverse event. The objective was to demonstrate the lowering of carbon dioxide serum levels, which is usually asymptomatic but may facilitate the occurrence of metabolic acidosis in patients using topiramate. METHODS: We evaluated, prospectively, the carbon dioxide serum levels of 18 patients seen at the epilepsy clinic of our university hospital, before and 3 months after introducing topiramate. RESULTS: Five patients were female and 13 were male, age ranging from 2 to 16 years old (mean=9.3. Carbon dioxide mean serum levels were 25 and 21.2 mmol/L (normal = 22 to 30, before and 3 months after introducing topiramate, respectively. Dose ranged from 2.08 to 11.76 mg/kg/day (mean=6.7mg/kg/day. Adverse events were anorexia, nausea and somnolence. CONCLUSION: We conclude that the lowering of carbon dioxide serum levels induced by topiramate is mostly asymptomatic, but may facilitate the occurrence of metabolic acidosis. Since patients in use of topiramate have refractory epilepsy, they may need epilepsy surgery, and must be carefully monitored for the risk of metabolic acidosis during surgery.INTRODUÇÃO: Acidose metabólica induzida por topiramato é evento adverso pouco frequente, mas bem documentado. Nosso objetivo foi demonstrar a diminuição dos níveis de dióxido de carbono, muitas vezes assintomática, mas que pode predispor ao aparecimento de acidose metabólica. MATERIAL E MÉTODO: Avaliamos prospectivamente os níveis de dióxido de carbono de 18 pacientes acompanhados no ambulatório de epilepsia infantil da UNICAMP, antes e 3 meses após o início do uso de topiramato. RESULTADOS: Foram avaliados 18 pacientes com idade entre 2 e 16 anos (média = 9,3 anos. Cinco pacientes eram do sexo feminino e 13, do sexo masculino. Os níveis médios de dióxido de carbono antes e após o uso de topiramato foram 25 e 21,2 mmol/L (normal = 22 a 30

  2. Activation of P-glycoprotein (Pgp)-mediated drug efflux by extracellular acidosis: in vivo imaging with 68Ga-labelled PET tracer

    In vitro it has been shown that the functional activity of P-glycoprotein (Pgp), an important drug transporter responsible for multidrug resistance, can be strongly increased by extracellular acidosis. Here mitogen-activated protein kinases (MAPK) (p38, ERK1/2) seem to play an important role for signal transduction. However, it is unclear whether these effects are also relevant in vivo. With the newly developed PET tracer Schiff base-based 68Ga-MFL6.MZ the functional Pgp activity was visualized under acidic conditions and during inhibition of MAPKs non-invasively by means of microPET in rat tumours. Tumours were acidified either by inspiratory hypoxia (8% O2) or by injection of lactic acid. Inhibitors of the MAPK were injected intratumourally. With increasing tumour volume the tumour pH changed from 7.0 to 6.7 and simultaneously the Pgp activity increased almost linearly. When the tumour was acidified by direct lactic acid injection the PET tracer uptake was reduced by 20% indicating a higher transport rate out of the cells. Changing the inspiratory O2 fraction to 8% dynamically led to a reduction of extracellular pH and in parallel to a decrease of tracer concentration. While inhibition of the p38 pathway reduced the Pgp transport rate, inhibition of ERK1/2 had practically no impact. An acidic extracellular environment significantly stimulates the Pgp activity. The p38 MAPK pathway plays an important role for Pgp regulation in vivo, whereas ERK1/2 is of minor importance. From these results new strategies for overcoming multidrug resistance (e.g. reducing tumour acidosis, inhibition of p38) may be developed. (orig.)

  3. Activation of P-glycoprotein (Pgp)-mediated drug efflux by extracellular acidosis: in vivo imaging with {sup 68}Ga-labelled PET tracer

    Thews, Oliver; Dillenburg, Wolfgang [University Medicine Mainz, Institute of Physiology and Pathophysiology, Mainz (Germany); Fellner, Marco; Roesch, Frank [University of Mainz, Institute of Nuclear Chemistry, Mainz (Germany); Buchholz, Hans-Georg; Bausbacher, Nicole; Schreckenberger, Mathias [University Medicine Mainz, Department of Nuclear Medicine, Mainz (Germany)

    2010-10-15

    In vitro it has been shown that the functional activity of P-glycoprotein (Pgp), an important drug transporter responsible for multidrug resistance, can be strongly increased by extracellular acidosis. Here mitogen-activated protein kinases (MAPK) (p38, ERK1/2) seem to play an important role for signal transduction. However, it is unclear whether these effects are also relevant in vivo. With the newly developed PET tracer Schiff base-based {sup 68}Ga-MFL6.MZ the functional Pgp activity was visualized under acidic conditions and during inhibition of MAPKs non-invasively by means of microPET in rat tumours. Tumours were acidified either by inspiratory hypoxia (8% O{sub 2}) or by injection of lactic acid. Inhibitors of the MAPK were injected intratumourally. With increasing tumour volume the tumour pH changed from 7.0 to 6.7 and simultaneously the Pgp activity increased almost linearly. When the tumour was acidified by direct lactic acid injection the PET tracer uptake was reduced by 20% indicating a higher transport rate out of the cells. Changing the inspiratory O{sub 2} fraction to 8% dynamically led to a reduction of extracellular pH and in parallel to a decrease of tracer concentration. While inhibition of the p38 pathway reduced the Pgp transport rate, inhibition of ERK1/2 had practically no impact. An acidic extracellular environment significantly stimulates the Pgp activity. The p38 MAPK pathway plays an important role for Pgp regulation in vivo, whereas ERK1/2 is of minor importance. From these results new strategies for overcoming multidrug resistance (e.g. reducing tumour acidosis, inhibition of p38) may be developed. (orig.)

  4. Glucocorticoid activity and metabolism with NaCl-induced low-grade metabolic acidosis and oral alkalization: results of two randomized controlled trials.

    Buehlmeier, Judith; Remer, Thomas; Frings-Meuthen, Petra; Maser-Gluth, Christiane; Heer, Martina

    2016-04-01

    Low-grade metabolic acidosis (LGMA), as induced by high dietary acid load or sodium chloride (NaCl) intake, has been shown to increase bone and protein catabolism. Underlying mechanisms are not fully understood, but from clinical metabolic acidosis interactions of acid-base balance with glucocorticoid (GC) metabolism are known. We aimed to investigate GC activity/metabolism under alkaline supplementation and NaCl-induced LGMA. Eight young, healthy, normal-weight men participated in two crossover designed interventional studies. In Study A, two 10-day high NaCl diet (32 g/d) periods were conducted, one supplemented with 90 mmol KHCO3/day. In Study B, participants received a high and a low NaCl diet (31 vs. 3 g/day), each for 14 days. During low NaCl, the diet was moderately acidified by replacement of a bicarbonate-rich mineral water (consumed during high NaCl) with a non-alkalizing drinking water. In repeatedly collected 24-h urine samples, potentially bioactive-free GCs (urinary-free cortisol + free cortisone) were analyzed, as well as tetrahydrocortisol (THF), 5α-THF, and tetrahydrocortisone (THE). With supplementation of 90 mmol KHCO3, the marker of total adrenal GC secretion (THF + 5α-THF + THE) dropped (p = 0.047) and potentially bioactive-free GCs were reduced (p = 0.003). In Study B, however, GC secretion and potentially bioactive-free GCs did not exhibit the expected fall with NaCl-reduction as net acid excretion was raised by 30 mEq/d. Diet-induced acidification/alkalization affects GC activity and metabolism, which in case of long-term ingestion of habitually acidifying western diets may constitute an independent risk factor for bone degradation and cardiometabolic diseases. PMID:26349936

  5. A novel heterozygous mutation in the ATP6V0A4 gene encoding the V-ATPase a4 subunit in an adult patient with incomplete distal renal tubular acidosis.

    Imai, Eri; Kaneko, Shuzo; Mori, Takayasu; Okado, Tomokazu; Uchida, Shinichi; Tsukamoto, Yusuke

    2016-06-01

    A 40-year-old Japanese man who had a medical history of hypokalemic periodic paralysis 4 months prior was hospitalized to undergo a cholecystectomy. Hypokalemia, nephrocalcinosis and alkaluria suggesting distal renal tubular acidosis (dRTA) were detected, but metabolic acidosis was not evident. An ammonium chloride/furosemide-fludrocortisone/bicarbonate loading test demonstrated a remarkable disability in urinary H(+) excretion. A novel heterozygous mutation in the ATP6V0A4 gene encoding the vacuolar H(+)-ATPase (V-ATPase) a4 subunit p.S544L was detected. Among cases of V-ATPase a4 mutations, this is the first case in which a heterozygous mutation developed to an incomplete or latent form of dRTA. PMID:27274828

  6. L-Arginine Affects Aerobic Capacity and Muscle Metabolism in MELAS (Mitochondrial Encephalomyopathy, Lactic Acidosis and Stroke-Like Episodes Syndrome.

    Lance H Rodan

    Full Text Available To study the effects of L-arginine (L-Arg on total body aerobic capacity and muscle metabolism as assessed by (31Phosphorus Magnetic Resonance Spectroscopy ((31P-MRS in patients with MELAS (Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like episodes syndrome.We performed a case control study in 3 MELAS siblings (m.3243A>G tRNA(leu(UUR in MTTL1 gene with different % blood mutant mtDNA to evaluate total body maximal aerobic capacity (VO(2peak using graded cycle ergometry and muscle metabolism using 31P-MRS. We then ran a clinical trial pilot study in MELAS sibs to assess response of these parameters to single dose and a 6-week steady-state trial of oral L-Arginine.At baseline (no L-Arg, MELAS had lower serum Arg (p = 0.001. On 3(1P-MRS muscle at rest, MELAS subjects had increased phosphocreatine (PCr (p = 0.05, decreased ATP (p = 0.018, and decreased intracellular Mg(2+ (p = 0.0002 when compared to matched controls. With L-arginine therapy, the following trends were noted in MELAS siblings on cycle ergometry: (1 increase in mean % maximum work at anaerobic threshold (AT (2 increase in % maximum heart rate at AT (3 small increase in VO(2peak. On (31P-MRS the following mean trends were noted: (1 A blunted decrease in pH after exercise (less acidosis (2 increase in Pi/PCr ratio (ADP suggesting increased work capacity (3 a faster half time of PCr recovery (marker of mitochondrial activity following 5 minutes of moderate intensity exercise (4 increase in torque.These results suggest an improvement in aerobic capacity and muscle metabolism in MELAS subjects in response to supplementation with L-Arg. Intramyocellular hypomagnesemia is a novel finding that warrants further study.Class III evidence that L-arginine improves aerobic capacity and muscle metabolism in MELAS subjects.ClinicalTrials.gov NCT01603446.

  7. Deficiency of the reduced nicotinamide adenine dinucleotide dehydrogenase component of complex I of mitochondrial electron transport. Fatal infantile lactic acidosis and hypermetabolism with skeletal-cardiac myopathy and encephalopathy.

    Hoppel, C L; Kerr, D S; Dahms, B; Roessmann, U

    1987-01-01

    A mitochondrial defect was investigated in an infant with fatal congenital lactic acidosis (3-14 mM), high lactate-to-pyruvate ratio, hypotonia, and cardiomyopathy. His sister had died with a similar disorder. Resting oxygen consumption was 150% of controls. Pathological findings included increased numbers of skeletal muscle mitochondria (many with proliferated, concentric cristae), cardiomegaly, fatty infiltration of the viscera, and spongy encephalopathy. Mitochondria from liver and muscle ...

  8. Acidosis differentially modulates inactivation in NaV1.2, NaV1.4, and NaV1.5 channels

    PeterRuben

    2012-06-01

    Full Text Available NaV channels play a crucial role in neuronal and muscle excitability. Using whole-cell recordings we studied effects of low extracellular pH on the biophysical properties of NaV1.2, NaV1.4, and NaV1.5, expressed in cultured mammalian cells. Low pH produced different effects on different channel subtypes. Whereas NaV1.4 exhibited very low sensitivity to acidosis, primarily limited to partial block of macroscopic currents, the effects of low pH on gating in NaV1.2 and NaV1.5 were profound. In NaV1.2 low pH reduced apparent valence of steady-state fast inactivation, shifted the τ(V to depolarizing potentials and decreased channels availability during onset to slow and use-dependent inactivation. In contrast, low pH delayed open-state inactivation in NaV1.5, right-shifted the voltage-dependence of window current, and increased channel availability during onset to slow and use-dependent inactivation. These results suggest that protons affect channel availability in an isoform-specific manner. A computer model incorporating these results demonstrates their effects on membrane excitability.

  9. PRIMARY SJOGREN’S SYNDROME AND DISTAL RENAL TUBULAR ACIDOSIS: PRESENTING WITH NEPHROGENIC DIABETES INSI PIDUS SECONDARY TO SEVERE HYPOKALEMIA-A CASE REPORT

    Ksh. Achouba

    2013-02-01

    Full Text Available NTRODUCTION: Sjogren’s syndrome is a slowly progressing autoimmun e disease characterized by lymphocytic infiltration of the exo crine glands, mainly the lacrimal and salivary glands, resulting in their impaired secreto ry function. Simultaneously, systemic involvement and symptoms of cutaneous, respiratory, r enal, hepatic, neurologic, and vascular systems often occur.[ 1 ] This syndrome can present either alone (as primary Sjogren’s syndrome or in the context of an underlying connec tive tissue disease (as secondary Sjogren’s syndrome.[ 2 ] Renal involvement is a well recognized extra glan dular manifestation of primary Sjogren’s syndrome (pSS. Most common manifestations are related to tubular dysfunction, resulting from chronic interstitial nephritis, which can manifest as distal renal tubular acidosis (dRTA, proximal RTA(pRTA, tubular proteinuria, or nephrogenic diabetes insipidus.[ 3 , 4 ] Hypokalemic periodic paralysis, urolithiasis, or osteo malacia are uncommon renal manifestations of pSS.[ 1 ] Here, we present a case of primary Sjogren’s syndr ome predominantly presenting as a renal manifestation in the form of nephrogenic Diabetes Insipidus secondary to severe hypokalemia due to dRTA .

  10. EVALUATION OF MITOCHONDRIAL ENCEPHALOMYOPATHY WITH LACTIC ACIDOSIS AND STROKE-LIKE EPISODES WITH MAGNETIC RESONANCE IMAGING AND PROTON MAGNETIC RESONANCE SPECTROSCOPY

    Feng Feng; Hui You; Jing Gao; Xiao-zhen Li; Chun-ling Meng; Hong-yi Sun; Zheng-yu Jin; Yu-pu Guo

    2006-01-01

    Objective To study the characteristics of spectra on proton magnetic resonance spectroscopy (1H-MRS) and its value in patients with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS).Methods Seven clinically diagnosed patients with MELAS underwent magnetic resonance imaging (MRI) and 1H-MRS examinations.The 1H-MRS techniques,characteristics of the spectra,and its correlation with the laboratory tests were analyzed.Results Cerebral abnormalities were revealed in all 7 patients on conventional MR images,and most abnormal signals were observed in bilateral occipital,parietal,and temporal lobes.We found 4 cases with basal ganglia involvement,2 cases with mild frontal lobe lesions,and 1 case with involvement of lateral cerebral peduncles and thalami.Additionally,1 patient was involved with left insular lobe.Spectra from prominent lesions in brain parenchyma showed lactate doublet peak in 6 patients,3 of whom were also noted lactate peak in ventricular cerebrospinal fluid (CSF).Conclusion 1H-MRS may provide more direct information about the metabolism changes,which aids to affirm the diagnosis,and may replace the conventional invasive method of quantifying lactate in CSF.

  11. SUSCEPTIBILIDADE DE BOVINOS DAS RAÇAS JERSEY E GIR À ACIDOSE LÁCTICA RUMINAL: II - ACIDOSE METABÓLICAE METABOLIZAÇÃO DO LACTATO-L SUSCEPTIBILITY OF JERSEY AND GIR STEERS TO RUMEN LACTIC ACIDOSIS: II - METABOLIC ACIDOSIS AND L-LACTATE METABOLISM

    Celso Akio Maruta

    2002-02-01

    Full Text Available Quatro garrotes Jersey (J (Bos taurus e quatro Gir (G (Bos indicus foram utilizados para comparar a susceptibilidade de zebuínos e taurinos à acidose láctica ruminal (ALR. Neste trabalho, acompanhou-se o grau da acidose metabólica (AM e a metabolização do lactato-L. A ALR foi induzida com a administração de sacarose intraruminal. Amostras de sangue foram colhidas nos seguintes momentos: zero, 14, 16, 18, 20, 22 e 24 horas. Foram determinadas as concentrações de lactato total, de seus isômeros L e D e o perfil hemogasométrico. Nos momentos mais críticos observados (14ªh a 18ªh, a AM foi severa em ambas as raças, porém, ao término do experimento, esta passou a grau moderado nos garrotes G, mantendo-se severa nos J. Os animais J absorveram, do rúmen, maiores quantidades de lactato-D, o qual apresentou correlação negativa com o pH sangüíneo (r = - 0,78. Por outro lado, o lactato-L foi mais absorvido e utilizado nos bovinos G, contribuindo para a restauração parcial do equilíbrio ácido-básico e gerando alterações nas pCO2 e pO2. Os garrotes zebuínos da raça Gir apresentaram menor susceptibilidade à AM que os taurinos da raça Jersey.In order to compare the susceptibility to acute rumen lactic acidosis (RLA, four Jersey (J (Bos taurus and four Gir (G (Bos indicus steers were used to evaluate the degree of metabolic acidosis (MA and the metabolism of L-lactate during the RLA. The RLA was induced by the administration of sucrose into the rumen. Blood samples were collected at following times: zero, 14th,16th, 18th, 20th, 22nd and 24th h. Total lactic acid and its isomers, and blood gas determination were measured. At the most critical moments (14th to 18th h the MA was severe in both breeds, but the MA became moderate in the G steers and remained severe in the J steers at the end of the trial. Higher amounts of D-lactate was absorbed from the rumen to the blood of the J steers; the higher the D-lactate plasma level, the

  12. 10例HIV/AIDS患者HAART后继发高乳酸血症或乳酸酸中毒临床分析%Clinical analysis of hyperlactacidemia/lactic acidosis after receiving HAART in 10 HIV/AIDS patients

    黄维; 黄葵; 蓝珂; 邬剑威; 刘宁; 蒙江明

    2012-01-01

    目的 探讨HIV/AIDS患者高效抗反转录病毒治疗(highly active antiretroviral therapy,HAART)后继发高乳酸血症或乳酸酸中毒的临床表现和治疗方案.方法 回顾性分析10例HIV/AIDS患者HAART后继发高乳酸血症或乳酸酸中毒的临床表现、实验室检测结果和治疗效果等资料.结果 10例在继发高乳酸血症或乳酸酸中毒前均服用过含有核苷类反转录酶抑制剂(nucleoside reverse transcriptase inhibitors,NRTIs)组合的HAART方案,临床症状以乏力、恶心、腹胀、肌肉酸痛和呼吸困难多见,血乳酸浓度为5.14~10.74mmol/L,其中8例出现高乳酸血症或乳酸酸中毒的相关症状,2例未出现.6例经换药或停药处理后好转,4例死亡.结论 引起高乳酸血症或乳酸酸中毒的主要原因是使用含有NRTIs的组合方案,其中司他夫定最为常见,其次为齐多夫定.治疗时应立刻换药或停药.%Objective To investigate the clinical manifestations and treatment of HIV/AIDS patients who are affected with hy-perlactacidemia/lactic acidosis after receiving highly active antiretroviral therapy (HAART). Methods The clinical manifestations, laboratory findings and treatment efficacy were retrospectively analyzed in 10 HIV/AIDS patients who were affected with hyperlacta-cidemia/lactic acidosis after receiving HAART. Results All the 10 HIV/AIDS patients had received HAART regimens including nu-cleoside reverse transcriptase inhibitors (NRTIs) before being affected with hyperlactacidemia/lactic acidosis. The common clinical symptoms were fatigue, nausea, abdominal distension, muscle aches and difficulty of breathing. The blood lactic acid level of the 10 patients was 5.14-10.74 mmol/L, symptoms related to hyperlactacidemia/lactic acidosis occurring in 8 patients. Six patients were improved on cessation or switching to another medication, and 4 died. Conclusions The major cause that leads to hyperlactacidemia/ lactic acidosis is receiving HAART including

  13. Acidose metabólica na infância: por que, quando e como tratá-la? Metabolic acidosis in childhood: why, when and how to treat

    Olberes V. B. Andrade

    2007-05-01

    controvérsia, o único ponto concordante refere-se à abordagem mais precoce da doença de base e dos mecanismos geradores da acidemia metabólica. Outras alternativas terapêuticas são promissoras; entretanto, os efeitos adversos e a falta de trabalhos controlados em pediatria não determinam evidências suficientes que recomendem sua utilização de rotina.OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in

  14. Metabolismo oxidativo dos neutrófilos de ovinos tratados com monensina sódica e experimentalmente submetidos à acidose ruminal Oxidative metabolism of the neutrophils in sheep treated with sodium monensin and experimentally submitted to ruminal acidosis

    José Augusto B. Afonso

    2002-10-01

    Full Text Available A acidose láctica ruminal é causada pela ingestão excessiva de carboidratos de fermentação rápida sem uma prévia adaptação dos mocroorganismos, podendo com isso gerar distúrbios metabólicos graves aos ruminantes. Este trabalho tem por objetivo estudar o metabolismo oxidativo dos neutrófilos em ovinos tratados com a monensina sódica na acidose láctica ruminal induzida experimentalmente. Foram empregados 18 ovinos, machos, mestiços (Ideal x Merino, fistulados no rúmen; dos quais nove receberam 33 mg/kg da dieta do ionóforo ao dia, durante 30 dias, os demais ovinos pertenceram ao grupo controle. A acidose foi induzida fornecendo 15g de sacarose/kg de peso corporal. A avaliação clínica e as amostras de rúmen e sangüíneas foram obtidas antes (momento controle 0h e às 6h, 12h, 24h e 48h pós-indução. Em ambos os grupos os animais apresentaram manifestações clínicas de acidose láctica ruminal 6 horas pós-indução. A partir deste período se observou uma diminuição significativa (pRuminal acidosis is due to excessive ingestion of carbohydrates of rapid fermentation without previous adaptation of the microorganisms, causing severe metabolic disturbances to the animals. The objective of the present study was to assess the neutrophilic oxidative metabolism in sheep treated with sodium monensin in experimentally induced ruminal lactic acidosis. A total of 18 male sheep, half-bred (Ideal x Merino, fistulated in the rumen, were used; nine of them received 33 mg/kg of the ionophore diet per day, for 30 days; the others were controls. The acidosis was induced by supplying 15g of sucrose/kg of body weight. The clinical evaluation and the rumen and blood samples were obtained before (0h and at 6, 12, 24 and 48 hours post-induction. In both groups, all the animals presented clinical manifestations of ruminal lactic acidosis 6 hours after the induction. From this period on, a significant pH decrease (P<0.05 was observed in the

  15. Safety Analysis of Vinegar Enema in Hepatic Encephalopathy Complicated with Metabolic Acidosis%食醋灌肠在肝性脑病合并代谢性酸中毒中的安全性分析

    魏晓广; 郑佳

    2016-01-01

    目的:分析食醋灌肠在肝性脑病合并代谢性酸中毒中的安全性。方法选取我院收治的48例肝性脑病合并代谢性酸中毒患者作为研究对象,随机分为两组,各24例。对照组采用乳果糖治疗,观察组采用食醋灌肠进行治疗。对比观察两组患者治疗效果及不良反应发生情况。结果观察组总有效率为91.67%,明显优于对照组70.83%,差异显著(P<0.05);对照组不良反应发生率为25.0%,观察组未见不良反应,组间比较差异显著(P<0.05)。结论对肝性脑病合并代谢性酸中毒患者实施食醋灌肠的方法进行治疗,临床效果显著,且不良反应发生率低,安全有效,值得推广运用。%Objective To analyze the safety of vinegar enema in hepatic encephalopathy complicated with metabolic acidosis. Methods 48 cases of patients with hepatic encephalopathy and metabolic acidosis were randomly divided into two groups, each of 24 cases. The control group was given lactulose treatment, the observation group was treated with vinegar enema treatment. The treatment effect and adverse reaction of the two groups were compared and observed.ResultsThe total effective rate of the observation group was 91.67%, which was significantly better than that of the control group (70.83%), and the difference was signiifcant (P<0.05); The adverse reaction rate of control group was 25.0%, no adverse reaction was observed in the observation group, and the difference was signiifcant (P<0.05).Conclusion In patients with hepatic encephalopathy complicated with metabolic acidosis implementation vinegar enema method of treatment, significant clinical effect and adverse reactions occurred rate is low, and is safe and effective, worthy of popularization and application.

  16. 缺氧和酸中毒对成骨细胞功能影响研究进展%Recent Advances in Effects of Hypoxia and Acidosis on the Proliferation and Differentiation of Osteoblast

    任原; 王茜; 李琪佳; 王志强

    2015-01-01

    局部pH值和氧分压(pO2)的变化可影响成骨细胞功能。成骨细胞对pH值直接影响极其敏感院酸中毒抑制成骨细胞的矿物沉积。成骨细胞对小范围pH变化反应机制较复杂,涉及对细胞膜离子通道、受体以及细胞内的直接影响。研究表明缺氧严重抑制成骨细胞的生长和分化,促进成骨细胞凋亡。在体内,由于血管灌注的减少和糖酵解代谢的增加,组织缺氧通常伴有酸中毒。血液供应的中断,使成骨细胞pO2减少和pH值降低,而对成骨细胞活动产生负面影响。该文就缺氧和酸中毒对成骨细胞的功能影响及近年研究进展作一综述。%The function of osteoblast is affected by local pH and oxygen tension. Osteoblasts are extremely sensitive to the direct effects of pH: acidosis inhibits mineral deposition by osteoblasts. The mechanisms by which osteoblasts sense small pH changes are complex, involving in channels, receptors in the cell membrane and the direct intracellular effects. Reseach shows that severe hypoxia inhibits osteoblast growth and differention, and promotes the apoptosis of osteoblasts. In vivo, tissue hypoxia usually ac-companied by acidosis due to reduced perfusion and increased glycolytic metabolism. Disruption of the blood supply can engender negative effects on osteoblasts via the direct actions of reduced pO2 and pH on osteoblasts. This article aims to review recent re-search progress which the effects of hypoxia and acidosis on proliferation and differentiation of osteoblast function.

  17. A primary Sjögren's syndrome patient with distal renal tubular acidosis, who presented with symptoms of hypokalemic periodic paralysis: Report of a case study and review of the literature.

    Soy, Mehmet; Pamuk, Omer Nuri; Gerenli, Murat; Celik, Yahya

    2005-11-01

    Although renal tubular acidosis (RTA), secondary to autoimmune interstitial nephritis, develops in a large proportion of patients with Sjögren's syndrome (SS), most of the subjects are asymptomatic. Here, we shall present a 39-year-old female patient who came to us with hypokalemic periodic paralysis (HPP), and who was later diagnosed with distal RTA. The patient, who had xerostomia and xerophthalmia for a long period of time, was diagnosed with primary SS from serologic and histologic findings. The patient recovered by being prescribed potassium replacement therapy. Although renal biopsy was not performed, corticosteroids were administered because HPP indicated severe interstitial nephritis. HPP did not reoccur during a 2-year follow-up period. We also review cases with SS-related distal RTA and HPP. PMID:15690142

  18. Controvérsias acerca da acidose hipercápnica na síndrome do desconforto respiratório agudo Controversies involving hypercapnic acidosis in acute respiratory distress syndrome

    Liliane Nardelli

    2009-12-01

    distress syndrome is the ventilatory support. However, mechanical ventilation can worsen lung injury. In this context, a protective ventilatory strategy with low tidal volume has been proposed. The use of low tidal volume reduced the mortality rate of acute respiratory distress syndrome patients, but result in hypercapnic acidosis. The current article presents a review of literature on the effects of permissive hypercapnia in acute respiratory distress syndrome. To that end, we carried out a systematic review of scientific literature based on established criteria for documental analysis including clinical and experimental articles, using as data bases MedLine, LILACS, SciELO, PubMed, Cochrane. Hypercapnic acidosis has been considered by some authors as a modulator of the inflammatory process of acute respiratory distress syndrome. However, clinical and experimental studies on the effects of hypercapnic acidosis have shown controversial results. Therefore it is important to better elucidate the role of hypercapnic acidosis in acute respiratory distress syndrome.

  19. 急慢性代谢性酸中毒对红细胞内外pH值的影响%Effects of acute or chronic metabolic acidosis on intracellular pH of rat erythrocytes

    王贤东; 袁媛; 王冬; 赫曼; 刘若彬

    2009-01-01

    Objecfive To investigate the effects of acute or chronic metabolic acidosis on intracellular pH of rat erythrocytes.Methods Acute metabolic acidosis in Wistar rats was induced by infusion of 4mmol/kg HCl for 4 hours;Chronic metabolic acidosis rats was induced by addition of 0.28 mol/L NH4CI to drinking water for 7 days.The control groups were given 0.9%NaCl in the same time.At 0,2and 4h after HCl infusion in acute group,and at 0,1,3,5 and 7 days after NH4Cl administration in chronic group,0.5ml blood samples were taken.All blood samples were placed in test tubes with heparin anticoagulant solution.Blood gas was analyzed.Carbonic anhydrase activity in rat erythrocytes was assayed by following the hydration of CO2 according to the method described by Wilbur and Anderson.And after stained by BCECF-AM fluorescent probe,the changes of intracellular pH were observed,and the ability of NHE1 were measured by detected recovery rate of intraeellular pH by laser scanning confocal microscopy.Results Acute metabolic acidosis inhibits NHE1 activity(P<0.05)and no changes in pHi and carbonic anhydrase activity of rat erythrocyte were seen.On the contrast.it was showed increasing activity of NHE 1 and carbonic anhydrase with decreasing phi in rats erythrocytesin chronic metabolic acidosis over five days(P<0.05).Conclusion These results suggest that an acute acid load does not alter pHi while chronic metabolic acidosis does reduce pHi of rat crythrocyte.%目的 观察急性或慢性代谢性酸中毒对大鼠红细胞内pH(pHi)、碳酸酐酶(carbonic and hydrase,CA)和钠-氢交换蛋白Ⅰ(Na+-H+ exchanger Ⅰ,NHE Ⅰ)活性的影响.方法 将24只Wistar大鼠随机分为急性组和慢性组.急性组分为:急性对照组(A组)和急性代谢性酸中毒组(B组);慢性组分为:慢性对照组(C组)和慢性代谢性酸中毒组(D组)(n=6).急性组采用静脉输注4 mmol·kg1-·h-1 HCl 4 h,慢性组采用0.28 mol/L NH4Cl喂饲7 d,构建大鼠急性和慢性代谢性酸

  20. Double effects of propofol on cardiac function of rats with metabolic acidosis%丙泊酚对代谢性酸中毒心脏功能的双重影响

    徐彦秋; 马兰; 曹焕军; 李力兵

    2012-01-01

    Objective To study the effect of propofol on cardiac function of rats with metabolic acidosis. Methods A metabolic acidosis model of in vitro rat heart was established with modified Langendoff apparatus. Twenty-four SD rats were randomly divided into control group, 25mmol/L propofol group(PL group) and 50mmol/L propofol group(PH group), 8 in each group. Metabolic acidosis was induced by perfusion with K-H solution(pH=7.4) for 40min, then with acidic K-H solution(pH=6-5) for 20 min and K-H solution(pH =7.4) for 30min. Propofol was added into the K-H solution 25min after stable perfusion. Heart rate (HR), left ventricular develop pressure(LVDP), left ventricular pressure ± dP/dtmax, perfusion circuit pressure and myocardial water content(MWC) were recorded before acidosis and 1, 5, 10, 20 and 30min after reperfusion. Results The HR, LVDP and left ventricular pressure ± dP/ dtmax were lower in PL and PH groups than in control group and significantly lower in PH group than in control group during the lOmin reperfusion(Pacidosis. The effect of 25mmol/L propofol is better than 50mmol/L propofol on recovery of cardiac function and improvement of cardiac muscle reperfusion and edema.%目的 探讨丙泊酚对代谢性酸中毒心脏功能的影响.方法 应用改良Langendorff装置,制备离体心脏代谢性酸中毒模型.将24只SD大鼠随机分为对照组(C组)、丙泊酚25μmol/L组(PL组)和丙泊酚50μmol/L组(PH组),每组8只.C组用pH=7.4的K-H液平衡灌注40min,然后用pH=6.5的K-H液酸化20min

  1. 重度乳酸性酸中毒并心脏骤停一例诊治分析%Characteristics of Severe Lactic Acidosis Complicated with Cardiac Arrest and the Related Literature Review

    刘红升; 苏琴; 曹阳; 姚咏明; 赵晓东

    2015-01-01

    目的:探讨重度乳酸性酸中毒(lactic acidosis, LA)的临床特征及治疗方法,以提高救治成功率。方法对我院收治的重度 LA 并心脏骤停1例的临床资料进行回顾性分析。结果本例因腹泻3 d、剧烈上腹痛1 h 以急性心肌梗死(心梗)急诊入院。有糖尿病史,长期口服二甲双胍,未定期检测血糖。入院后出现腰背剧痛,经相关检查排除急性心梗、主动脉夹层,查血乳酸脱氢酶277.0 U/ L,乳酸17 mmol/ L,血气分析示代谢性酸中毒,入院诊断为糖尿病、重度 LA。入院1 h 后发生心脏骤停,经积极复苏抢救,病情逐步缓解,1个月后临床治愈出院。结论重度 LA 可以剧烈胸腹部疼痛为主要表现,甚至发生心脏骤停,及时诊断及正确评估病情对预后极为重要,积极液体复苏及有效呼吸支持、早期血液透析是救治成功的保证。%Objective To investigate the clinical features and the treatment of severe lactic acidosis (LA) and to im-prove the success rate. Methods We carried out a retrospective analysis of clinical data of a patient suffering from cardiac ar-rest with severe LA and a review of the related literature review was made. Results The patient suffered from diarrhea for 3 d, severe abdominal pain for 1 h and was admitted into our hospital for acute myocardial infarction. The patient had a history of diabetes and diabetic nephropathy and took a long-term oral metformin without testing blood sugar regularly. Relevant exam-inations ruled out acute myocardial infarction and aortic dissection, and then, and the blood lactate dehydrogenase was 277. 0 U/ L, and lactic acid was 17 mmol/ L and blood gas analysis revealed metabolic acidosis. Above all, the patient was di-agnosed with diabetes and severe LA. The patient suffered sudden cardiac arrest one hour after admission, then the condition was alleviated gradually after active recovery treatment, and in the end the patient was clinically cured and was

  2. The measurement of urine pH to predict the amount of buffer used in the treatment of acute rumen lactic acidosis in cattle Mensuração do pH de urina para predizer a quantidade de tampão empregado para o tratamento de acidose láctica ruminal aguda em bovinos

    Celso Akio Maruta

    2008-06-01

    Full Text Available The purpose of the present study was to establish a practical, fast, precise and low-cost procedure to estimate the degree of metabolic acidosis in cattle with acute rumen lactic acidosis for further treatment. The rumen acidosis was induced experimentally in 40 crossbreed rumen-cannulated 1.5-year-old steers. The induction caused the development of the most characteristic clinical signs of acute rumen lactic acidosis, severe rumen acidosis and a moderate metabolic acidosis, which was evidenced by low blood pH, and blood bicarbonate concentration and base excess (BE. A highly positive correlation (r=0.80 between urinary pH and BE concentration, and between urinary pH and blood pH (r=0.75 was observed. The BE concentration estimated by urinary pH was similar to that determined by venous blood gas analysis (P>0.99. Furthermore, the results presented by the predictive formula were very significant. In conclusion, urinary pH is a good tool to predict the quantity of buffers needed to treat metabolic acidosis in cattle with acute rumen lactic acidosis.O presente estudo teve como objetivo desenvolver um procedimento de baixo custo, preciso, rápido e prático para estimar o grau de acidose metabólica, para tratar bovinos com quadros de acidose láctica ruminal. A acidose ruminal foi induzida experimentalmente em 40 novilhos mestiços de 1,5 anos de idade, implantados com cânula ruminal. Essa indução causou o surgimento de sinais clínicos muito típicos da enfermidade aguda, com o aparecimento de pronunciada acidose ruminal e acidose metabólica de grau moderado, caracterizado por baixo pH sangüíneo e diminutos teores de bicarbonato e excesso de base (BE no sangue. Verificou-se uma alta correlação positiva (r = 0,80 entre o pH urinário e o BE e entre o pH urinário e o pH sangüíneo (r = 0,75. A concentração de BE estimado pelo pH urinário foi similar à obtida pela análise do hemogasômetro (P = 0,99. Além disso, os resultados

  3. 二甲双胍引起乳酸性酸中毒的风险与糖尿病患者的肾功能%Risk of lactic acidosis caused by metformin and renal function of diabetic patients

    张林; 胡茂清

    2010-01-01

    二甲双胍是治疗2型糖尿病的一线药物,其有导致乳酸性酸中毒的风险.肾小球滤过率是评估糖尿病患者是否应用二甲双胍的标准之一.然而越来越多的证据表明二甲双胍与糖尿病患者乳酸性酸中毒的发生似乎无明显的相关性,目前尚无高质量的临床证据来指导二甲双胍在糖尿病合并肾功能不全患者中的应用,但临床上尚不能仅仅依据肾小球滤过率水平来判断是否使用二甲双胍,使用之前应评估患者使用前后的效益-风险比.在糖尿病合并肾功能不全人群中应用二甲双胍的标准尚需更多的循证医学证据.%Mefformin is in the first line of treating diabetes, though it might increase the risk of lactic acidosis. Glomerular filtration rate is one of the indexs that determines whether mefformin should be used or not. However,more and more clinical studies show that the relationship between mefformin and lactic acidosis is not clear. There are few high quality clinical evidences to guide the use of mefformin in diabetic subjects with chronic kidney disease. But in clinical practice,whether mefformin is used in these diabetic subjects or not does not just depend on glomerular filtration rate, efficiency-risk ratio should be evaluated at first. The standard of using mefformin in diabetic subjects with chronic kidney disease should be provided by more evi-dences.

  4. Premature Children Late-onset Metabolic Acidosis Analysis of 89 Cases%早产儿晚发性代谢性酸中毒89例分析

    郝宝生; 王艳

    2013-01-01

    Objective To study the incidence of late metabolic acidosis among premature infant. Method: Summary of clinical data of 89 cases of LMA patients from Mar 2005 to June 2008 and analysis of the gestational age, birth weight and feeding, timing of occurrence, blood gas analysis and treatment result. Results ① The gestational age 2.5kg accounting for 14.49%; ② breastfeeding 8 cases (11.5%), occurred in 2 ~ 3w 36 cases (52.17%); ③blood gas analysis showed that lower pH, BE negative increase, PCO2 normal or slightly lower, PO2 normal; ④short SB oral treatment I excel ent outcomes. Conclusion:The incidence of late metabolic acidosis among premature infant is higher. The smal er the gestational age at birth, lower birth weight, the higher incidence of LMA;Artificial feeding showed higher incidence; clinical symptoms is not typical, Timely blood gas analysis would be helpful for early diagnosis. Treatment is simple and with early intervention, prognosis is good.%目的了解早产儿晚发性代谢性酸中毒的情况。方法总结2005年3月~2008年6月共89例LMA患儿的资料,对LMA发生的出生胎龄、出生体重、喂养方式、发生时间及血气分析及治疗结果进行分析。结果①出生胎龄2.5kg占14.49%;②母乳喂养8例(11.5%),发生时间在2~3w36例(52.17%);③血气分析结果表明,pH值降低,BE负值增大,PCO2正常或稍低,PO2正常;④治疗予短期SB口服,疗效良好。结论早产儿晚发性代谢性酸中毒发生率较高。出生胎龄越小,出生体重越低,发生率越高;人工喂养发生率高;临床表现不典型,及时进行血气分析以早期明确诊断;本病治疗简单,早期积极干预,预后良好。

  5. 60 cases obese children Ⅱ diabetes TongZheng acidosis clinical analysis%肥胖儿童2型糖尿病酮症酸中毒60例的临床分析

    谷玉龙

    2012-01-01

    objective To improve the clinical pediatricians to start to in obesity symptoms of child obesity type 2 diabetes TongZheng acidosis (DKA) and tall lipemia (HL) understanding. Methods Retrospective analysis in January 2001 to December 2011 60 cases were 0 -6 years of age FeiPanXing type 2 diabetes TongZheng acidosis and hyperlipidemia obese children clinical data. Results The 60 cases obese children, boys than girls, a ratio of 1.8:1.2, namely, girls for 24 cases, the boy for 36 cases, age: 4.21 + /-1.56 years;before the disease were no diabetes history and related symptoms, there were no history of hyperlipemia;before the disease were no boozing, overeating and cholelith disease history;are obese size, body mass index 29.41 + /-2.07;reached DKA diagnosis standard. Conclusions children with type 2 diabetes FeiPanXing to obesity clinic of, should be routine check blood fat; adjust diet and exercise can relieve the obese child's 2 diabetes symptoms.%目的:提高临床医师对以肥胖为首发症状的儿童2型糖尿病酮症酸中毒(DKA)并高脂血症(HL)的认识.方法:回顾性分析我院2001年1月至2011年12月收治的60例0~6岁2型糖尿病DKA并高脂血症肥胖儿童的临床资料.结果:60例肥胖儿童年龄(4.21±1.56)岁,其中女童24例,男童36例,男:女为1.8∶1.2;病前均无糖尿病史及相关症状,均无高脂血症史;病前均无暴饮、暴食和胆石症史;均为肥胖体型,体质指数(29.41±2.07);均达到DKA诊断标准.结论:儿童肥胖型2型糖尿以肥胖就诊的,应常规查血脂;调整饮食和运动可以缓解肥胖儿童的糖尿病症状.

  6. Metabolic acidosis and its effect on calcium and phosphorus metabolism in maintenance hemodialysis patients%维持性血液透析患者代谢性酸中毒对钙磷代谢的影响

    黎晓磊; 邵咏红; 孔耀中

    2012-01-01

    分析比较维持性血液透析(MHD)患者的代谢性酸中毒对钙磷代谢的影响.方法:选择MHD患者120例,测定透析前碳酸氢根(HCO3-)、血尿素氮(BUN)、肌酐(CR)、钙(Ca)、磷(P)、碱性磷酸酶(ALP)、甲状旁腺激素(iPTH)及透析后BUN和CR,计算钙磷乘积(Ca×P)、Kt/V.根据HCO3-分为3组:A组(HCO3-< 20 mmol/L)、B组(HCO3-为20~24 mmol/L)和C组(HCO3-≥24 mmol/L),比较3组酸中毒对钙磷紊乱的影响.结果:B、C组的P、ALP及iPTH均低于A组(P<0.05),C组的P、Ca×P低于A、B组(P<0.05).HCO3-浓度与P、iPTH、ALP及Ca×P呈负相关(P<0.05).结论:对于MHD患者,HCO3-< 20 mmol/L较HCO3-≥20 mmol/L者易合并高磷血症、低钙血症,可刺激iPTH的合成,最终导致肾性骨病及转移性钙化.%Objective To evaluate the effect of metabolic acidosis on calcium and phosphorus metabolism in maintenance hemodialysis(MHD) patients. Methods 120 MHD patients were enrolled in the present study. Predialysis laboratory detections including HC03", BUN creatinine, calcium, phosphorus, alkaline phosphatase (ALP) and intact parathyroid hormone (iPTH) were performed. Calcium-phosphate product and Kt/V were also determined. The patients were randomized into 3 groups: group A(HCO3- < 20 mmol/L), group B (20 mmol/L≤HCO-3< 24 mmol/L), group C (HCO3-≥ 24 mmol/L). Results The concentrations of phosphorus, ALP and iPTH were decreased in groups B and C in comparation to that in group A (P < 0.05). Compared with group A and B, the phosphorus and calcium-phosphate product level in group C were decreased (P < 0.05). The serum HCO3" level correlated negatively with the serum phosphorus, iPTH, ALP and calcium-phosphate product (P < 0.05). Conclusions Correction of metabolic acidosis (bicarbonate level -S 20 mmol/L) may prevent the deleterious long-term consequences such as CKD-MBD, but further investigation of the long-term effect still needs to be done.

  7. Clinical Significance of Early Correction of Metabolic Acidosis in Patients with Chronic Kidney Disease%早期纠正慢性肾脏病患者代谢性酸中毒的临床意义

    田秋菊

    2015-01-01

    目的:探讨早期纠正慢性肾脏病患者代谢性酸中毒的临床意义。方法将该院于2014年1月-2014年12月收治的符合慢性肾脏病2、3期且TCO2跃22 mmol/L的80例患者随机分为治疗组和对照组。对照组给予常规治疗,治疗组在对照组的基础上给予NaHCO3片1.0~1.5 g/d,分次口服,同时给予产碱的水果蔬菜。主要观察指标为血尿素氮、血肌酐、血pH值、血TCO2、电解质及血压。结果治疗组血pH值、血TCO2有所提高,血尿素氮、血肌酐略有升高,但差异无统计学意义。对照组血pH值、血TCO2进一步下降,血尿素氮、血肌酐明显升高,差异有统计学意义。两组治疗前后电解质、血压均无明显变化。结论NaHCO3片和产碱的水果蔬菜饮食疗法能纠正血浆TCO2跃22 mmol/L慢性肾脏病患者的代谢性酸中毒,并延缓肾功能进展,具有肾脏保护作用,且不引起电解质紊乱及血压升高。%Objective To study the clinical effect of early correction of metabolic acidosis in patients with chronic kidney disease(CKD). Methods A total of 80 patients from 2014 January to 2014 December in our hospital with CKD at stages II-III and TCO2>22mmol/L were enrolled in the study. The patients were randomly divided into treatment group and control group. The con-trol group was given conventional treatment. The treatment group was given NaHCO3 1.0~1.5 g/d and alkali production of fruits and vegetables based on conventional treatment. The main parameters including serum urea nitrogen, serum creatinine, PH value, TCO2, electrolyte and blood pressure were measured. Results The PH, TCO2, blood urea nitrogen, and serum creatinine slightly im-proved in treatment group, but there was no significant difference. The pH value and TCO2 fell further and serum urea nitrogen and serum creatinine significantly improved. There was significant difference after treatment. There were no obvious changes in electrolytes and

  8. The changes of hematology and biochemical parameters in the beef cattle with subacute ruminal acidosis%肉牛亚急性瘤胃酸中毒血液学及生化指标变化分析

    赵晨旭; 王晓旭; 孙国权; 张良; 陈灰; 杨文涛; 刘兆喜; 王哲; 刘国文

    2013-01-01

    为了解肉牛发生亚急性瘤胃酸中毒时血液学和相应生化指标的变化,对瘤胃液pH在5.2~5.5、5.6~5.8和5.9~6.8之间的24头肉牛进行了血液学及相应生化指标的分析.结果表明:随着pH值的降低,血液中红细胞(RBC)数量、血红蛋白(Hb)浓度、红细胞压积(PCV)均显著增加;白细胞(WBC)总数上升,白细胞分类(WBC-DC)也有相应的变化,嗜酸性粒细胞和淋巴细胞呈下降趋势,中性杆状核粒细胞和中性分叶核粒细胞呈上升趋势,单核细胞略微升高;血气指标pO2显著增加,pCO2、HCO3-浓度显著减少;生化指标Ca2+、Cl-显著减少,Na+和尿素氮显著增加,K+差异不显著.肉牛发生轻度和中度亚急性瘤胃酸中毒时,pCO2以及HCO3-含量显著降低,表明机体碱储备不足,缓冲能力下降,存在代偿性酸中毒;同时根据水合状态和血象指标,表明亚急性瘤胃酸中毒病牛存在轻度脱水和炎性反应.%The aim of this study was to investigate the changes of hematology and biochemical parameters in beef cattle with subacute ruminal acidosis. We analyzed the hematology and biochemical parameters of 24 beef cattle with ruminal pH value in 5. 2-5. 5,5. 6-5. 8 and 5. 9-6. 8. The results showed that red blood cell (RBC), haemoglobin (Hb), packed cell volume(PCV)significant-ly increased with the reducing pH value, the number of white blood celKWBOwas increased. The leukocyte differential count was changed in the different degree, the proportion of eosinophilic leukocyte and lymphocyte was decreased,neutrophilic stab and segmented granulocyte was increased, mononuclear leucocyte was increased slightly. The pO2 was significantly increased. The pCO2 and HCO3- were significantly decreased. The levels of Ca2+ and Cl- were significantly decreased, the levels of Na+ and urea nitrogen were significantly increased,and there was no significant difference in the levels of K+. The decreased pCO2 and HCO3- in the slight and moderate

  9. Adaptation to High Grain Diets Proceeds Through Minimal Immune System Stimulation and Differences in Extracellular Matrix Protein Expression in A Model of Subacute Ruminal Acidosis in Non-lactating Dairy Cows

    L. Dionissopoulos

    2012-01-01

    Full Text Available Problem statement: Subacute Ruminal Acidosis (SARA is a metabolic disorder affecting approximately 20% of all dairy cattle in North America. Although the presence of SARA has been described for some time, the etiology of the disorder remains uncertain. For example, many animals diagnosed with SARA seem to remodel and adapt their epithelium to accommodate the stresses imposed by SARA, but not before exacting a significant health and economic toll. Specifically, a search is on in which a desire to identify the system and associated pathways that are causative agents in the progression and development of SARA is evident. We hypothesize that adaptation to SARA is facilitated by the immune system. Approach: In order to answer of this question, 4 mature, non-lactating dairy cattle were transitioned from a High Fiber (HF; 0% grain diet to High Grain (HG; 65% grain diet. Having fed the HG diet for three weeks, the cattle were then transitioned back to the HF diet for an additional three weeks to facilitate adaptation. SARA was diagnosed by pH data only during the first week and not during the remaining weeks, indicating that adaptation to the HG diet took place within one week. Results: In this study, significant (pConclusion: These results indicate that the immune system is involved in the adaptation of the rumen epithelium to a HG diet, but to a lesser extent than was previously thought. This is the first time an attempt has been made to link the immune system and wound healing in the adaptation of the bovine rumen to a HG diet."""

  10. Effect of acarbose addition on acute and subacute rumen acidosis in an in vitro fermentation study%酸中毒条件下添加阿卡波糖对瘤胃微生物发酵的影响

    毛胜勇; 何文波; 朱伟云

    2012-01-01

    The effect of acarbose addition on ruminant fermentation was investigated in three experiments. In the first and second experiments, the effects of acarbose addition on subacute rumen acidosis was studied. The final concentration of acarbose in the media was 0, 0. 1, 0. 2 or 0. 4 mg/mL. In the first study, the substrate consisted of 0. 8 g cracked corn and 0. 2 g Chinese dry grass. As compared with the control, the acarbose addition increased the pH value and the ratio of acetate to propionate, and decreased acetate, propionate, butyrate, isobutyrate, total volatile fatty acid and lactic acid concentrations. In the second experiment, the substrates consisted of cracked sorghum, corn, barley and wheat. The acarbose supplement increased pH, NH3-N, lac-tate concentration and the ratio of the acetate to propionate, and decreased acetate, propionate, butyrate and TVFA concentration. In the third experiment, the effect of acarbose addition on acute rumen acidosis was investigated, the pH, acetate, propionate, acetate, propionate, valerate, isovalerate and TVFA concentrations were reduced by acarbose addition, while the pH value was improved. There were no significant changes in the isobutyrate, butyrate, and isovalerate concentrations. In general, these results indicated that acarbose addition increased the pH value and reduced lactic acid concentration, and it has the potential to prevent rumen acidosis.%利用体外培养技术,评估了急性与亚急性酸中毒条件下添加阿卡波糖对瘤胃微生物发酵的影响.设3个实验,实验1和实验2体外摸拟了亚急性酸中毒(5.0<pH<5.6)、实验3模拟了急性酸中毒条件(pH<5.0),各实验中阿卡波糖添加量均为0,0.1,0.2和0.4 mg/mL.实验1中底物组成为0.8g玉米和0.2g粉碎羊草,实验2以高梁、玉米、小麦和大麦为底物,实验3发酵底物为0.75g玉米、0.25g纤维二糖、0.25g甘露糖和0.25g木糖;各实验组均设4个重复,体外培养24h.结果表明,实验1

  11. 替比夫定与干扰素联用致乳酸性酸中毒并横纹肌溶解症%Telbivudine co-administration with interferon induced lactic acidosis and rhabdomyolysis: one case report

    曲彩红; 谢俊强; 黄建华

    2013-01-01

    A 23-γears-old male patient with chronic viral hepatitis type B developed rhabdomyolysis and lactic acidosis during receiving telhivudine and interferon Alfa-2a for anti-HBV treatment. He appeared muscular soreness, lower extremity weakness, palpitation, and shortness of breath and chest pain. Laboratory examination showed AST217 U·L-1, ALT 144 U·L-1, GGT56 U·L-1, TBIL29.7 μmol·L-1, NA 1288.3 μmol·L-1, CK 925 U·L-1, LDH 991 U·L-1, and MGB 419. 5 μmol·L-1. After withdrawal of relevant drugs and symptomatic treatment, his conditions were improved and stabilized, and he was discharged 1 month later. Clinical physicians should pay attention to drug-induced myopathy induced by nucleotide analogues combined with interferon.%1例23岁青年男性在使用替比夫定与干扰素α-2a联合抗乙肝病毒治疗的过程中出现四肢肌肉酸痛、双下肢无力,心悸、气促伴胸痛等乳酸性酸中毒并横纹肌溶解症严重症状.实验室检查示:AST 217U.L-1,ALT 144 U·L-1,GGT 56 U.L-1,TBIL 29.7 μmol·L-1,NA 1 288.3 μmol·L-1;CK 925 U·L-1,LDH 991U.L-1,MGB 419.5 μg·L-1.经停用相关药物及对症治疗,病情好转并趋于稳定,1月后出院.临床医生应当对核苷(酸)类似物和干扰素联用引起的药源性肌病高度重视.

  12. Brain carbonic acid acidosis after acetazolamide

    Heuser, D; Astrup, J; Lassen, N A;

    1975-01-01

    In cats in barbiturate anesthesia extracellular pH and potassium were continously recorded from brian cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood-brain-barrier to HCO3-minus and H+ions as indicated by the development of brain...

  13. Topiramate and Metabolic Acidosis in Infants

    J Gordon Millichap

    2002-08-01

    Full Text Available The acid-base metabolism was investigated in 9 infants and toddlers, aged 5 months to 2.3 years (median, 6 months, treated with topiramate (TPM for seizures at Johannes Gutenberg University, Mainz, Germany.

  14. BUTYRATE-MEDIATED GENOMIC CHANGES INVOLVED IN NON-SPECIFIC HOST DEFENSES, MATRIX REMODELING AND THE IMMUNE RESPONSE IN THE RUMEN EPITHELIUM OF COWS AFFLICTED WITH SUBACUTE RUMINAL ACIDOSIS

    Louis Dionissopoulos

    2013-01-01

    Full Text Available Subacute Ruminal Acidosis (SARA is a disorder in cattle which can lead to chronic inflammation in the rumen epithelium, known as rumenitis. Butyrate has been shown to attenuate some of the detrimental effects of inflammatory gastroenteral disorders but the molecular mechanisms mediated by butyrate have not been defined. The objective of this study was to define the inflammatory-related genomic changes responsible for the beneficial effects of butyrate. Experimentally, 16 fistulated dairy cows at mid-lactation were fed a SARA-inducing (45% non-fiber carbohydrate diet beginning 2 days before the beginning of treatment and continuing throughout the experiment. Cows were then evenly divided into treatment groups where a carrier with (n = 8 or without (n = 8 supplemental butyrate (2.5% initial DM intake was deposited into the rumen daily for 7 days. The minimum rumen pH was higher in cows with supplemental butyrate (4.96±0.09 to 5.20±0.05, p = 0.040, but mean pH, maximum pH and the duration for which rumen pH was below 5.6 was unaffected. Free plasma Lipopolysaccharide (LPS concentration was unaffected by treatment as was the concentration of Serum Amyloid A (SAA, although the LPS Binding Protein (LBP concentration was increased by the addition of butyrate to the rumen (6.91±0.29 to 7.93±0.29 μg mL-1, p = 0.024. Of the rumen Short Chain Fatty Acids (SCFA tested, only butyrate showed a pronounced treatment effect, rising from 8.60±0.94 to 21.60±0.94 mM (p≤0.0001. Plasma Beta-Hydroxybutyrate (BHBA concentration also increased (799.50±265.24 to 3261.63±265.24 μM, p≤0.001. Butyrate infusion did not affect milk parameters (total fat, lactose, total protein and LOS; however, when related to dry matter intake, milk production efficiency was increased (p = 0.035. Microarray and qRT-PCR analyses of rumen papillae biopsies collected on day 7 found that butyrate administration affected (p≤0.05 the expression of genes

  15. Effect of propofol on intracellular pH of erythrocytes in rats with acute or chronic metabolic acidosis%异丙酚对急性和慢性代谢性酸中毒大鼠红细胞内pH的影响

    袁媛; 张诗海; 姚尚龙; 王贤东; 王冬

    2008-01-01

    Objective To investigate the effect of propofol on erythrocyte intracellular pH (phi) in rats with acute or chronic metabolic acidosis. Methods Adult Wistar rats of both sexes weighing 290-330 g were used in this study. In the first part, acute metabolic acidosis was induced by 0.15 mol/L HCI (4 mmol/kg) infusion via tail vein for 4 h and then forty rats were randomly divided into 4 groups ( n = 10) : control group (F) 10% fat emulsion 10 ml·kg-1·h-1 , acetazolamide 20 mg·kg-1·h-1 group (Z), propofol 10mg·kg-1·h-1 group (P1) and propofol 20 mg·kg-1·h-1 group ( P2 ). In the second part, chronic metabolic acidosis was induced by drinking water containing NH4 CI 0.28 mol/L (535 mg/kg) for 5 days and then forty rats were randomly divided into 4 groups ( n = 10) receiving the same drugs respectively as that of the first part. Blood samples were taken from femoral artery immediately before and at 1, 3 and 6 h during drug administration for determination of carbonic anhydrase (CA) activity, phi and sedinm-hydrogan exchanger-1 (NHE-I) activity. Results In the first part, compared with group F, CA activity was significantly decreased after drug administration in group Z ( P 0.05).第二部分与F组比较,Z组、P1组和P2组pHi和CA活性降低(P0.05).结论 静脉输注异丙酚10、20 mg·kg-1·h-1可导致慢性代谢性酸中毒大鼠红细胞phi降低,其机制与抑制CA活性有关;而对急性代谢性酸中毒大鼠红细胞pHi无影响.

  16. Modelo Matemático para Predição da Acidose Metabólica no Nascimento em Gestações com Diástole Zero ou Reversa Mathematical Model to Predict Metabolic Acidosis at Birth in Pregnancies with Absent or Reversed End-Diastolic Velocity

    Roseli Mieko Yamamoto Nomura

    2002-05-01

    Full Text Available Objetivos: elaborar modelo matemático baseado em parâmetros da cardiotocografia (CTG anteparto de repouso para predição da acidose metabólica no nascimento, caracterizada por valores do excesso de bases (BE inferiores a -10 mEq/L, em gestações com diagnóstico de diástole zero (DZ ou reversa (DR na dopplervelocimetria das artérias umbilicais. Métodos: foi estudada a última cardiotocografia de 127 gestantes de alto risco com diagnóstico de DZ ou DR, pela análise visual do traçado. Os parâmetros da CTG estudados foram a variabilidade da FCF, acelerações transitórias, desacelerações e padrão pseudo-sinusoidal. Entre as características da gravidez foram analisadas a idade gestacional, o intervalo em dias entre o diagnóstico da DZ ou DR e o parto. O modelo de regressão logística foi aplicado na determinação do melhor modelo matemático para predição da acidose. Resultados: a acidose metabólica ocorreu em 51 casos (40,2%. O modelo matemático para predição da acidose contemplou os seguintes parâmetros: intervalo em dias entre o diagnóstico da DZ ou DR e o parto (X1, idade gestacional em semanas (X2, variabilidade da FCF Purpose: to develop a mathematical model based on the fetal heart rate (FHR monitoring to predict metabolic acidosis at birth (base excess < -10 mEq/L, in pregnancies with absent or reversed end-diastolic velocity (AREDV in the umbilical arteries. Methods: the last FHR tracing of 127 AREDV cases was studied by visual analysis. The analyzed parameters included: gestational age, interval between AREDV diagnosis and delivery, FHR variability, FHR accelerations, decelerations, and sinusoidal- like pattern. Multivariate logistic regression was applied to find the best mathematical model to predict acidosis. Results: metabolic acidosis at birth occurred in 51 cases (40.2%. The model included the parameters: interval between AREDV diagnosis and delivery (X1, gestational age in weeks (X2, FHR variability <5

  17. 桥本甲状腺炎合并干燥综合征肾小管酸中毒致低钾血症的临诊应对%Approach to the patient with hypokalemia caused by Hashimoto′s thyroiditis associated with primary Sjogren′s syndrome and renal tubular acidosis

    张洪梅; 张伟伟; 李晓永; 陈寒蓓; 杨震; 钮忆欣; 苏青

    2016-01-01

    Hypokalemia is a common clinical symptom. It is quite important to clarify the cause of hypokalemia. Autoimmune thyroid disease and primary Sjogren syndrome ( pSS ) have a common genetic predisposition. The coexistence of both diseases is frequent. Renal tubular acidosis ( RTA) is one of the causes of hypokalemia, which can be primary and secondary to other diseases in etiology. Primary RTA is more common in children. As for adults, RTA is often secondary to pSS. In this paper, we reported a case of hypokalemia caused by Hashimoto’s thyroiditis associated with primary Sjogren’s syndrome and renal tubular acidosis in order to call attention to the special cause and treatment of hypokalemia.%低钾血症临床上较为常见,明确低血钾的原因至关重要。自身免疫性甲状腺疾病及干燥综合征有共同的遗传易感性,往往同时发生,肾小管性酸中毒为低钾血症病因之一,按病因分原发性和继发性,原发性多见于儿童,成人以继发性肾小管酸中毒多见,多继发于原发性干燥综合征。本文详细描述了1例桥本甲状腺炎合并干燥综合征肾小管酸中毒导致低钾血症的诊疗过程,以使临床医生重视低钾血症的病因,及时诊治。

  18. 线粒体脑肌病伴高乳酸血症及卒中样发作综合征的病因及病机研究进展%Research Progress of Mitochondrial Encephalopathy with Lactic Acidosis and Stroke-Like Episodes in Etiopathogenisis and Pathogenesis

    陈燕; 曹秉振

    2011-01-01

    Mitochondrial encephalopathy with lactic acidosis and stroke - like episodes ( MELAS syndrome ) is the most common form of mitochondrial dieases and coused by an A to G transition mutation at position 3243 of the mitochondrial genome. The disease is maternal inheritance , usually involved central nerve system and skeletal muscle. The most frequent clinical manifestations were headache, fatigue or movement intolerance, mental impairment, stroke - like episodes and lactic acidosis.In recent years the pathogenesis, genetic mutation characteristics, pathology, clinical manifestation of MELAS svndrome has made great progress. This review emphatically discusses the etiology and pathogenesis of the disease.%线粒体脑肌病伴高乳酸血症及卒中样发作(MELAS)综合征是人类线粒体疾病中最常见的表现形式,该病主要是由线粒体基因组第3243位点的腺嘌呤突变为鸟嘌呤所致.呈母系遗传,主要累及中枢神经系统和骨骼肌.头痛、抽搐、运动耐受差、智能障碍、脑卒中样发作、血乳酸水平升高为本组患者的主要临床表现.近年来MELAS综合征的发病机制、基因突变特点、病理改变、临床表现等方面取得了较大进展,本文着重讨论该病的病因及发病机制.

  19. Avaliação da acidose metabólica em pacientes graves: método de Stewart-Fencl-Figge versus a abordagem tradicional de henderson-hasselbalch Assessment of metabolic acidosis in critically ill patients: method of Stewart-Fencl-Figge versus the traditional henderson-hasselbalch approach

    Manuela Borges Gavaza Barbosa

    2006-12-01

    of metabolic acidosis giving emphasis to the of Stewart-Fencl-Figge method versus the traditional method of Henderson-Hasselbalch. CONTENTS: Metabolic acidosis is a common issue in critically ill patients, an important cause of myocardial contractility depression and sensible marker of impaired tissue oxygenation. Traditionally, is evaluated by the Henderson-Hasselbalch approach in which an arterial blood sample provides information about the presence and type of acid base disturbance. However, this method is not always capable to explain the causes of the metabolic acidosis and, therefore, several studies have explored mechanisms to improve its interpretation. The Stewart-Fencl-Figge method calculated through a mathematical formula, where in addition to arterial blood gas levels, serum levels of electrolytes, lactate and albumin are used, supplies trustworthy information allowing detection of mixed metabolic abnormalities and quantification of the magnitude of each component, mainly in patients with multiple organic dysfunctions. In these individuals, the presence of unmeasured anions in the plasma is an important mechanism of metabolic acidosis and its early detection fundamental to avoid deleterious effect on the organism. CONCLUSIONS: The traditional Henderson-Hasselbalch approach fails in analyzing the underlying mechanisms of metabolic acidosis and possesses many variables that intervene with its result especially in the critically ill patient. The Stewart-Fencl-Figge method offers a broader analysis of metabolic acidosis, indicating its mechanisms and guiding a better therapeutically strategy. As an alternative, the albumin-corrected and lactate-corrected anion gap seems to be as useful as the Stewart approach in identifying the unmeasured anions.

  20. Oedema disease is associated with metabolic acidosis and small intestinal acidosis

    Nabuurs, M.J.A.; Weijgert, van de E.; Grootendorst, A.F.; Niewold, T.A.

    2001-01-01

    Limited information is available about the pathogenesis and pathophysiology of oedema disease (OD). Oedema disease is caused by specific enterotoxemic Escherichia coli (SLTIIv-toxin producing) strains; however, the same strains are also found in non-afflicted pigs. Furthermore, it is unclear how the

  1. Electrophysiological effects of lidocaine on myocardial tissue in guinea-pig left ventricular outflow tract under conditions of hypoxia, acidosis and treatment with epinephrine%利多卡因对低氧、酸中毒及肾上腺素条件下豚鼠左心室流出道心肌组织电活动的影响

    赵兰平; 王雪芳; 杜会博; 薛淑芳; 陈彦静

    2013-01-01

    AIM; To study the electrophysiological effects of lidocaine on the myocardial tissue in guinea-pig left ventricular outflow tract under the conditions of hypoxia, acidosis and treatment with epinephrine. METHODS: The action potentials of pacemaker cells in guinea-pig left ventricular outflow tract were recorded by conventional technique with intracellular microelectrodes. The effects of lidocaine on the spontaneous slow response potentials were investigated under the conditions of hypoxia, acidosis and treatment with epinephrine (EPI). RESULTS: Lidocaine markedly decreased the rate of pacemaker firing ( RPF) , the velocity of diastolic depolarization ( VDD) , the maximal rate of depolarization ( Vmax), the maximal diastolic potential (MDP) and the amplitude of action potential ( APA). Lidocaine also shortened the 50% and 80% of duration of action potential (APD50 and APD80). At the concentrations from 0.1 μmol/L to 10 μmol/L, the effects of lidocaine were more significant. Under the condition of hypoxia and perfusion with deprived glucose content for 15 min, VDD, RPF, Vmax, MDP and APA significantly decreased, and APD50 notably shortened. Under the condition of hypoxia, lidocaine at 1 μmol/L significantly decreased VDD, RPF, Vmax and APA as compared with the cells treated with hypoxia only. Perfusion with pH 6.8 solution for 10 min, VDD, RPF, Vmax and APA significantly decreased, MDP notably increased, and APD50 and APD80 markedly shortened. Under the condition of acidosis for 10 min, lidocaine significantly decreased VDD, RPF and Vmax, and lengthened APD50 and APD80 as compared with the cells under the condition of acidosis alone. Perfusion with EPI at 10 μmol/L for 10 min resulted in significant increases in VDD, RPF, Vmax, MDP and APA, and notable shortenings of APD50 and APD80, were also observed. Compared with 10 μmol/L EPI group, 1 μmol/L lidocaine +10 μmol/L EPI significantly reduced VDD, RPF, MDP and APA, and lengthened APD50, and APD80. CONCLUSION

  2. Protection of benthiactzine on mixed type acidosis of concomitant respiratory failure and circulatory failure induced by intoxication of cholinesterase inhibitor%宾赛克嗪对胆碱酯酶抑制剂中毒所致呼吸衰竭和循环衰竭时混合型酸中毒的影响

    宋丽雪; 唐渊; 龙超良; 王汝欢; 张津津; 汪海

    2012-01-01

    new antidote benthiactzine on mixed type acidosis of concomitant respiratory failure and circulatory failure induced by intoxication of cholinesterase inhibitor ( ChEI) . Methods Seven male dogs,weighing(12 - 15)kg,were injected intermuscularly 1/3 LD soman(l LD = 10 μg/kg)per ten minutes. The mean the pressure of carbondioxide decreased to 60 mmHg and the pressure of oxygen increased to 50 mmHg was defined as respirato ry failure. The mean the blood pressure decreased to (40-45) mmHg was defined as circulatory failure . The changes of arterial blood were evaluated by an eight-channel direct -writing oscillograph, and were observed before and after soman injection. Statistical analysis of the data wag performed using the self control t test with the SAS 6.12 Software Program. Results The results indicated that PaCO2 and PO2 were (45. 5 ±12.3) mmHg and (87. 8 ±14. 3) mmHg with significant difference (P<0.01,n=7); and BE,BB, SB and CH+ were ( -6.7 ±1.7) mmol/L, (41.1 ±1.8) mmol/L, (18.8 ±1.2) mmol/L, and (50.4 ± 10. 5) mmol/L, respectively. When it be continually treated above 6 h, the life feature be recovered in the acidosis dog. When the acidosis induced 2 h by the soman(4 LD) in dog, the blood pressure decreased , MAP was below 45 mmHg, and caused respiratory failure and circulatory failure. After treatment with benthiactzine 1 h, PaCO2, CH+ and PO2 changed to (40. 2 ±7. 9) mmHg, (61.3 ±5.4) mmol/L, (114.5 ±27.1) mmHg,respectively, The other symptoms has not been continuously worsened , and acid poisoning was partially controlled . Conclusion Intoxiciation of cholinest erase inhibitors could lead to compensated primary acute respiratory acidosis complicating continuous metabolic aci -dosis. After treatment with benthiactzine , the symptoms of acidosis will be relieved , and broken away from the acidosis state.

  3. Clinical features of child mitochondrial encephalopathy with lactic acidosis and stroke with status epileptics%以癫痫持续状态起病的线粒体脑肌病伴乳酸血症和卒中样发作患儿临床特点

    方琼; 陈琅; 陈巧彬; 杨芳

    2015-01-01

    目的:探讨线粒体脑肌病合并乳酸血症与卒中样发作(MELAS)出现癫痫持续状态患儿的临床特点及治疗。方法回顾性分析4例以癫痫持续状态起病并最终确诊为MEILAS患儿的临床、脑电图、影像学及治疗。结果4例患儿均以癫痫持续状态起病,血清乳酸、血氨、心肌酶升高,血钠降低,伴代谢性酸中毒;发作期及发作间期脑电图均有相应表现;头颅影像学发现基底节钙化、脑萎缩,急性期可见皮层水肿;基因检测提示mtDNA3243位点突变。结论MELAS的癫痫发作较难控制,应尽早诊断,选择合适的抗癫痫药物及相关对症治疗,以减轻脑损伤。%Objective To investigate the clinical features and treatment of a group of patients of mitochondrial encepha-lomyopathy with actic acidosis and stroke (MELAS) with onset of status epileptics. Methods Clinical features, EEGs, image ifndings, and therapeutic data of 4 cases with onset of status epileptics patients ifnally diagnosed as MELAS were retrospectively reviewed. Results Four Patients were onset with status epileptics. The levels of serum lactic acid, ammonia, myocardial enzymes were increased, and the serum sodium level was reduced, and accompanied with metabolic acidosis. EEG found corresponding paroxysmal and interictal activities. Brain images showed basal ganglia calciifcation, brain atrophy, and acute cortex edema. Genetic detection found mtDNA3243 mutation. Conclusions The status epilepticus was commonly present in MELAS. The treatment of epileptic attack in this disease was dififcult, which needs early diagnosis. Appropriate anti-leptic drugs and relevant treatment to symptoms are important to alleviate cerebral injury.

  4. Influência da forma de indução à acidose na determinação da intensidade de lactato mínimo em corredores de longa distância Influence of the acidosis induction manner in the determination of minimal lactate threshold in endurance runners

    Vanessa Santhiago

    2008-08-01

    Full Text Available O objetivo principal deste estudo foi verificar se diferentes formas de indução à acidose interferem na determinação da intensidade do lactato mínimo (LACmin em corredores de longa distância. Desse modo, 14 corredores de provas fundas do atletismo participaram do estudo. Os atletas realizaram três protocolos: 1 teste incremental em esteira rolante, com incrementos de 1km.h-1 a cada três minutos até a exaustão, para a determinação das intensidades de limiar anaeróbio (OBLA, de limiar aeróbio (Laer, consumo máximo de oxigênio (VO2max e intensidade de consumo máximo de oxigênio (vVO2max; 2 teste de lactato mínimo em pista de atletismo (LACminp, que consistiu de dois esforços máximos de 233m na pista de atletismo com intervalo de um minuto entre cada repetição, com oito minutos de recuperação passiva, seguido de um teste incremental semelhante ao do protocolo 1; e 3 teste de lactato mínimo em esteira rolante (LACmine, constituído de dois esforços máximos de um minuto e 45 segundos com intervalo de um minuto, na intensidade de 120% da vVO2max, seguido dos mesmos procedimentos do protocolo 2. Foram coletadas amostras de sangue do lóbulo da orelha ao final de cada estágio em todos os protocolos e no 7º minuto de recuperação passiva dos testes de LACmine e LACminp. A análise de variância (ANOVA mostrou que ocorreram diferenças significativas entre as intensidades de LACmine (13,23 ± 1,78km.h-1 e OBLA (14,67 ± 1,44km.h-1. Dessa maneira, a partir dos resultados obtidos no presente estudo, é possível concluir que a determinação da intensidade correspondente ao lactato mínimo é dependente do protocolo utilizado para a indução à acidose. Além disso, o LACmine subestimou a intensidade correspondente ao OBLA, não podendo ser utilizado para a mensuração da capacidade aeróbia de corredores fundistas.The purpose of this study was to verify if different induction forms to the acidosis can interfere in the

  5. Série de treinamento intervalado de alta intensidade como índice de determinação da tolerância à acidose na predição da performance anaeróbia de natação High intensity interval training series as indices of acidosis tolerance determination in swimming anaerobic performance prediction

    Rafael Deminice

    2007-06-01

    Full Text Available O objetivo do presente estudo foi determinar a tolerância à acidose através de uma série de nados intervalados de alta intensidade e relacionar com a velocidade de limiar anaeróbio (VLan, concentração de lactato sanguíneo de pico ([Lac]pico, capacidade de trabalho anaeróbio (CTA, freqüência de braçada (fB, comprimento de braçada (CB e índice de braçada (IB na predição da performance de 100m de natação. Dez nadadores realizaram seis nados máximos de 100m no estilo crawl com intervalo de seis minutos. Amostras de sangue foram coletadas cinco minutos após cada nado para posterior análise de lactacidemia ([Lac]. Através da razão entre [Lac] e os respectivos tempos de execução dos seis nados, determinou-se a tolerância à acidose (TA. O número de braçadas realizadas durante os seis esforços foi anotado para determinação da fB, CB, IB. Um nado máximo de 100m foi utilizado como parâmetro de performance (P100 e amostras de sangue foram coletadas para determinação da concentração de lactato sanguíneo de pico ([Lac]pico. Três esforços progressivos de 400m foram realizados para determinação da VLan correspondente à concentração fixa de 3,5mM de lactato. Esforços máximos de 200 e 400m foram realizados para determinação da CTA por regressão linear (coeficiente linear. Os resultados apresentaram significativas correlações (p The aim of the present study was to determine the acidosis tolerance through one high intensity interval swim serie and to relate with anaerobic threshold speed (ATS, blood lactate peak concentration ([Lac]peak, anaerobic work capacity (AWC, stroke rate (SR, stroke length (SL and stroke index (SI in swimming 100 m performance prediction. Ten swimmers performed six maximal swims along 100 m by crawl style with 6 minutes for a rest. Blood samples were taken 5 minutes before each swim for lactate analyses ([Lac]. Through the division of the [Lac] for the time to complete the 6 swims, was

  6. 代谢性酸中毒诱导新生大鼠视网膜新生血管缺氧诱导因子-lα的表达及其意义%Expression and significance of hypoxia-inducible factor-1α in retinal neovascularization induced by metabolic acidosis in newborn rats

    张玉真; 王娟; 乔立兴; 蒋犁

    2011-01-01

    Objective To investigate the expression and significance of hypoxia-inducible factor-1α (HIF-1α) in the retinal neovascularization by metabolic acidosis in newborn rats. Methods One hundred and twenty newborn SD rats were randomly divided into acidosis (experiment) and normoxia (control) groups. A total of 60 newborn rats in experiment group underwent tubal feeding day for 6 days and followed by a period of recovery. The rats in the two groups were sacrificed at the 3rd, 5th, 8th, 10th, 13th and 20th day after birth, respectively. The morphologic changes of retinal vessels were estimated by observing the vascular pattern in adenosine diphosphatase stained retina flat mounts. The newborn vessels were quantified by HE staining. Immunohistochemical method was used to detect HIF-1α expression. Results In experiment group, numerous neovascularization and un-perfused area at the periphery of vessels occurred on the 10th day. The result of HE staining showed that in experiment group of 10-day old,the number of neovascular nuclei extending into the vireo was 28.78±7.53, and that of the control group was 1.22±1.48 (t=11.169,P<0.01). The results of immunohistochemistry revealed that the expression of HIF-1α protein were stronger in the experiment group than in the control group on the 8th, 10th and 13th day, and there were significant differences between the two groups (108.87±15.21, 183.68±26.58 and 129.42±9.85 vs 74.98±4.50, 76.38± 3.38 and 74.78±1.86, t=4.625, 9.023 and 9.672,P<0.05). Conclusions HIF-lα might play an important role in retinal neovascularization.%目的 探讨缺氧诱导因子-lα(hypoxia-inducible factor-lα,HIF-lα)在代谢性酸中毒诱导视网膜新生血管中的表达和意义.方法 将120只新生SD大鼠随机分为酸中毒模型组和正常对照组,各60只.酸中毒模型组出生后第2天开始按535 mg/(kg·d)的剂量管饲氯化铵溶液 (质量浓度为50 mg/ml),2次/d,连续6 d,停药进入恢复期.2

  7. [Distal renal tubular acidosis: report of 3 cases].

    Guibaud, P; Parchoux, B; Langue, J; Bouissou, F; Barthe, P; Larbre, F

    1979-06-01

    Three observations of R.T.A. with nerve deafness are reported. Case 1 and 2 concern consanguinous brothers whose parents are not affected, which confirm the syndrom as an autosomal recessive entity. The third, sporadic, case relates to a 13-year-old non consanguinous girl. Metabolic abnormalities and renal evolution with nephrocalcinosis was such as in Albright disease. However a progressive nerve deafness makes distinction. The authors underline the importance of this sometimes difficult distinction for genetic counseling. PMID:541679

  8. Postoperative metabolic acidosis following the minimally invasive radiofrequency maze procedure

    Raymond Patrick Hom; Anna Dubovoy; Elizabeth Jewell; Milo Engoren

    2016-01-01

    Purpose: Atrial fibrillation (AF) is the most common arrhythmia treated in the world. While medical treatment with antiarrhythmic drugs remains the primary treatment modality, symptomatic refractory AF often requires treatment with a catheter or surgical ablation. One minimally invasive therapy is the Mini-Maze procedure, which utilizes epicardial radiofrequency ablation via a subxiphoid approach to rid the heart of arrhythmogenic atrial foci without a median sternotomy or cardiopulmonary byp...

  9. Tolerance of hypercapnic acidosis by the European eel, Anguilla anguilla

    McKenzie, DJ; Dalla Valle, AZ; Steffensen, JF;

    2000-01-01

    uptake. Eels exposed for 3 months to chronic hypercapnia (Pw,CO2 values of control, 15, 30 or 45 mmHg) were anaesthetised, cannulated and recovered as described above, at the appropriate Pw,CO2. In all groups, Pa,CO2 was about 3 mmHg above Pw,CO2, and hypercapnic eels exhibited a marked accumulation......Eels reared intensively in recirculated water can experience chronic hypercapnia from accumulation of metabolic CO2, with water CO2 partial pressures (Pw,CO2) exceeding 30 mmHg, far above that hitherto considered normal for fish (1 to 3 mmHg). The effects on eels of acute and chronic hypercapnia...... to progressive hypercapnia (20 min at Pw,CO2 values of 10, 20, 40, 60 and 80 mmHg) caused a linear increase in arterial PCO2 (Pa,CO2) from 3.5 ± 0.4 mmHg in normocapnia to 44.9 ± 2.6 at Pw,CO2 = 80 mmHg, coupled to respective declines in arterial pH (pHa) from 7.86 ± 0.02 to 7.16 ± 0.04 and in arterial total O2...

  10. Genetics Home Reference: renal tubular acidosis with deafness

    ... Prevention: Hearing Loss in Children Centre for Genetics Education (Australia): Deafness and Hearing Loss Gallaudet University: Laurent Clerc National Deaf Education Center KidsHealth: What's Hearing Loss? MalaCards: renal tubular ...

  11. Productivity, digestion, and health responses to hindgut acidosis in ruminants

    The role of large intestinal or hindgut fermentation in ruminant nutrition has received little research attention in recent decades. Though the contribution of the hindgut to total tract nutrient digestion is substantially less than the contribution from the rumen, hindgut fermentation impacts anima...

  12. Caracterização físico-química da acidose metabólica induzida pela expansão volêmica inicial com solução salina a 0,9% em pacientes com sepse grave e choque séptico Physicochemical characterization of metabolic acidosis induced by normal saline resuscitation of patients with severe sepsis and septic shock

    Marcelo Park

    2011-06-01

    Full Text Available OBJETIVO: O objetivo deste estudo foi caracterizar e quantificar a acidose metabólica causada pela expansão volêmica inicial na reanimação de pacientes com sepse grave e choque séptico. MÉTODOS: Uma coleta de sangue para caracterização físico-química do equilíbrio ácido-básico antes e após a expansão volêmica com 30 mL/kg de solução salina a 0,9%. O diagnóstico e a quantificação da acidose metabólica foram feitas com o uso do "standard base excess" (SBE. RESULTADOS: Oito pacientes com 58 ± 13 anos e APACHE II de 20 ± 4 foram expandidos com 2000 ± 370 mL de solução salina a 0,9%. Houve queda do pH de 7,404 ± 0,080 para 7,367 ± 0,086 (P=0,018 associada a elevação da PCO2 de 30 ± 5 mmHg para 32 ± 2 mmHg (P=0,215 e queda do SBE de -4,4 ± 5,6 para -6,0 ± 5,7 mEq/L (P=0,039. Esta queda do SBE foi associada ao poder acidificante de dois fatores: elevação não significativa do "strong ion gap" (SIG de 6,1 ± 3,4 para 7,7 ± 4,0 mEq/L (P=0,134 e queda não significativa do "strong ion diference" aparente inorgânico (SIDai de 40 ± 5 para 38 ± 4 mEq/L (P=0,318. Em contraposição, houve queda da albumina sérica de 3,1 ± 1,0 para 2,6 ± 0,8 mEq/L (P=0,003, que teve um poder alcalinizante sobre o SBE. A elevação do cloro sérico de 103 ± 10 para 106 ± 7 mEq/L (POBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9% saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE. RESULTS: Eight patients with a mean age of 58 ± 13 years and mean APACHE II scores of 20 ± 4 were expanded using 2,000 ± 370 mL of 0.9% saline solution. Blood pH dropped

  13. Heteroplasmy levels of mitochondrial tRNALeu(UUR) A3243G mutation and clinical features in a Chinese family with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome%线粒体脑肌病伴高乳酸血症和脑卒中样发作综合征一家系临床特征及线粒体基因A3243G位点点突变异质性水平

    何振巍; 张朝东

    2010-01-01

    目的 调查1个疑似患有母系遗传性线粒体脑肌病伴高乳酸血症和脑卒中样发作(MELAS)综合征家系的临床表现、生物化学检测数据和影像学资料,并探索其与血细胞线粒体基因突变异质性水平的关联性.方法 收集先证者和11位其母系家系成员的一般情况、抽搐及脑卒中样发作等病史,检测家系成员的血常规和运动前后血浆乳酸水平等生化指标,并做头颅磁共振检查.用聚合酶链反应(PCR)-限制性内切酶片段长度多态和DNA测序法检测其成员是否存在线粒体基因组A3243G点突变,并用荧光实时定量PCR定量该突变的水平.结果 该家系部分成员存在抽搐、脑卒中样发作和高乳酸血症等MELAS综合征典型症状,以及身材矮小、运动不耐受和发热、偏头痛等非典型症状.发作期头颅磁共振成像符合MELAS综合征的典型特点,且普遍存在小脑萎缩.母系亲属均存在线粒体基因的A3243G位点点突变,突变异质性水平越高,症状越典型且严重.结论 该调查家系确诊母系遗传性MELAS综合征,其致病基因为线粒体A3243G点突变.外周血血细胞线粒体基因突变异质性水平与亲缘关系、抽搐早现性和血乳酸值等临床表型存在相关性.%Objective To investigate the clinical manifestation, biochemically detected data, and radiographic features of a pedigree with suspected mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome, and to explore the correlations between the clinical features and the mutant heteroplasmy levels of mitochondrial genome. Methods The personal details, histories of stroke-like episodes and seizures within the proband and 11 members in the maternal lineage of the family were collected. Routine blood examinations and plasma lactate levels before and after movements of these family members were detected, followed by cephalic MRI examinations. Polymerase chain reaction

  14. Hallazgos neurorradiológicos de la Acidosis Glutárica tipo I

    Luis, E.; Larrache, J. (Javier); Garcia-de-Eulate, R. (Reyes); Narbona, J. (Juan); Zubieta, J L

    2007-01-01

    Glutaric aciduria type I is a rare disorder of organic acid metabolism caused by deficiency of glutaryl-CoA dehydrogenase, a mitochondrial enzyme. Improper degeneration of amino acids: tryptophan, lysine, and hydroxylysine, results in increased levels of glutaric acid, which typically becomes clinically manifest as an acute dystonic crisis in young children. Accumulation of glutaric acid causes neurotoxicity in the basal ganglia and fronto-tempor...

  15. Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study

    Dubin, Arnaldo; Murias, Gastón; Maskin, Bernardo; Pozo, Mario O; Sottile, Juan P; Barán, Marcelo; Edul, Vanina S Kanoore; Canales, Héctor S; Badie, Julio C; Etcheverry, Graciela; Estenssoro, Elisa

    2005-01-01

    Introduction Increased intramucosal–arterial carbon dioxide tension (PCO2) difference (ΔPCO2) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in ΔPCO2. Methods In 19 anesthetized and mechanically ventilated sheep, we measured cardiac output, superior mesenteric blood flow, lactate, gases, hemoglobi...

  16. Lactic acidosis in the rectal lumen of patients with septic shock measured by luminal equilibrium dialysis

    Due, V; Bonde, J; Espersen, K;

    2002-01-01

    Gut ischaemia may contribute to morbidity in sepsis, but little is known about the metabolic state of the gut mucosa in such patients.......Gut ischaemia may contribute to morbidity in sepsis, but little is known about the metabolic state of the gut mucosa in such patients....

  17. Umbilical cord blood lactate: a valuable tool in the assessment of fetal metabolic acidosis

    Gjerris, Anne Cathrine Roslev; Staer-Jensen, Jette; Jørgensen, Jan Stener;

    2008-01-01

    The aim of the present study was (1) to evaluate the relationship between umbilical cord arterial blood lactate and pH, standard base excess (SBE), and actual base excess (ABE) at delivery and (2) to suggest a cut-off level of umbilical cord arterial blood lactate in predicting fetal asphyxia usi...

  18. Umbilical cord blood lactate: a valuable tool in the assessment of fetal metabolic acidosis

    Gjerris, A.C.; Staer-Jensen, J.; Jorgensen, J.S.;

    2008-01-01

    OBJECTIVE: The aim of the present study was (1) to evaluate the relationship between umbilical cord arterial blood lactate and pH, standard base excess (SBE), and actual base excess (ABE) at delivery and (2) to suggest a cut-off level of umbilical cord arterial blood lactate in predicting fetal a...

  19. Metabolic acidosis with a high anion: A drug-drug interaction between paracetamol and flucloxacillin

    Jessurun, N.T.; Van Hunse, F.; Van Puijenbroek, E.

    2015-01-01

    Background: Five-oxoproline is a product of disordered glutathione metabolism in the gamma glutamyl cycle: glutathione deficiency removes the feedback inhibition resulting in the formation of γ -glutamylcysteine and elevated concentrations of γ -glutamylcysteine leading to the formation of 5-oxoprol

  20. Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium

    Street, D.; Nielsen, Jens Jung; Bangsbo, Jens;

    2005-01-01

    Skeletal muscle releases potassium during activity. Interstitial potassium accumulation is important for muscle function and the development of fatigue resulting from exercise. In the present study we used sodium citrate ingestion as a tool to investigate the relationship between interstitial H+ ...

  1. Marble brain syndrome: osteopetrosis, renal acidosis and calcification of the brain

    Jacquemin, C.; Mullaney, P.; Svedberg, E. [King Khaled Eye Specialist Hospital, Riyadh (Saudi Arabia)

    1998-10-01

    Cerebral calcification in children is frequently associated with systemic metabolic disease. We present a case of ``marble brain syntrome``, which showed this abnormality. (orig.) (orig.) With 2 figs.

  2. Phosphate and acidosis act synergistically to depress peak power in rat muscle fibers

    Nelson, Cassandra R.; Debold, Edward P.; Fitts, Robert H.

    2014-01-01

    Skeletal muscle fatigue is characterized by the buildup of H+ and inorganic phosphate (Pi), metabolites that are thought to cause fatigue by inhibiting muscle force, velocity, and power. While the individual effects of elevated H+ or Pi have been well characterized, the effects of simultaneously elevating the ions, as occurs during fatigue in vivo, are still poorly understood. To address this, we exposed slow and fast rat skinned muscle fibers to fatiguing levels of H+ (pH 6.2) and Pi (30 mM)...

  3. A truncating PET100 variant causing fatal infantile lactic acidosis and isolated cytochrome c oxidase deficiency.

    Oláhová, Monika; Haack, Tobias B; Alston, Charlotte L; Houghton, Jessica Ac; He, Langping; Morris, Andrew Am; Brown, Garry K; McFarland, Robert; Chrzanowska-Lightowlers, Zofia Ma; Lightowlers, Robert N; Prokisch, Holger; Taylor, Robert W

    2015-07-01

    Isolated mitochondrial complex IV (cytochrome c oxidase) deficiency is an important cause of mitochondrial disease in children and adults. It is genetically heterogeneous, given that both mtDNA-encoded and nuclear-encoded gene products contribute to structural components and assembly factors. Pathogenic variants within these proteins are associated with clinical variability ranging from isolated organ involvement to multisystem disease presentations. Defects in more than 10 complex IV assembly factors have been described including a recent Lebanese founder mutation in PET100 in patients presenting with Leigh syndrome. We report the clinical and molecular investigation of a patient with a fatal, neonatal-onset isolated complex IV deficiency associated with multiorgan involvement born to consanguineous, first-cousin British Asian parents. Exome sequencing revealed a homozygous truncating variant (c.142C>T, p.(Gln48*)) in the PET100 gene that results in a complete loss of enzyme activity and assembly of the holocomplex. Our report confirms PET100 mutation as an important cause of isolated complex IV deficiency outside of the Lebanese population, extending the phenotypic spectrum associated with abnormalities within this gene. PMID:25293719

  4. Hypertrophic cardiomyopathy, cataract, developmental delay, lactic acidosis: A novel subtype of 3-methylglutaconic aciduria

    G. Di Rosa; F. Deodato; F.J. Loupatty; C. Rizzo; R. Carrozzo; F.M. Santorelli; S. Boenzi; A. D'Amico; G. Tozzi; E. Bertini; A. Maiorana; R.J.A. Wanders; C. Dionisi-Vici

    2006-01-01

    3-Methylglutaconic aciduria is the biochemical marker of several inherited metabolic diseases. Four types of 3-methylglutaconic aciduria can be distinguished. In the type I form, accumulation of 3-methylglutaconate is due to deficient activity of 3-methylglutaconyl-CoA hydratase, an enzyme of the le

  5. Metabolic multianalyte microphysiometry reveals extracellular acidosis is an essential mediator of neuronal preconditioning.

    McKenzie, Jennifer R; Palubinsky, Amy M; Brown, Jacquelynn E; McLaughlin, Bethann; Cliffel, David E

    2012-07-18

    Metabolic adaptation to stress is a crucial yet poorly understood phenomenon, particularly in the central nervous system (CNS). The ability to identify essential metabolic events which predict neuronal fate in response to injury is critical to developing predictive markers of outcome, for interpreting CNS spectroscopic imaging, and for providing a richer understanding of the relevance of clinical indices of stress which are routinely collected. In this work, real-time multianalyte microphysiometry was used to dynamically assess multiple markers of aerobic and anaerobic respiration through simultaneous electrochemical measurement of extracellular glucose, lactate, oxygen, and acid. Pure neuronal cultures and mixed cultures of neurons and glia were compared following a 90 min exposure to aglycemia. This stress was cytotoxic to neurons yet resulted in no appreciable increase in cell death in age-matched mixed cultures. The metabolic profile of the cultures was similar in that aglycemia resulted in decreases in extracellular acidification and lactate release in both pure neurons and mixed cultures. However, oxygen consumption was only diminished in the neuron enriched cultures. The differences became more pronounced when cells were returned to glucose-containing media upon which extracellular acidification and oxygen consumption never returned to baseline in cells fated to die. Taken together, these data suggest that lactate release is not predictive of neuronal survival. Moreover, they reveal a previously unappreciated relationship of astrocytes in maintaining oxygen uptake and a correlation between metabolic recovery of neurons and extracellular acidification. PMID:22860220

  6. Progress in Diagnosing Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like Episodes

    Ying-Xin Wang

    2015-01-01

    Conclusions: MELAS involves multiple systems with variable clinical symptoms and recurrent episodes. The prognosis of MELAS patients depends on timely diagnosis. Therefore, overall diagnosis of MELAS should be based on the maternal inheritance family history, clinical manifestation, and findings from serial MRI, muscle biopsy, and genetics.

  7. Rumen Microbiome Composition in Cattle during Grain-Induced Subacute Ruminal Acidosis (SARA)

    Danscher, Anne Mette; Derakshani, Hooman; Li, Shucong;

    2014-01-01

    genus level. The rumen bacterial communities were altered in response to SARA (P=0.01). The proportion of several taxa was significantly higher in SARA samples, including S24-7, Erysipelotrichales. Lactobacillus, C lostridia, Moryella, Butyrivibrio, Olsenella, and C oprococcus. Microbiome profiling of...... rumen during SARA could provide new knowledge of the pathogenesis and might be used as a biological marker of the disease....

  8. Extreme hyponatremia with moderate metabolic acidosis during hysteroscopic myomectomy -A case report-

    Jo, Youn Yi; Jeon, Hyun Joo; Choi, Eunkyeong; Choi, Yong-Seon

    2011-01-01

    Excess absorption of fluid distention media remains an unpredictable complication of operative hysteroscopy and may lead to lethal conditions. We report an extreme hyponatremia, caused by using an electrolyte-free 5 : 1 sorbitol/mannitol solution as distention/irrigation fluid for hysteroscopic myomectomy. A 34-year-old female developed severe pulmonary edema and extreme hyponatremia (83 mmol/L) during transcervical endoscopic myomectomy. A brain computed tomography showed mild brain swelling...

  9. Genetics Home Reference: SLC4A1-associated distal renal tubular acidosis

    ... hemolysis), causing a shortage of red blood cells ( anemia ). Hemolytic anemia can lead to unusually pale skin (pallor), extreme ... these abnormal red blood cells may lead to hemolytic anemia. Some people have nonhereditary forms of distal renal ...

  10. Mitochondrial myopathy, encephalopathy, lactate acidosis with stroke-like episodes syndrome (MELAS: A case report

    Petrović Igor N.

    2012-01-01

    Full Text Available Introduction. Mitochondrial encephalopathy, lactacidosis and stroke-like episodes (MELAS represent a multisystemic dysfunction due to various mutations in mitochondrial DNA. Here we report a patient with genetically confirmed MELAS. Case Outline. A patient is presented whose clinical features involved short stature, easy tendency to fatigue, recurrent seizures, progressive cognitive decline, myopathy, sensorineural deafness, diabetes mellitus as well as stroke-like episodes. The major clinical feature of migraine type headache was not present. Neuroimaging studies revealed signs of ischemic infarctions localized in the posterior regions of the brain cortex. Electron microscopy of the skeletal muscle biopsy showed subsarcolemmal accumulation of a large number of mitochondria with paracristal inclusions in the skeletal muscle cells. The diagnosis of MELAS was definitively confirmed by the detection of a specific point mutation A to G at nucleotide position 3243 of mitochondrial DNA. Conclusion. When a relatively young patient without common risk factors for ischemic stroke presents with signs of occipitally localized brain infarctions accompanied with multisystemic dysfunction, MELAS syndrome, it is necessary to conduct investigations in order to diagnose the disease.

  11. The Ovine Fetal and Placental Inflammatory Response to Umbilical Cord Occlusions With Worsening Acidosis.

    Xu, Alex; Matushewski, Brad; Cao, Mingju; Hammond, Robert; Frasch, Martin G; Richardson, Bryan S

    2015-11-01

    We hypothesized that repetitive umbilical cord occlusions (UCOs) leading to severe acidemia will stimulate a placental and thereby fetal inflammatory response which will be exacerbated by chronic hypoxemia and low-grade bacterial infection. Chronically instrumented fetal sheep served as controls or underwent repetitive UCOs for up to 4 hours or until fetal arterial pH was 55% and placental cotyledons processed for measurement of macrophage, neutrophil, and mast cell counts. Repetitive UCOs resulted in severe fetal acidemia with pH approaching 7.00 for all 3 UCO groups. Neutrophils, while unchanged within the cotyledon fetal and intermediate zones, were ∼2-fold higher within the zona intima for all 3 UCO groups. However, no differences were observed in macrophage counts among the treatment groups and no cotyledon mast cells were seen. Fetal plasma and amniotic fluid cytokines remained little changed post-UCOs and/or at 1 and 48 hours of recovery in the normoxic-UCO and hypoxic-UCO groups but increased several fold in the LPS-UCO group with IL-6 plasma values at 1 hour recovery highly correlated with the nadir pH attained (r = -.97). As such, repetitive UCOs with severe acidemia can induce a placental inflammatory response and more so with simulated low-grade infection and likely contributing to cytokine release in the umbilical circulation. PMID:25878209

  12. Melas (mitochondrial, encephalopathy, lactic acidosis and stroke like episodes): relato de um caso

    Lineu Cesar Werneck; Haydée Abdalla; Alfredo Lohr

    1987-01-01

    Relato de caso de menino de 12 anos de idade que apresentou diversas crises convulsivas, cefaléia e vômitos de difícil controle, concomitantes a sinais neurológicos focais. Esses episódios eram recorrentes e apresentavam regressão, com permanência de discreto déficit. A investigação revelou aumento do ácido láctico plasmático, lesões semelhantes a infartos cerebrais e calcificações nos gânglios da base. A biópsia muscular mostrou inúmeras fibras granulares (ragged-reds) e diminuição da citocr...

  13. Yeast mediates lactic acidosis suppression after antibiotic cocktail treatment in short small bowel?

    Bongaerts, G.P.A.; Severijnen, R.S.V.M.; Skladal, D.; Bakkeren, J.A.J.; Sperl, W.

    2005-01-01

    During acidotic periods in a girl with a short small bowel, very high D-lactic acid concentrations were measured in blood and urine; the patient's characteristic faecal flora contained mainly lactobacilli, and during antibiotic cocktail treatment also many yeasts. In this case report we sought to un

  14. Neonatal lactic acidosis, complex I/IV deficiency, and fetal cerebral disruption

    van Straaten, HLM; van Tintelen, JP; Trijbels, JMF; van den Heuvel, LP; Troost, D; Rozemuller, JM; Duran, M; de Vries, LS; Schuelke, M; Barth, PG

    2005-01-01

    Cerebral developmental abnormalities occur in various inborn errors of metabolism including peroxisomal deficiencies, pyruvate dehydrogenase complex deficiency and others. Associations with abnormalities of the respiratory chain are rare. Here we report male and female siblings with microcephaly, a

  15. Genetics Home Reference: pseudohypoaldosteronism type 2

    ... high levels of chloride (hyperchloremia) and acid (metabolic acidosis) in their blood (together, referred to as hyperchloremic metabolic acidosis). People with hyperkalemia, hyperchloremia, and metabolic acidosis can ...

  16. The effect of metabolic acidosis on maximal force production and muscle recruitment during repeated, submaximal calf contractions to task failure

    Siegler, Jason; Poulsen, Mathias Krogh; Nielsen, Niels-Peter;

    2014-01-01

    Obesity is an increasing problem worldwide leading to cardiovascular morbidity. Only limited information exists on the transcriptional regulation of arterial K+ and Ca2+ channels in obesity. We quantified, by real-time PCR, mRNA expression of K+ channels and L-type Ca2+ channels (LTCC) in small m...

  17. Persistence of acidosis in alloxan-induced diabetic rats treated with the juice of Asystasia gangetica leaves

    Rotimi, Solomon O; Omotosho, Omolola E.; Rotimi, Oluwakemi A.

    2011-01-01

    Background: Diabetes mellitus is gradually becoming a global health burden leading to an increase in the search for herbal hypoglycemic agents as alternatives to synthetic ones. Asystasia gangetica is one of the herbs used in folklore system of medicine for managing hypoglycaemia associated with diabetes. Materials and Methods: The influence of the juice of A. gangetica leaf on alloxan-induced diabetic rats was assessed by treating diabetic rats with 25%, 50% and 75% fresh juice and glibencla...

  18. Role of extracellular and intracellular acidosis for hypercapnia-induced inhibition of tension of isolated rat cerebral arteries

    Tian, R; Vogel, P; Lassen, N A;

    1995-01-01

    Ho was measured with a glass electrode. In all studies, Ca(2+)-dependent basal tension (in the absence of any agonist) and tension in the presence of arginine vasopressin were investigated. Control solution was physiological saline bubbled with 5% CO2 and containing 25 mmol/L HCO3- (pH 7.45 to 7...

  19. Severe myositis on commencement of efavirenz, abacavir and lamivudine, in the absence of lactic acidosis or classical abacavir hypersensitivity

    Parsonage, Mirella Jane; Barlow, Gavin; Lillie, Patrick; Moss, Peter; Adams, Katherine; Thaker, Hiten

    2009-01-01

    Myositis in HIV may be due to HIV itself, or to opportunistic infection, malignancy or drug treatment. Severe myositis or rhabdomyolysis have never been reported with the commonly used nucleoside reverse transcriptase inhibitor abacavir, although creatine phosphokinase may rise modestly, particularly if abacavir hypersensitivity occurs. We report an unusual case of abacavir use associated with a thousand-fold rise in creatine phosphokinase in the absence of features of hypersensitivity. The c...

  20. Incomplete renal tubular acidosis as a predisposing factor for calcium phosphate stones in neuropathic bladder: a case report

    Vaidyanathan, Subramanian; Soni, Bakul M.; Watson, Ian D; Singh, Gurpreet; Peter L. Hughes; Mansour, Paul

    2008-01-01

    We present a male tetraplegic patient, who developed stones in neuropathic bladder six times within a span of three years. Unusual features of this case are: (1) This patient started developing stones in urinary bladder thirteen years after sustaining spinal cord injury. (2) He was performing intermittent catheterisation and did not have an indwelling catheter. (3) The presenting symptom of vesical lithiasis was abdominal spasms and not urine infection. (4) The major component of the stones w...

  1. Mutations in GTPBP3 Cause a Mitochondrial Translation Defect Associated with Hypertrophic Cardiomyopathy, Lactic Acidosis, and Encephalopathy

    Kopajtich, Robert; Nicholls, Thomas J.; Rorbach, Joanna; Metodiev, Metodi D.; Freisinger, Peter; Mandel, Hanna; Vanlander, Arnaud; Ghezzi, Daniele; Carrozzo, Rosalba; Taylor, Robert W.; Marquard, Klaus; Murayama, Kei; Wieland, Thomas; Schwarzmayr, Thomas; Mayr, Johannes A.

    2014-01-01

    Respiratory chain deficiencies exhibit a wide variety of clinical phenotypes resulting from defective mitochondrial energy production through oxidative phosphorylation. These defects can be caused by either mutations in the mtDNA or mutations in nuclear genes coding for mitochondrial proteins. The underlying pathomechanisms can affect numerous pathways involved in mitochondrial physiology. By whole-exome and candidate gene sequencing, we identified 11 individuals from 9 families carrying comp...

  2. Osteopathy of renal tubular acidosis: Case report%肾小管酸中毒性骨病1例

    李欣欣

    2011-01-01

    @@ 患者男,49岁.因"腰腿疼痛3年,加重1个月"来诊.患者既往有慢性乙型肝炎病史,长期服用多种抗病毒药物.入院查体:腰椎及髋部压痛明显,直腿抬高试验及"4"字征(-).实验室检查:HLA B27(-).尿常规检查:尿蛋白(-),尿糖:(+),尿pH值7.00;电解质:TCO2 17.21 mmol/L,K+ 3.26 mmol/L,Cl- 106.00 mmol/L;肾功能检查:Cr 106.00 μmol/L,Bun 6.90 mmol/L.血钙1.92 mmol/L,血磷1.80 mmol/L.

  3. Carnosine inhibits carbonic anhydrase IX-mediated extracellular acidosis and suppresses growth of HeLa tumor xenografts

    Ditte, Zuzana; Ditte, Peter; Labudova, Martina; Simko, Veronika; Iuliano, Filippo; Zatovicova, Miriam; Csaderova, Lucia; Pastorekova, Silvia; Pastorek, Jaromir

    2014-01-01

    Background Carbonic anhydrase IX (CA IX) is a transmembrane enzyme that is present in many types of solid tumors. Expression of CA IX is driven predominantly by the hypoxia-inducible factor (HIF) pathway and helps to maintain intracellular pH homeostasis under hypoxic conditions, resulting in acidification of the tumor microenvironment. Carnosine (β-alanyl-L-histidine) is an anti-tumorigenic agent that inhibits the proliferation of cancer cells. In this study, we investigated the role of CA I...

  4. Genetics Home Reference: mitochondrial complex III deficiency

    ... chemical called lactic acid in the body (lactic acidosis). Some affected individuals also have buildup of molecules ... Additional Information & Resources MedlinePlus (4 links) Encyclopedia: Lactic Acidosis Encyclopedia: Metabolic Acidosis Health Topic: Genetic Brain Disorders ...

  5. Tc(V)-DMS tumor localization mechanism: a pH-sensitive Tc(V)-DMS-enhanced target/nontarget ratio by glucose-mediated acidosis

    Since the conception of the pentavalent technetium polynuclear complex of dimercaptosuccinic acid, Tc(V)-DMS, a great number of papers published on its clinical applicability forced us to question ''how tumor tissue appropriates the Tc(V)-DMS.'' Preliminary in vitro studies with Ehrlich ascites tumor cells (EATC) indicated the pH-sensitive character of this tumor agent. From this finding and the well-established notion that malignant tumors are more acidic than normal tissue, the in vivo correlation of Tc(V)-DMS accumulation in tumor tissue with its tissue acidification was considered of interest. The systemic lowering of tumor tissue pH by the stimulation of aerobic glycolysis has been well reported. In the present paper, the response of Tc(V)-DMS tumor accumulation to acidification induced by the glucose administration was explored in EATC-bearing mice. Measurement of tumor tissue pH was carried out by direct microelectrode technique and by histochemical umbelliferone technique in tumor tissue excised from EATC bearing mice. The regional acidity distribution is correlated with the regional radioactivity distribution registered by autoradiography. Evidence related to the pH sensitiveness of Tc(V)-DMS in response to glycolytic acidification was gathered; the pH measurement and the in vivo biodistribution of the double-tracer macroautoradiography with C-14 deoxyglucose (C-14-DG) demonstrated that the regional tissue distribution of Tc(V)-DMS was superimposed to that of C-14-DG. The glucose interventional modality offers the premier foundation for the interpretation of Tc(V)-DMS accumulation in diagnostic studies of malignant tumors

  6. PRIMARY SJOGREN’S SYNDROME AND DISTAL RENAL TUBULAR ACIDOSIS: PRESENTING WITH NEPHROGENIC DIABETES INSI PIDUS SECONDARY TO SEVERE HYPOKALEMIA-A CASE REPORT

    Ksh. Achouba; Banashree Devi; Kh. Lokeshwar; Ram

    2013-01-01

    NTRODUCTION: Sjogren’s syndrome is a slowly progressing autoimmun e disease characterized by lymphocytic infiltration of the exo crine glands, mainly the lacrimal and salivary glands, resulting in their impaired secreto ry function. Simultaneously, systemic involvement and symptoms of cutaneous, respiratory, r enal, hepatic, neurologic, and vascular systems often occur.[ 1 ] This syndrome can present either alone (as primary Sjogren’s syndrome) or in the...

  7. Uso de bicarbonato de sódio na acidose metabólica do paciente gravemente enfermo Sodium bicarbonate in the critically lll patient with metabolic acidosis

    Paulo Novis Rocha

    2009-01-01

    A acidose lática é um distúrbio do equilíbrio ácido-base muito frequente em pacientes internados em unidades de terapia intensiva e está associado a um mau prognóstico. Embora exista um acúmulo substancial de evidências de que níveis críticos de acidemia provocam inúmeros efeitos adversos sobre o funcionamento celular, a utilização de bicarbonato de sódio para o tratamento da acidose lática em pacientes gravemente enfermos permanece alvo de controvérsias. Neste artigo, pretendemos: 1) analisa...

  8. Brain Injury and Inflammatory Response to Umbilical Cord Occlusions Is Limited With Worsening Acidosis in the Near-Term Ovine Fetus.

    Xu, Alex; Matushewski, Brad; Nygard, Karen; Hammond, Robert; Frasch, Martin G; Richardson, Bryan S

    2016-07-01

    We hypothesized that repetitive umbilical cord occlusions (UCOs) with worsening fetal acidemia will lead to an inflammatory response within the brain and thereby brain injury which will be exacerbated by chronic hypoxemia and low-grade infection. Chronically instrumented fetal sheep served as controls (N = 10) or underwent repeated UCOs for up to 4 hours or until arterial pH was 55% and hematoxylin and eosin-and apoptosis-cleaved caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labeling [TUNEL]). Repetitive UCOs resulted in severe acidemia in most animals with pH approaching 7.00 for all 3 UCO groups. However, there was no significant effect on measures of brain inflammation or injury, except in the LPS-UCO animals where TUNEL-positive cells were increased in the hippocampus, although small animal numbers in the hypoxic-UCO group may have limited the ability to detect significance in their TUNEL cell findings. We were therefore unable to confirm our working hypothesis since the near-term ovine fetal brain showed remarkable tolerance for these cord occlusion insults and likely involving protective metabolic mechanisms, despite the severe acidemia noted. PMID:26704527

  9. Effects of acarbose on ruminal fermentation, blood metabolites and microbial profile involved in ruminal acidosis in lactating cows fed a high-carbohydrate ration.

    Blanch, Marta; Calsamiglia, Sergio; Devant, Maria; Bach, Alex

    2010-02-01

    The objective was to evaluate the effects of an inhibitor of alpha-amylase and glucosidase (acarbose, Pfizer Limited, Corby, UK) on ruminal fermentation, blood metabolism and microbial profile in dairy cows in a 2x2 cross-over experiment. Eight Holstein cows fitted with rumen cannulas (milk yield, 24.3+/-2.35 kg/d, body weight, 622+/-54 kg, days in milk, 183+/-67, 5 multiparous and 3 primiparous) were used. Treatments were: control (no additive, CTR) and alpha-amylase and glucosidase inhibitor (0.75 g acarbose-premix/cow per d, AMI). Animals were given ad-libitum access to a high non-fibre carbohydrate (NFC) partial mixed ration (PMR) containing 17.6% crude protein, 28.3% neutral detergent fibre, and 46.5% NFC in the dry matter and supplementary concentrate during milking. Blood samples were taken to determine blood glucose, insulin and urea within the first hour after the morning feeding on two separate days in each period. Samples of ruminal contents were collected during 3 d in each period at 0, 4 and 8 h after feeding to determine volatile fatty acid and ammonia-N concentrations and to quantify protozoa, Streptococcus bovis and Megasphaera elsdenii. Rumen pH was recorded electronically at 22-min intervals during 6 d in each period. Results were analysed using a mixed-effects model. Cows on AMI treatment spent less time with ruminal pH bovis to Meg. elsdenii ratio than CTR (4.09 and 26.8+/-12.0, respectively). These results indicate that dietary supplementation with acarbose in dairy cattle fed high-production rations may be effective in reducing the time for which rumen pH is suboptimal, with no negative effects on ruminal fermentation and blood metabolites. PMID:20053317

  10. Disease: H00241 [KEGG MEDICUS

    Full Text Available H00241 Combined proximal and distal renal tubular acidosis (RTA type 3) Renal tubular acidosis... (RTA) is characterized by metabolic acidosis, a severe disturbance of extracellular pH homeostas...0 PMID:11045400 (gene) Rodriguez-Soriano J New insights into the pathogenesis of renal tubular acidosis--fro...riguez Soriano J Renal tubular acidosis: the clinical entity. J Am Soc Nephrol 13

  11. Disease: H00429 [KEGG MEDICUS

    Full Text Available H00429 Proximal renal tubular acidosis (RTA type 2) Renal tubular acidosis (RTA) is... characterized by metabolic acidosis, a severe disturbance of extracellular pH homeostasis, due to renal imp...4278 PMID:11045400 (gene) Rodriguez-Soriano J New insights into the pathogenesis of renal tubular acidosis--...(gene, env_factor, marker) Rodriguez Soriano J Renal tubular acidosis: the clinical entity. J Am Soc Nephrol... 13:2160-70 (2002) PMID:11095551 (env_factor, drug) Kurtzman NA Renal tubular acidosis syndromes. South Med

  12. Disease: H00428 [KEGG MEDICUS

    Full Text Available H00428 Distal renal tubular acidosis (RTA type 1) Renal tubular acidosis (RTA) is c...haracterized by metabolic acidosis, a severe disturbance of extracellular pH homeostasis, due to renal impai...a DM, Oliveira EA, Silva AC Molecular pathophysiology of renal tubular acidosis. Curr Genomics 10:51-9 (2009...) PMID:11045400 (gene) Rodriguez-Soriano J New insights into the pathogenesis of renal tubular acidosis...ne, env_factor, marker) Rodriguez Soriano J Renal tubular acidosis: the clinical

  13. Genetics Home Reference: glutaric acidemia type II

    ... blood and tissues to become too acidic (metabolic acidosis). Glutaric acidemia type II usually appears in infancy ... sudden episode called a metabolic crisis, in which acidosis and low blood sugar (hypoglycemia) cause weakness, behavior ...

  14. Short bowel syndrome

    ... B12 Too much acid in the blood (metabolic acidosis due to diarrhea) Gallstones Kidney stones Malnutrition Weakened ... PA: Saunders Elsevier; 2011:chap 142. Read More Acidosis Crohn disease Gallstones Kidney stones Malabsorption Necrotizing enterocolitis ...

  15. Genetics Home Reference: 3-hydroxy-3-methylglutaryl-CoA lyase deficiency

    ... cause the blood to become too acidic (metabolic acidosis). If untreated, the disorder can lead to breathing ... byproducts called organic acids can result in metabolic acidosis. A shortage of ketones often leads to hypoglycemia. ...

  16. Ethylene glycol poisoning

    ... causes disturbances in the body's chemistry, including metabolic acidosis . The disturbances may be severe enough to cause ... given through a vein (IV) to reverse severe acidosis Antidotes that slow the formation of the poisonous ...

  17. Potassium test

    ... also be done if your provider suspects metabolic acidosis (for example, caused by uncontrolled diabetes) or alkalosis ( ... Hypoaldosteronism (very rare) Kidney failure Metabolic or respiratory acidosis Red blood cell destruction Too much potassium in ...

  18. Genetics Home Reference: glutathione synthetase deficiency

    ... elevated acidity in the blood and tissues (metabolic acidosis). In addition to the features present in moderate ... Kaabachi N, Hachicha M. Hemolytic anemia and metabolic acidosis: think about glutathione synthetase deficiency. Fetal Pediatr Pathol. ...

  19. Interstitial nephritis

    ... kidney damage in older people. Possible Complications Metabolic acidosis can occur because the kidneys aren't able ... stage kidney disease Injury - kidney and ureter Metabolic acidosis Renal Urine output - decreased Update Date 9/22/ ...

  20. Genetics Home Reference: 3-methylglutaconyl-CoA hydratase deficiency

    ... elevated levels of acid in their blood (metabolic acidosis) and excrete large amounts of acid in their ... Testing Registry: 3-Methylglutaconic aciduria MedlinePlus Encyclopedia: Metabolic Acidosis These resources from MedlinePlus offer information about the ...

  1. Chloride Test

    ... electrolyte or metabolic panel, may be ordered when acidosis or alkalosis is suspected or when someone has ... base is lost from the body (producing metabolic acidosis ) or when a person hyperventilates (causing respiratory alkalosis ). ...

  2. Maple syrup urine disease

    ... burning fat) and excess acid in the blood (acidosis). Treatment When the condition is diagnosed, and during ... York, NY: Springer; 2012:chap 19. Read More Acidosis Amino acids Metabolism Seizures Update Date 4/20/ ...

  3. Osteomalacia

    ... Disorders of vitamin D metabolism Kidney failure and acidosis Lack of enough phosphates in the diet Liver ... PA: Saunders Elsevier; 2011:chap 253. Read More Acidosis Acute kidney failure Lactose intolerance Malabsorption Rickets Seizures ...

  4. Lactic acid test

    ... test is most often done to diagnose lactic acidosis . Normal Results 4.5 to 19.8 mg/ ... PA: Elsevier Saunders; 2016:chap 118. Read More Acidosis Aerobic Anaerobic Heart failure - overview Hepatic Metabolism Muscle ...

  5. Metabolismo oxidativo dos neutrófilos de ovinos tratados com monensina sódica e experimentalmente submetidos à acidose ruminal Oxidative metabolism of the neutrophils in sheep treated with sodium monensin and experimentally submitted to ruminal acidosis

    José Augusto B. Afonso; Ciarlini, Paulo C; Márcio R.G. Kuchembuck; Aguemi Kohayagawa; Lúcia P.Z. Feltrin; Luciana D.R. Pinoti Ciarlini; Cecília B. Laposy; Carla L. de Mendonça; Regina K. Takahira

    2002-01-01

    A acidose láctica ruminal é causada pela ingestão excessiva de carboidratos de fermentação rápida sem uma prévia adaptação dos mocroorganismos, podendo com isso gerar distúrbios metabólicos graves aos ruminantes. Este trabalho tem por objetivo estudar o metabolismo oxidativo dos neutrófilos em ovinos tratados com a monensina sódica na acidose láctica ruminal induzida experimentalmente. Foram empregados 18 ovinos, machos, mestiços (Ideal x Merino), fistulados no rúmen; dos quais nove receberam...

  6. 硫胺素对反刍动物瘤胃内代谢规律及其瘤胃酸中毒的影响%Effect of Thiamin on Rumen Metabolism and Acidosis in Ruminant

    郝志敏

    2010-01-01

    @@ 1 概述``硫胺素(又称为维生素B1)属水溶性维生素,是动物体内能量代谢途径中重要的辅酶.它以硫胺素焦磷酸辅酶(TPP)的形式参与碳水化合物代谢过程中α-酮酸的氧化脱羧反应,是动物体内整个能量代谢过程和支链氨基酸代谢所必需的水溶性维生素;同时对神经和大脑功能也有重要作用(Combs,1992)[1].

  7. Relationship between hyperunconjugated bilirubinemia and metabolic acidosis in newborns%新生儿高未结合胆红素血症与代谢性酸中毒的关系

    张晓云

    2004-01-01

    目的探讨代谢性酸中毒对新生儿高未结合胆红素血症的影响.方法对200例新生儿高未结合胆红素血症患儿进行血浆二氧化碳结合力(CO2CP)检测.结果 CO2CP低于正常值182例(91 %).结论及时发现并纠正代谢性酸中毒,有利于新生儿高未结合胆红素血症患儿黄疸的消退.

  8. Proposal of a new method of judging metabolic acidosis and metabolic alkalosis in the condition of high anion gap%改进高阴离子间隙代谢性酸中毒判断方法

    周寿生

    2008-01-01

    目的 改进高AG代酸的判断方法.方法 通过分析人体血浆中阴离子间变化的特殊关系,提出高AG代酸判断新方法.结果 到目前为止国内外在对高AG代酸的判断中的确存在明显的过度判断问题,判断方法需要改进.结论 对于高AG代酸过去一直没有较好的判断方法,误判漏判现象常有发生.改进判断方法后可以防止误判漏判.

  9. Observation of Curative Effectiveness of Vitamin C in the Treatment of Metabolic Acidosis Following Heart Surgery%维生素C治疗心脏手术后代谢性碱中毒疗效观察

    杜菊

    2004-01-01

    对心脏术后并发代谢性碱中毒的16例病人采用维生素C治疗,对比分析治疗前后动脉血pH值和碱剩余(BE)的变化情况.结果维生素C治疗前后pH值分别是7.56±0.07和7.46士0.05,BE分别为(12.40士3.10)mmol/L和(6.30±3.00)mmol/L,BE值前后比较,P<0.01.提示维生素C能纠正心脏术后代谢性碱中毒.

  10. Effect of Correction of Metabolic Acidosis on Skeletal Muscle Protein Degrada- tion in Uremic Patients%纠正酸中毒对尿毒症患者骨骼肌蛋白质分解率的影响

    王远程; 兰天飙; 张晓燕; 王旭

    2003-01-01

    目的:测定尿毒症患者尿3-MEH/Cr的变化及纠正代谢性酸中毒对其影响.方法:采用氨基酸自动分析仪测定尿毒症患者尿中3-MEH排泄量,以尿3-MEH/Cr比值作为骨骼肌蛋白质分解率指标.结果:在代谢性酸中毒情况下,给予低蛋白饮食,3-MEH/Cr比值升高.纠正代谢性酸中毒后3-MEH/Cr比值明显下降(P<0.01).结论:尿3-MEH/Cr可作为蛋白质营养状况的指标,纠正代谢性酸中毒并限制蛋白质饮食可显著降低尿毒症患者骨骼肌蛋白质分解率.

  11. Unequal Sized Pupils Due to Escitalopram; Adverse Events to Dietary Supplements Causing Emergency Department Visits; Compulsive Masturbation Due to Pramipexole; Metformin-Induced Lactic Acidosis Masquerading As an Acute Myocardial Infarction.

    Mancano, Michael A

    2016-05-01

    The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) Med Watch program (800-FDA-1088). If you have reported an interesting, preventable ADR to Med Watch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: mmancano@temple.edu). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA's Med Watchprogram and Temple University School of Pharmacy. ISMP is an FDA Med Watch partner. PMID:27303087

  12. SUSCEPTIBILIDADE DE BOVINOS DAS RAÇAS JERSEY E GIR À ACIDOSE LÁCTICA RUMINAL: I - VARIÁVEIS RUMINAIS E FECAIS SUSCEPTIBILITY OF JERSEY AND GIR STEERS TO RUMEN LACTIC ACIDOSIS: I - RUMINAL AND FAECAL VARIABLES

    Celso Akio Maruta; Enrico Lippi Ortolani

    2002-01-01

    Quatro garrotes Jersey (J) (Bos taurus) e quatro Gir (G) (Bos indicus), providos de cânula ruminal, foram utilizados para comparar a susceptibilidade à acidose láctica ruminal (ALR) aguda. Para a uniformização da microbiota ruminal, os animais receberam uma alimentação padronizada por dois meses antes da indução da ALR. Esta foi realizada com o uso de sacarose administrada diretamente no rúmen, de acordo com peso metabólico corrigido. Amostras de suco ruminal e fezes foram colhidas no decorre...

  13. A Case Study of Primary Sjogren's Syndrome Complicated by Distal End Renal Tubule Acidosis and Renal Osteopathy%原发性干燥综合征并远端肾小管酸中毒及肾性骨病

    周新荣; 张木勋

    2009-01-01

    目的:提高原发性干燥综合征并远端肾小管酸中毒及肾性骨病的临床诊治水平.方法:报告1例原发性干燥综合征并远端肾小管酸中毒及肾性骨病病例,并结合文献进行复习.结果:本例因间断乏力、低血钾10年,全身关节疼痛10个月入院.入我院后行唾液腺发射体层成像(ECT)示双侧唾液腺摄取及排泄功能均严重受损,眼科检查滤纸试验、角膜染色和泪膜破碎时间均阳性,确诊为原发性干燥综合征并远端肾小管酸中毒及肾性骨病.予10%枸橼酸钾、小剂量泼尼松(20 mg/d)及补钙等对症治疗,骨痛渐缓解,血钾恢复正常,病情好转出院.结论:干燥综合征起病隐匿,临床表现多种多样,易误诊或漏诊,出现肾脏损害时,多表现为远端肾小管酸中毒及低钾麻痹,严重者可出现肾钙化、肾结石及骨软化,应引起临床医生高度重视.

  14. Acid-Base and the Skeleton

    Bushinsky, David A.

    2008-09-01

    Chronic metabolic acidosis increases urine calcium (Ca) excretion in the absence of a concomitant increase in intestinal Ca absorption resulting in a net loss of total body. The source of this additional urine Ca is almost certainly the skeleton, the primary reservoir of body Ca. In vitro metabolic acidosis, modeled as a primary reduction in medium bicarbonate concentration, acutely (24 h) cell-mediated mechanisms predominate. In cultured neonatal mouse calvariae, acidosis-induced, cell-mediated Ca efflux is mediated by effects on both osteoblasts and osteoclasts. Metabolic acidosis inhibits extracellular matrix production by osteoblasts, as determined by measurement of collagen levels and levels for the non-collagenous matrix proteins osteopontin and matrix gla protein. Metabolic acidosis upregulates osteoblastic expression of RANKL (Receptor Activator of NFκB Ligand), an important osteoclastogenic and osteoclast-activating factor. Acidosis also increases osteoclastic activity as measured by release of β-glucuronidase, an enzyme whose secretion correlates with osteoclast-mediated bone resorption.

  15. Hjertestopbehandling. Nyere aspekter af kardiopulmonal genoplivning

    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 on...... account of hyperventilation and venous acidosis. No communications exist about the favourable effect of administration of bicarbonate during cardiac arrest. On the other hand, several conditions suggest that bicarbonate increases the intracellular acidosis with poorer possibilities for resuscitation with...

  16. Risk factors in patients surgically treated for peptic ulcer perforation

    Møller, Morten Hylander; Shah, Kamran; Bendix, Jørgen;

    2009-01-01

    Society of Anaesthesiologists) class, age, shock upon admission, preoperative metabolic acidosis, elevated concentration of creatinine upon admission, subnormal concentration of albumin upon admission and insufficient postoperative nutrition. CONCLUSIONS: Thus, preoperative metabolic acidosis, renal...... admission and preoperative metabolic acidosis are independently related to 30-day mortality could indicate that patients with peptic ulcer perforation are septic upon admission, and thus might benefit from a perioperative care protocol with early source control and early goal-directed therapy according to...

  17. Clinical and Virological Outcome of European Patients Infected With HIV

    2016-02-29

    HIV; Hepatitis B; Hepatitis C; AIDS; Coinfection; Cardiovascular Diseases; Diabetes Mellitus; Acidosis, Lactic; Renal Insufficiency; Fractures, Bone; End Stage Liver Disease; Kidney Failure, Chronic; Proteinuria

  18. Acid-base balance, dentinogenesis and dental caries:experimental studies in rats

    Bäckman, T. (Tuula)

    1999-01-01

    Abstract High-sucrose diet and metabolic acidosis have some similar effects on bone and they both reduce the formation of dentine. This series of experiments was conducted in order to get information about the effects of acidosis and alkalosis on dentine during primary dentinogenesis and also to ascertain if high-sucrose diet affects dentine formation via acidosis. Chronic metabolic acidosis (0.25 mol/L of NH4Cl in drinking water), chronic metabolic alkalosis (0.25 mol/L of NaHCO3 in drink...

  19. Nephrocalcinosis

    ... Bartter syndrome Chronic glomerulonephritis Familial hypomagnesemia Medullary sponge kidney Primary hyperoxaluria Renal transplant rejection Renal tubular acidosis Renal cortical necrosis Other possible ...

  20. Effects of hypercapnia and NO synthase inhibition in sustained hypoxic pulmonary vasoconstriction

    Ketabchi Farzaneh

    2012-01-01

    Full Text Available Abstract Background Acute respiratory disorders may lead to sustained alveolar hypoxia with hypercapnia resulting in impaired pulmonary gas exchange. Hypoxic pulmonary vasoconstriction (HPV optimizes gas exchange during local acute (0-30 min, as well as sustained (> 30 min hypoxia by matching blood perfusion to alveolar ventilation. Hypercapnia with acidosis improves pulmonary gas exchange in repetitive conditions of acute hypoxia by potentiating HPV and preventing pulmonary endothelial dysfunction. This study investigated, if the beneficial effects of hypercapnia with acidosis are preserved during sustained hypoxia as it occurs, e.g in permissive hypercapnic ventilation in intensive care units. Furthermore, the effects of NO synthase inhibitors under such conditions were examined. Method We employed isolated perfused and ventilated rabbit lungs to determine the influence of hypercapnia with or without acidosis (pH corrected with sodium bicarbonate, and inhibitors of endothelial as well as inducible NO synthase on acute or sustained HPV (180 min and endothelial permeability. Results In hypercapnic acidosis, HPV was intensified in sustained hypoxia, in contrast to hypercapnia without acidosis when HPV was amplified during both phases. L-NG-Nitroarginine (L-NNA, a non-selective NO synthase inhibitor, enhanced acute as well as sustained HPV under all conditions, however, the amplification of sustained HPV induced by hypercapnia with or without acidosis compared to normocapnia disappeared. In contrast 1400 W, a selective inhibitor of inducible NO synthase (iNOS, decreased HPV in normocapnia and hypercapnia without acidosis at late time points of sustained HPV and selectively reversed the amplification of sustained HPV during hypercapnia without acidosis. Hypoxic hypercapnia without acidosis increased capillary filtration coefficient (Kfc. This increase disappeared after administration of 1400 W. Conclusion Hypercapnia with and without acidosis

  1. Posterior spinal instrumented fusion for idiopathic scoliosis in patients with multisystemic neurodegenerative disorder: a report of two cases.

    Loh, K W; Chan, C Yw; Chiu, C K; Bin Hasan, M S; Kwan, M K

    2016-08-01

    Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) syndrome is a progressive multisystemic neurodegenerative disorder. MELAS syndrome impairs oxidative phosphorylation and predisposes patients to lactic acidosis, particularly under metabolic stress. We report 2 siblings with MELAS-associated idiopathic scoliosis who underwent posterior spinal instrumented fusion with measures taken to minimise anaesthetic and surgical stress, blood loss, and operating time. PMID:27574278

  2. Optic nerve pH and PO2

    Pedersen, Daniella B; Stefánsson, Einar; Kiilgaard, Jens Folke;

    2006-01-01

    how optic nerve pH (ONpH) and ONPO(2) are affected by: (1) carbonic anhydrase inhibition; (2) respiratory acidosis, and (3) metabolic acidosis. We measured ONpH with a glass pH electrode and ONPO(2) with a polarographic oxygen electrode. One of the electrodes was placed in the vitreous cavity 0.5 mm...

  3. Hyperchloremische metabole acidose bij een patiënt met een brickerlis

    Poppel, P.C.M. van; Stehouwer, C.D.A.; Beutler, J.J.; Korst, M.B.; Beerlage, H.P.; Hoogeveen, E.K.

    2009-01-01

    A 79-year-old male with a Bricker loop and chronic renal failure was admitted to hospital because progressive dyspnoea. This was due to severe hyperchloraemic metabolic acidosis. Hyperchloraemic acidosis can occur if urinary diversions are constructed from the colon or ileum. Contact between intesti

  4. Increased levels of inflammatory mediators in children with severe Plasmodium falciparum malaria with respiratory distress

    Awandare, Gordon A; Goka, Bamenla; Boeuf, Philippe;

    2006-01-01

    BACKGROUND: Respiratory distress (RD), a symptom of underlying metabolic acidosis, has been identified as a major risk factor for mortality in children with severe malaria in Africa, yet the molecular mediators involved in the pathogenesis of RD have not been identified. METHODS: We studied...... involved in the pathogenesis of the underlying metabolic acidosis....

  5. Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning

    Roberts, Darren M; Yates, Christopher; Megarbane, Bruno;

    2015-01-01

    to methanol: coma, seizures, new vision deficits, metabolic acidosis with blood pH ≤7.15, persistent metabolic acidosis despite adequate supportive measures and antidotes, serum anion gap higher than 24 mmol/L; or, serum methanol concentration 1) greater than 700 mg/L (21.8 mmol/L) in the context of...

  6. Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-Nitro-L-arginine induces cortical spreading ischemia when K+0+ is increased in the subarachnoid space

    Dreier, J.P.; Körner, K.; Ebert, Nathalie;

    1998-01-01

    Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)......Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)...

  7. Svaer metabolisk acidose hos en kronisk alkoholiker

    Sonne, Morten Egede; Rudolph, Søren Finnemann; Pott, Frank Christian

    2008-01-01

    Severe metabolic acidosis is associated with poor prognosis. We present a patient with profound alcohol and starvation-related combined lactic and keto acidosis (lactate = 29 mM; pH = 6.83) who made a good recovery following 18 hours of intensive care therapy. A brief summary of the proposed...... mechanism by which these metabolic derangements develop is presented....

  8. Hypokalemic rhabdomyolysis: an unusual presentation of Sjogren's syndrome

    Cherif, Eya; Ben Hassine, Lamia; Kechaou, Ines; Khalfallah, Narjess

    2013-01-01

    Hypokalaemic rhabdomyolysis represents a medical emergency requiring rapid diagnosis and appropriate aetiological treatment. Renal tubular acidosis is a common cause of hypokalemia which can be idiopathic or secondary to systemic disorders such as Sjogren's syndrome. It can remain asymptomatic or manifest with metabolic abnormalities including hypokalemia paralysis, hypocalcaemia and hyperchloremic metabolic acidosis. Rhabdomyolysis presenting with severe hypokalemia as the first manifestatio...

  9. Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule

    de Seigneux, Sophie; Malte, Hans; Dimke, Henrik;

    2007-01-01

    The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either ...

  10. Efeitos da correção da acidose metabólica com bicarbonato de sódio sobre o catabolismo protéico na insuficiência renal crônica The effects of the correction of metabolic acidosis with sodium bicarbonate on protein catabolism in chronic kidney failure

    Mafra, Denise; Burini, Roberto Carlos

    2001-01-01

    A desnutrição protéico-energética constitui problema comum aos pacientes com insuficiência renal crônica, influenciando diretamente na sua morbi-mortalidade. A acidose metabólica tem papel no catabolismo protéico, ativando a via proteolítica proteasoma-ubiquitina, dependente de adenosina trifosfato, e conjuntamente com glicocorticóides induz uma maior atividade na desidrogenase que degrada os aminoácidos de cadeia ramificada. Esta revisão teve como objetivo descrever o mecanismo pelo qual a a...

  11. Nursing Care of Continuous Renal Replacement Therapy in the Treatment of Hereditary Metabolic Disease with Acute Organic Acidosis%CRRT治疗遗传性代谢缺陷病合并重症有机酸血症的护理

    胡艳群; 李君

    2005-01-01

    采用连续性肾脏替代疗法(CRRT)治疗遗传性代谢缺陷病合并重症有机酸血症9例.结果患者各项生化及血气指标均较治疗前好转.提出连续监测生命体征,准确记录每小时出入量,严格配制置换液,预防感染,保持血管通路通畅等护理,是CRRT顺利进行的保证.

  12. Electrophysiological effects of amiodarone on pacemaker cells in guinea-pig left ventricular outflow tract under conditions of hypoxia, acidosis and treatment with epinephrine%胺碘酮对低O2、酸中毒及肾上腺素条件下豚鼠左心室流出道自律细胞电活动的影响

    赵兰平; 王雪芳; 陈彦静; 杜会博; 胡兴光; 季振慧

    2010-01-01

    目的:研究胺碘酮对豚鼠左心室流出道自律细胞电活动的影响以及胺碘酮对低O2、酸中毒和肾上腺素(EPI)所致该部位自律性改变的影响.方法:采用标准玻璃微电极细胞内电位记录技术,分别观测胺碘酮对豚鼠左心室流出道自发慢反应电位的影响,以及胺碘酮对无糖低氧、pH6.8和EPI导致的该电位改变的影响.结果:(1)0.1 μmol/L胺碘酮可使左心室流出道自发慢反应电位自发放电频率(RPF)减慢,最大舒张电位(MDP)绝对值减小,复极80%时间(APD80)延长(P<0.05);1 μmol/L胺碘酮可引起4相自动除极速度(VDD)和0相最大除极速度(Vmax)减慢,动作电位幅度(APA)减小,复极50%时间(APD50)延长(P<0.05),RPF减慢,MDP减小和APD80延长(P<0.01);10μmol/L胺碘酮可使VDD进一步减慢,APA进一步减小(P<0.01),其它指标的改变维持1 μmol/L胺碘酮灌流时的水平.(2)低O2可使VDD、RPF和Vmax减慢,MDP和APA减小,APD50缩短(P<0.05);和低O2组相比,1 μmol/L胺碘酮+低O2可使RPF和Vmax进一步减慢,MDP增大,APD80延长(P<0.05),VDD进一步减慢,APD50延长(P<0.01).(3)pH6.8的灌流液可使VDD和RPF减慢,APD80缩短(P<0.05),Vmax减慢,APA减小(P<0.01);与pH6.8组相比,pH6.8的1 μmol/L胺碘酮可使RPF进一步减慢,MDP和APA进一步减小,APD80延长(P<0.05),VDD进一步减慢,APD50延长(P<0.01).(4)10 μmol/L EPI可使VDD、RPF和Vmax加快,MDP增大,APD50和APD80缩短(P<0.05),APA增大(P<0.01);μmol/L胺碘酮+10 μmol/L EPI可使VDD和RPF减慢,MDP和APA减小,Vmax减慢,APD50和APD80延长(P<0.05,P<0.01).结论:胺碘酮可降低豚鼠左心室流出道的自律性,同时对低O2、酸中毒和EPI所致的该部位自律性改变有一定的影响.

  13. Atypical MR lenticular signal change in infantile isovaleric acidemia.

    Wani, Nisar A; Qureshi, Umer Amin; Jehangir, Majid; Ahmad, Kaiser; Hussain, Zahid

    2016-01-01

    Isovaleric acidemia (IVA) is an inborn error of branched chain amino acid metabolism that may manifest as acute neonatal metabolic acidosis or as chronic intermittent form with developmental delay or recurrent episodes of acute metabolic acidosis. Early diagnosis is the key to prevent morbidity and mortality. Brain imaging abnormalities are rarely described in IVA. We report a case of chronic intermittent IVA with acute presentation in a 4-month-old infant who presented with acute metabolic acidosis. Brain magnetic resonance imaging (MRI) revealed symmetric signal intensity changes in bilateral lentiform nuclei with an unreported T1-weighted (T1W) symmetric hyperintense ring-like appearance in bilateral putamen. PMID:27081237

  14. [Hypokalemic paralysis revealing Sjögren's syndrome associated with auto-immune thyroiditis].

    Baaj, Mohamed; Safi, Somaya; Hassikou, Hassna; Tabache, Fatima; Mouden, Karim; Hadri, Larbi

    2010-02-01

    We report a case of 36-year-old woman, admitted for hypotonic tetraparesis. Laboratory tests revealed severe hypokalaemia, acidosis, hyperchloremia and alkaline urinary pH allowing the diagnosis of distal tubular acidosis. Additional investigations led to the diagnosis of primary Sjögren's syndrome associated with Hashimoto's thyroïditis. The evolution was favorable under potassium citrate alkalinisation, the corticosteroid therapy and hormonal substitution. Based on this observation, the pathogenesis of distal tubular acidosis during auto-immune diseases (Sjögren's syndrome, monoclonal hypergammaglobulinemia, hypothyroidism) was discussed as well as its consequences and management. PMID:19836323

  15. Citric acid urine test

    ... usually done while you are on a normal diet. Ask your provider for more information. ... acidosis and a tendency to form calcium kidney stones. The ... acid levels: A high carbohydrate diet Estrogen therapy Vitamin D

  16. Changes in plasma potassium concentration during carbon dioxide pneumoperitoneum

    Perner, A; Bugge, K; Lyng, K M;

    1999-01-01

    to either carbon dioxide pneumoperitoneum or abdominal wall lifting for laparoscopic colectomy. Despite an increasing metabolic acidosis, prolonged carbon dioxide pneumoperitoneum resulted in only a slight increase in plasma potassium concentrations, which was both statistically and clinically...

  17. 21 CFR 201.80 - Specific requirements on content and format of labeling for human prescription drug and...

    2010-04-01

    ... metabolic or pharmacokinetic data in humans are unavailable, the labeling shall contain a statement about... delayed acidosis). (3) Oral LD50 of the drug in animals; concentrations of the drug in biologic...

  18. The intracellular to extracellular proton gradient following maximal whole body exercise and its implication for anaerobic energy production

    Voiantis, Stefanos; Secher, Niels H.; Quistorff, Bjørn

    2010-01-01

    intracellular acidosis and the decrease in PCr is that the anaerobic contribution to energy metabolism during maximal rowing corresponds to 4.47 ± 1.8 L O2, a value similar to that defined as the “accumulated oxygen deficit”. In conclusion, during maximal rowing the intracellular acidosis, expressed as proton......Maximal exercise elicits systemic acidosis where venous pH can drop to 6.74 and here we assessed how much lower the intracellular value (pHi) might be. The wrist flexor muscles are intensively involved in rowing and 31P-magnetic resonance spectroscopy allows for calculation of forearm pHi and...... concentration, surpasses ~4-fold the intravascular acidosis, while the resting gradient is ~2....

  19. Disease: H00473 [KEGG MEDICUS

    Full Text Available opathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome. Pharmacotherapy 30:1179-...ine therapy: pathophysiology of stroke-like episodes. Ann N Y Acad Sci 1201:104-10 (2010) PMID:21871538 Cosk

  20. Hipoglicemia neonatal: Un caso de galactosemia

    Bermúdez M.; Arteaga C.; Cifuentes Y.

    2001-01-01

    Se presenta la historia clínica de un recien nacido con un cuadro de hipoglicemia, que posteriormente desarrolla hiperbilirrubinemia conjugada, hepatomegalia, acidosis metabólica con anion gap aumentado y lactato normal e infeccion por E. coli

  1. METABOLISM, HEALTH AND EFFICIENCY OF COWS AT DIFFERENT LEVEL IN THE DIET OF CONCENTRATES IN THE TRANSITION PERIOD Обмен веществ, здоровье и продуктивность коров при разном уровне в рационе концентратов в переходный период

    Ryadchikov V. G.; Shlaychova O. G.; Dubinina D. P.; Sein T. A.

    2012-01-01

    In this article, we discussed the problems of the metabolic disease of cows in peripartum period and profitability of the consequent lactation. The article has materials about adaptation in postpartum and arise ketosis, acidosis, laminit and reproductively reasons

  2. Mucormycosis

    ... Long-term steroid use Metabolic acidosis Poor nutrition (malnutrition) Use of some medicines Mucormycosis may involve: A ... medicine. Outlook (Prognosis) Mucormycosis has an extremely high death rate, even when aggressive surgery is done. Risk ...

  3. Ribosome profiling reveals features of normal and disease-associated mitochondrial translation

    Rooijers, K.; Loayza-Puch, F.; Nijtmans, L.G.J.; Agami, R.

    2013-01-01

    Mitochondria are essential cellular organelles for generation of energy and their dysfunction may cause diabetes, Parkinson's disease and multi-systemic failure marked by failure to thrive, gastrointestinal problems, lactic acidosis and early lethality. Disease-associated mitochondrial mutations oft

  4. Rumen Microbiome Composition Determined Using Two Nutritional Models of Subacute Ruminal Acidosis▿

    Khafipour, Ehsan; Li, Shucong; Plaizier, Jan C.; Krause, Denis O

    2009-01-01

    Subacute ruminal acidosis (SARA) is a metabolic disease in dairy cattle that occurs during early and mid-lactation and has traditionally been characterized by low rumen pH, but lactic acid does not accumulate as in acute lactic acid acidosis. It is hypothesized that factors such as increased gut permeability, bacterial lipopolysaccharides, and inflammatory responses may have a role in the etiology of SARA. However, little is known about the nature of the rumen microbiome during SARA. In this ...

  5. Hashimoto Thyroiditis and Nephrocalcinosis in a Child with Down Syndrome

    Spahiu, Lidvana; Jashari, Haki; Mulliqi-Kotori, Vjosa; Elezi-Rugova, Blerta; Merovci, Besart

    2016-01-01

    Introduction: Hypothyroidism has been reported to affect renal function and structure. However, the association of hypothyroidism with distal renal tubular acidosis (dRTA) is rarely reported in children. Case Presentation: We present a 6-year-boy with Down syndrome admitted in our department due to vomiting, weakness, polyuria, polydipsia, irritability and weight loss in the last few weeks. Investigations revealed features of hypokalemia, metabolic acidosis and alkaline urine consistent with ...

  6. Hyperkalaemic quadriparesis secondary to chronic diclofenac treatment

    Patel, P; Mandal, B.; Greenway, M

    2001-01-01

    A 76 year old woman presented with a quadriparesis associated with hyperkalaemia. She had a 10 month history of treatment with oral diclofenac sodium. On admission she had hyperkalaemic metabolic acidosis with a normal anion gap and mild renal impairment. Her weakness resolved after withdrawal of diclofenac and medical correction of her hyperkalaemia. Non-steroidal anti-inflammatory drugs are known to cause hyperkalaemic acidosis and should be used with caution, especially in the presence of ...

  7. Ocular and skin manifestations in systemic pseudohypoaldosteronism

    Eliwa, Mahmoud Salah; El-Emmawie, Aymen Hussein; Saeed, Mahmood Ahmad

    2014-01-01

    Pseudohypoaldosteronism type-1 is a rare disorder characterised by end-organ resistance to aldosterone resulting in salt-losing crisis with hyponatraemic dehydration, hyperkalaemia and metabolic acidosis. We report two siblings with pseudohypoaldosteronism type-1 who presented early in neonatal period with hyponatraemia, severe hyperkalaemia and metabolic acidosis. Both babies had miliaria like skin rash which flared up during episodes of hyperkalaemia and hyponatraemia. They had visible dila...

  8. Hyperkalaemia induced by carbonic anhydrase inhibitor.

    Wakabayashi, Y.

    1991-01-01

    An 81-year-old man developed hyperkalaemic and hyperchloraemic metabolic acidosis following treatment with a carbonic anhydrase inhibitor for his glaucoma. He had mild renal failure and selective aldosterone deficiency was confirmed. In this case the treatment did not lead to hypokalaemia because of the limited potassium secretory capacity in the renal tubules from selective aldosterone deficiency; rather, it may have led to hyperkalaemia because metabolic acidosis induced by the carbonic anh...

  9. Hypokalemic paralysis associated with cystic disease of the kidney: case report

    Jayasinghe Saroj; Rodrigo Chaturaka; Gamakaranage Champika SSSK; Rajapakse Senaka

    2011-01-01

    Abstract Background Severe hypokalemia is known to cause muscle paralysis, and renal tubular acidosis is a recognized cause. Cystic disease of the kidney is associated with severe hypokalemia. Case presentation We report a 33-year-old male patient who presented with generalized limb weakness caused by severe hypokalemia due to renal tubular acidosis, who was found to have renal medullary cysts. Conclusion The association of cystic renal disease with hypokalemia, and the possible pathophysiolo...

  10. RENAL TUBULER ASİDOZA BAĞLI AĞIR HİPOPOTASEMİ VE SOLUNUM ARRESTİ İLE ORTAYA ÇIKAN BİR PRİMER SJÖGREN SENDROMU OLGUSU

    BAVUNOĞLU TÜFEKÇİ, Işıl; TUNÇKALE, Aydın; YİRMİBEŞÇİK, Sibel; AYATA, Ebru; Karter, Yesari; ÖZTÜRK, Esin; DOĞUSOY, Gülen

    2014-01-01

    Background.- Sjögren’s syndrome (SS) is an autoimmune exocrinopathy that involves both glandular and extraglandular systems. This disease may cause hypokalemic quadriparalysis due to distal renal tubuler acidosis (RTA).Observation.- We report here a 19-year-old girl who presented with life-threatening hypokalemic paralysis requiring admission to an intensive care unit. Biochemical investigations showed severe hypokalemia with hyperchloremic metabolic acidosis, a spot urine pH of 6.8, and a po...

  11. Renal ammonia excretion in response to hypokalemia: effect of collecting duct-specific Rh C glycoprotein deletion

    Lee, Hyun-Wook; Verlander, Jill W.; Bishop, Jesse M.; Handlogten, Mary E.; Han, Ki-Hwan; Weiner, I. David

    2012-01-01

    The Rhesus factor protein, Rh C glycoprotein (Rhcg), is an ammonia transporter whose expression in the collecting duct is necessary for normal ammonia excretion both in basal conditions and in response to metabolic acidosis. Hypokalemia is a common clinical condition associated with increased renal ammonia excretion. In contrast to basal conditions and metabolic acidosis, increased ammonia excretion during hypokalemia can lead to an acid-base disorder, metabolic alkalosis, rather than mainten...

  12. 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

    Olga Lucía Morales Múnera; Juan Camilo Villada Valencia; Ivan Dario Flórez Gómez; Nicolas Guillermo Pineda Trujillo

    2013-01-01

    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, hypo...

  13. A60

    A. Shihlyarova

    2015-11-01

    Conclusion: Modulating abnormalities in energy metabolism due to metabolic acidosis of tumor microenvironment on the background of systemic chemotherapy, one can achieve activation of additional pathogenetic mechanisms of inhibition of tumor growth and tumor cell death. It is necessary to emphasize the importance of the further search for factors of pathogenetic mechanisms and therapy of the influence on the tumor, including the modulation of acidosis of peritumoraly area that opens up new perspectives in solving this problem.

  14. The Effect of CO2-Pneumoperitoneum on Ventilation Perfusion Distribution of the Lung

    Strang, Christof

    2011-01-01

    Laparoscopic operations are a common and popular way for abdominal procedures. They are usually performed by insufflation of carbon dioxide (CO2) into the abdominal cavity. However, insufflation of CO2 may interfere with cardiac and circulatory as well as respiratory functions. The CO2-pneumoperitoneum (PP) may cause hypercarbia and acidosis. The direct effects of CO2 and acidosis lead to decreased cardiac contractility, sensitization of the myocardium to arrhythmogenic effects of catecholami...

  15. Predictive Value of Capnography for Suspected Diabetic Ketoacidosis in the Emergency Department

    Soleimanpour, Hassan; Taghizadieh, Ali; Niafar, Mitra; Rahmani, Farzad; Golzari, Samad EJ; Mehdizadeh Esfanjani, Robab

    2013-01-01

    Introduction: Metabolic acidosis confirmed by arterial blood gas (ABG) analysis is one of the diagnostic criteria for diabetic ketoacidosis (DKA). Given the direct relationship between end-tidal carbon dioxide (ETco2), arterial carbon dioxide (PaCO2) and metabolic acidosis, measuring ETco2 may serve as a surrogate for ABG in the assessment of possible DKA. The current study focuses on the predictive value of capnography in diagnosing DKA in patients referring to the emergency department (ED) ...

  16. Identification of peripartum near-miss for perinatal audit

    Kerkhofs, C; De Bruyn, C.; Mesens, T.; Theyskens, C.; Vanhoestenberghe, M.; E. Bruneel; Van Holsbeke, C; Bonnaerens, A.; Gyselaers, W.

    2014-01-01

    Introduction: Today, perinatal audit focuses basically on cases of perinatal mortality. In most centres in Western Europe, perinatal mortality is low. Identification of metabolic acidosis at birth may increase index cases eligible for evaluation of perinatal care, and this might improve quality of perinatal audit. The aim of this study is to assess the incidence of metabolic acidosis at birth in order to estimate its impact on perinatal audit. Patients and Methods: Cord blood was analysed for...

  17. Extracellular proton depression of peak and late Na+ current in the canine left ventricle

    Murphy, Lisa; Renodin, Danielle; Antzelevitch, Charles; Di Diego, José M.; Cordeiro, Jonathan M.

    2011-01-01

    Cardiac ischemia reduces excitability in ventricular tissue. Acidosis (one component of ischemia) affects a number of ion currents. We examined the effects of extracellular acidosis (pH 6.6) on peak and late Na+ current (INa) in canine ventricular cells. Epicardial and endocardial myocytes were isolated, and patch-clamp techniques were used to record INa. Action potential recordings from left ventricular wedges exposed to acidic Tyrode solution showed a widening of the QRS complex, indicating...

  18. Simple Diagnostic Tests to Detect Toxic Alcohol Intoxications

    Shin, Jai Moo; Sachs, George; Kraut, Jeffrey A.

    2008-01-01

    Methanol, ethylene glycol, and diethylene glycol intoxications can produce visual disturbances, neurological disturbances, acute renal failure, pulmonary dysfunction, cardiac dysfunction, metabolic acidosis, and death. Metabolic acidosis and an increased serum osmolality are important clues to their diagnosis. The former reflects the organic acids produced by metabolism of the parent alcohol, while the latter is due to accumulation of the offending alcohol. However, neither the clinical nor t...

  19. Behandling af metforminassocieret laktatacidose med hæmodialyse

    Schousboe, K.; Rasmussen, K.; El Fassi, D.;

    2012-01-01

    Metformin-associated lactate acidosis is rare but serious and characterized by metabolic acidosis and elevated lactate. We describe a single-institution experience of four cases in one year. Despite pH levels of 6.85 to 7.12 and lactate levels of 11-28 mmol/l three of the patients survived. Two o...... the patients had normal kidney function previous to hospitalization. Treatment includes fluid replacement, IV sodium bicarbonate and haemodialysis....

  20. Renal hücreli karsinom tanılı bir olguda tekrarlayan hiperkalemi atakları

    A. ALP; Akdam, H.; Ünsal, A; Uyanık, Ö; Ayhan, M; Çulhacı, N; Akar, H.; Yeniçerioğlu, Y

    2014-01-01

    Hyperkalemia is one of the most urgent entities in clinical practice. The importance of hyperkalemia arises from its cardiovascular effects that can be mortal. Relapsing hyperkalemia is rare and usually associated with renal disorders. Renal tubular acidosis is one of them. Although Type 4 renal tubular acidosis is generally associated with diabetes mellitus, this entity also may accompanied by other disorders. Renal cell carcinoma is the most common type of kidney cancer in adults and recent...

  1. Bone Disease in Medullary Sponge Kidney and Effect of Potassium Citrate Treatment

    Fabris, Antonia; Bernich, Patrizia; Abaterusso, Cataldo; Marchionna, Nicola; Canciani, Chiara; Nouvenne, Antonio; Zamboni, Mauro; Lupo, Antonio; Gambaro, Giovanni

    2009-01-01

    Background and objectives: In medullary sponge kidney (MSK)—a common malformative renal condition in patients with calcium nephrolithiasis—hypercalciuria, incomplete distal renal tubular acidosis, and hypocitraturia are common. Clinical conditions with concomitant hypercalciuria and/or incomplete distal renal tubular acidosis are almost invariably associated with bone disease, making osteopathy highly likely in MSK, too. Patients with MSK have never been investigated for osteopathy; neither h...

  2. Brinzolamide-induced retinopathy in neonatal rats: an alternative animal model of retinal neovascularization

    DYOMIN, Y. A.; BILETSKA, P.V.; GAPUNIN, I. D.

    2014-01-01

    Background and Purpose: Neovascular retinal pathology is steel uncertain. Thus, there is great need to investigate new modeling, diagnostic and treatment technologies. Brinzolamide induces a metabolic acidosis via an alternative biochemical mechanism (bicarbonate loss). In the present study the influence of brinzolamide-induced acidosis on preretinal neovascularization in neonatal rat was investigated. Materials and Methods. In our study we used newborn Wistar rats raised in two litter...

  3. Interpreting the Consequences of Metformin Accumulation in an Emergency Context: Impact of the Time Frame on the Blood Metformin Levels

    Jean-Daniel Lalau

    2014-01-01

    Full Text Available Objective. To clarify the link between metformin accumulation and its metabolic consequences by taking the time frame for metformin measurement into account. Research Design and Methods. Our database was studied for cases of metformin accumulation and lactic acidosis status available on admission, and then we selected patients in whom arterial pH, blood lactate, and plasma and erythrocyte metformin levels had been determined at the same time point. Results. Seventeen reports were studied on 16 patients, of whom 10 presented lactic acidosis. The time interval between admission and comprehensive testing ranged from 0 to 52 hours. The study parameters were determined simultaneously on admission in only 4 patients. In the 9 patients with lactic acidosis on admission and a delayed metformin assay, lactic acidosis persisted in 6 cases and had resolved in 3 cases by the time the blood sampling for metformin assay was performed. Conversely, lactic acidosis developed after admission in one case. Conclusions. Caution must be taken when interpreting the consequences of metformin accumulation in an emergency context: the patient’s lactic acidosis status will have changed by the time the metformin assay is performed, even though metformin accumulation may still be present.

  4. Acidic environment leads to ROS-induced MAPK signaling in cancer cells.

    Anne Riemann

    Full Text Available Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e, pH(i and mitogen-activated-protein-kinases (ERK1/2, p38 was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furthermore, p38 phosphorylation was elicited by sole intracellular lactacidosis at normal pH(e. Inhibition of ERK1/2 phosphorylation during acidosis led to necrotic cell death. No evidence for the involvement of the kinases c-SRC, PKC, PKA, PI3K or EGFR nor changes in cell volume in acidosis-induced MAPK activation was obtained. However, our data reveal that acidosis enhances the formation of reactive oxygen species (ROS, probably originating from mitochondria, which subsequently trigger MAPK phosphorylation. Scavenging of ROS prevented acidosis-induced MAPK phosphorylation whereas addition of H(2O(2 enhanced it. Finally, acidosis increased phosphorylation of the transcription factor CREB via p38, leading to increased transcriptional activity of a CRE-reporter even 24 h after switching the cells back to a normal environmental milieu. Thus, an acidic tumor microenvironment can induce a longer lasting p38-CREB-medited change in the transcriptional program, which may maintain the altered phenotype even when the cells leave the tumor environment.

  5. Con: Higher serum bicarbonate in dialysis patients is protective.

    Chauveau, Philippe; Rigothier, Claire; Combe, Christian

    2016-08-01

    Metabolic acidosis is often observed in advanced chronic kidney disease, with deleterious consequences on the nutritional status, bone and mineral status, inflammation and mortality. Through clearance of the daily acid load and a net gain in alkaline buffers, dialysis therapy is aimed at correcting metabolic acidosis. A normal bicarbonate serum concentration is the recommended target in dialysis patients. However, several studies have shown that a mild degree of metabolic acidosis in patients treated with dialysis is associated with better nutritional status, higher protein intake and improved survival. Conversely, a high bicarbonate serum concentration is associated with poor nutritional status and lower survival. It is likely that mild acidosis results from a dietary acid load linked to animal protein intake. In contrast, a high bicarbonate concentration in patients treated with dialysis could result mainly from an insufficient dietary acid load, i.e. low protein intake. Therefore, a high pre-dialysis serum bicarbonate concentration should prompt nephrologists to carry out nutritional investigations to detect insufficient dietary protein intake. In any case, a high bicarbonate concentration should be neither a goal of dialysis therapy nor an index of adequate dialysis, whereas mild acidosis could be considered as an indicator of appropriate protein intake. PMID:27411724

  6. Carbon dioxide in the critically ill: too much or too little of a good thing?

    Marhong, Jonathan; Fan, Eddy

    2014-10-01

    Hypercapnia and hypocapnia commonly complicate conditions that are present in critically ill patients. Both conditions have important physiologic effects that may impact the clinical management of these patients. For instance, hypercapnia results in bronchodilation and enhanced hypoxic vasoconstriction, leading to improved ventilation/perfusion matching. Hypocapnia reduces cerebral blood volume through arterial vasoconstriction. These effects have also been exploited for therapeutic aims. In patients with traumatic brain injury (TBI), hypocapnia is often utilized to control intracranial pressure. However, this effect is not sustained, and prolonged hypocapnia increases the risk of mortality and severe disability in patients with TBI. Hypercapnia and hypercapnic acidosis are common consequences of lung-protective ventilation in ARDS. Hypercapnic acidosis reduces ischemic lung injury and preserves lung compliance, but concern has arisen over hypercapnia-induced immunosuppression and the potential for bacterial proliferation in sepsis. Experimental studies suggest that buffering hypercapnic acidosis attenuates these effects, whereas hypocapnia appears to potentiate lung injury through increased capillary permeability and decreased lung compliance. Several areas of uncertainty surround the role of hypercapnia/hypocapnia in treating TBI and ARDS. Current data support recommendations to avoid hypocapnia in treating TBI, with the exception of emergent treatment of elevated intracranial pressure, while awaiting definitive management. Permissive hypercapnia is commonly accepted as a consequence of lung-protective ventilation in ARDS, but there is insufficient evidence to support the induction of hypercapnic acidosis in clinical practice. Buffering hypercapnic acidosis should be considered only for a specific clinical indication (eg, hemodynamic instability). For clinicians choosing to buffer hypercapnic acidosis, tris-hydroxymethyl aminomethane is recommended over sodium

  7. Control of lipid oxidation during exercise: role of energy state and mitochondrial factors

    Sahlin, K; Harris, R C

    2008-01-01

    and CHO oxidation and relative fuel utilization is mainly controlled by substrate availability and the capacity of the metabolic pathways. In the high-intensity domain (>60%VO(2max)) there is a pronounced decrease in energy state, which will stimulate glycolysis in excess of the substrate requirements...... of the oxidative processes. This will lead to acidosis, reduced levels of free Coenzyme A (CoASH) and reduced levels of free carnitine. Acidosis and reduced carnitine may limit the carnitine-mediated transfer of long-chain fatty acids (LCFA) into mitochondria and may thus explain the observed...

  8. Clinical, haematological and biochemical findings in milk-fed calves with chronic indigestion.

    Stocker, H; Lutz, H; Rüsch, P

    1999-09-11

    The principal clinical signs in 59 milk-fed calves with chronic indigestion were general malaise and depression, poor appetite, poor body condition, dehydration, a dull and scaly hair coat, alopecia and clay-like faeces. All the calves had metabolic acidosis, which was associated with an inability to stand up in more than half of them. There were significant differences in the severity of acidosis between the calves that could stand and those that could not. Other signs in some of the calves were dehydration, leucocytosis, and increased activities of liver enzymes. PMID:10515617

  9. Nutritional Strategies to Modulate Intracellular and Extracellular Buffering Capacity During High-Intensity Exercise

    Lancha Junior, Antonio Herbert; de Salles Painelli, Vitor; Saunders, Bryan; Artioli, Guilherme Giannini

    2015-01-01

    Intramuscular acidosis is a contributing factor to fatigue during high-intensity exercise. Many nutritional strategies aiming to increase intra- and extracellular buffering capacity have been investigated. Among these, supplementation of beta-alanine (~3–6.4 g/day for 4 weeks or longer), the rate-limiting factor to the intramuscular synthesis of carnosine (i.e. an intracellular buffer), has been shown to result in positive effects on exercise performance in which acidosis is a contributing fa...

  10. Differential uptake of Tc-99m DMSA and Tc-99m EC in renal tubular disorders: Report of two cases and review of the literature

    Tc-99m DMSA and Tc-99m EC studies are invaluable functional imaging modalities for renal structural and functional assessment. Normally, the relative renal function estimated by the two methods correlates well with each other. We here present two patients with renal tubular acidosis who showed impaired/altered DMSA uptake with normal EC renal dynamic study depicting the pitfall of DMSA imaging in tubular disorders. The two presented cases also depict distinct pattern of Tc-99m DMSA scintigraphic findings in patients with proximal and distal renal tubular acidosis, thus highlighting the factors affecting DMSA kinetics

  11. Comparison of Rumen Fluid pH by Continuous Telemetry System and Bench pH Meter in Sheep with Different Ranges of Ruminal pH

    2014-01-01

    We aimed to compare the measurements of sheep ruminal pH using a continuous telemetry system or a bench pH meter using sheep with different degrees of ruminal pH. Ruminal lactic acidosis was induced in nine adult crossbred Santa Ines sheep by the administration of 15 g of sucrose per kg/BW. Samples of rumen fluid were collected at the baseline, before the induction of acidosis (T 0) and at six, 12, 18, 24, 48, and 72 hours after the induction for pH measurement using a bench pH meter. During ...

  12. Stimulation of Na+ transport by stress protein and by its inhibitors by sheep maw epithelium

    Stress proteins - 'Heat shock proteins' (Hsp) are formed during sublethal stress and other impulses, and can play an important role in protecting the functions of sheep maw epithelium, such as transport of minerals and development of the epithelium itself. The paper is aimed at assessing the protective mechanism of Hsp originated during returning to the original state from temporary acidosis of sheep maw epithelium. The aim was to determine the activity of the Na+/H+ exchanger, which was affected by the expression of Hsp70 in ruminal acidosis by the method of radioactive indication. (authors)

  13. Metformin poisoning: which therapy?

    Ivo Casagranda

    2006-12-01

    Full Text Available Lactic acidosis is a rare but serious adverse effect in metformintreated- patients. The authors report a case of metformin-associated lactic acidosis and discuss the appropriated therapy. The patient was treated with bicarbonate iv and with two short dialysis session, also because of acute renal failure. Many authors do not agree with using bicarbonate, and about hemodialysis some authors suggest that the session should go on at least 12 hours. In this case the use of bicarbonate and short hemodialysis determinated a favourable outcame.

  14. quadriparesis in sjogren syndrome.

    nikhil srivastva

    2015-06-01

    Full Text Available Hypokalemic paralysis is a well recognised clinical presentation of Primary sjogren syndrome that occurs due to renal potassium loss caused by interstitial nephritis. However we report a case where a hypokalemic paralysis in a suspected case of sjogren syndrome was associated with high anion gap metabolic acidosis in the presence of a near normal Glomerular filtration rate (RTA and a failure to acidify urine pH 5.5 in the presence of systemic acidosis. [Natl J Med Res 2015; 5(2.000: 161-162

  15. Hypokalemic paralysis associated with cystic disease of the kidney: case report

    Jayasinghe Saroj

    2011-04-01

    Full Text Available Abstract Background Severe hypokalemia is known to cause muscle paralysis, and renal tubular acidosis is a recognized cause. Cystic disease of the kidney is associated with severe hypokalemia. Case presentation We report a 33-year-old male patient who presented with generalized limb weakness caused by severe hypokalemia due to renal tubular acidosis, who was found to have renal medullary cysts. Conclusion The association of cystic renal disease with hypokalemia, and the possible pathophysiological basis of the development of renal cysts in patients with severe hypokalemia, are discussed.

  16. Cetoacidosis alcohólica y complicaciones neurológicas reversibles de la hipofosfatemia Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia

    M.ª T. Fernández López

    2012-06-01

    Full Text Available Un paciente varón de 57 años alcohólico ingresó en nuestro hospital por alteración del nivel de conciencia y polirradiculitis. En el estudio analítico aparecía acidosis metabólica, hipopotasemia e hipofosfatemia. La cetoacidosis alcohólica es frecuente en estos pacientes. Todos ellos se presentan con una historia de abuso del alcohol, con cese del consumo los días previos por la aparición de náuseas, vómitos y dolor abdominal. Los datos básicos de laboratorio son: glucemia normal o baja, acidosis metabólica con anión GAP elevado, ausencia de alcohol en sangre y cetonuria. Los mayores peligros son la hipovolemia, hipopotasemia, hipoglucemia y acidosis. El abuso del alcohol puede provocar un amplio rango de trastornos electrolíticos y del equilibrio ácido-base, incluyendo hipofosfatemia, hipomagnesemia, hipocalcemia, hipopotasemia, acidosis metabólica y alcalosis respiratoria. El deterioro del nivel de conciencia puede observarse en relación con intoxicación etílica aguda, encefalopatía de Wernicke, síndrome de abstinencia, mielinolisis central pontina, encefalopatía hepática, hipoglucemia y trastornos electrolíticos.A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including

  17. Therapeutic plasma exchange as treatment for propofol infusion syndrome.

    Levin, Phillip D; Levin, Valentin; Weissman, Charles; Sprung, Charles L; Rund, Deborah

    2015-10-01

    Propofol infusion syndrome (PRIS), a rare complication of propofol sedation, is associated with high mortality. There is no specific therapy. A 16-year-old with head injury and status epilepticus is described. Three days after seizure resolution, whilst receiving propofol, he developed severe lactic acidosis, rhabdomyolysis, and hemodynamic instability. Suspected PRIS was treated with a single session of therapeutic plasma exchange (TPE). This was associated with immediate improvement in hemodynamic status, resolution of lactic acidosis within 24 h, normalization of CPK over 10 days, and a subsequent full recovery. TPE is suggested as a novel therapy for PRIS. PMID:25619501

  18. MLASA SYNDROME: A CASE REPORT

    R. Fallah

    2007-02-01

    Full Text Available AbstractMitochondrial myopathy, lactic acidosis, and sideroblastic anemia (MLASA syndrome is a rare autosomal recessive disorder of oxidative phosphorylation and iron metabolism. The association between myopathy and sideroblastic anemia was initially reported in 1974. Here we report an 8.5 year old boy with normal cognitive function, suffering from chronic progressive weakness in his lower extremities, inability to walk and palor. Microcytic sideroblastic anemia, mild lactic acidosis and inflammatory myopathy (myositis in muscle biopsy was detected and treated; the response to corticosteroid therapy and rehabilitation was excellent and the patient was ambulatory after four months.

  19. Acid-induced changes of brain protein buffering

    Kraig, Richard P.; Wagner, Robert J.

    1987-01-01

    Excessive cellular acidosis is thought to enhance destruction of brain from ischemia. Protein denaturation may contribute to such injury although the behavior of brain proteins to acidosis is poorly defined. As a first approach to detect acid-induced changes in brain proteins and to characterize buffer content, homogenates were acidified for 20 min (as low as pH 3.1), returned to baseline pH (6.9), and then titrated. Titration curves show a significant (P < 0.0001) and permanent increase in b...

  20. Optic nerve pH and PO2

    Pedersen, Daniella B; Stefánsson, Einar; Kiilgaard, Jens Folke;

    2006-01-01

    Earlier studies have demonstrated that carbonic anhydrase inhibitors (CAIs) increase optic nerve oxygen tension (ONPO(2)) in pigs. We hypothesized that the mechanism of this effect was either a CO(2) increase or a pH decrease in tissue and blood. To test this hypothesis we investigated and compared...... how optic nerve pH (ONpH) and ONPO(2) are affected by: (1) carbonic anhydrase inhibition; (2) respiratory acidosis, and (3) metabolic acidosis. We measured ONpH with a glass pH electrode and ONPO(2) with a polarographic oxygen electrode. One of the electrodes was placed in the vitreous cavity 0.5 mm...

  1. Metabolic studies of transient tyrosinemia in premature infants

    Fernbach, S. A.; Summons, R. E.; Pereira, W. E.; Duffield, A. M.

    1975-01-01

    The recently developed technique of gas chromatography-mass spectrometry supported by computer has considerably improved the analysis of physiologic fluids. This study attempted to demonstrate the value of this system in the investigation of metabolite patterns in urine in two metabolic problems of prematurity, transient tyrosinemia and late metabolic acidosis. Serial 24-hr urine specimens were analyzed in 9 infants. Transient tyrosinemia, characterized by 5- 10-fold increases over basal excretion of tyrosine, p-hydroxyphenyllactate, and p-hydroxyphenylpyruvate in urine, was noted in five of the infants. Late metabolic acidosis was seen in four infants, but bore no relation to transient tyrosinemia.

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

    Nijenhuis, T.; Renkema, K.Y.R.; 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

  3. "Herbal remedy is natural and safe"--truth or myth?

    Meeran, Mohammed; Murali, A; Balakrishnan, R; Narasimhan, Denesh

    2013-11-01

    Neem oil is often used externally as a traditional medicine in India. Its ingestion, even in small doses produces toxic effects like severe metabolic acidosis, seizures, renal failure and encephalopathy. Management is supportive and prognosis is generally good but fatalities may occur. Herein we report an unusual case of neem oil toxicity in a previously normal adult. PMID:24974507

  4. No effect of bicarbonate treatment on insulin sensitivity and glucose control in non-diabetic older adults

    Chronic mild metabolic acidosis is common among older adults, and limited evidence suggests that it may contribute to insulin resistance and type 2 diabetes. This analysis was conducted to determine whether bicarbonate supplementation, an alkalinizing treatment, improves insulin sensitivity or gluco...

  5. A dynamic mechanistic model of lactic acid metabolism in the rumen

    Mills, J.A.N.; Crompton, L.A.; Ellis, J.L.; Dijkstra, J.; Bannink, A.; Hook, S.E.; Benchaar, C.; France, J.

    2014-01-01

    Current feed evaluation systems for ruminants are too imprecise to describe diets in terms of their acidosis risk. The dynamic mechanistic model described herein arises from the integration of a lactic acid (La) metabolism module into an extant model of whole-rumen function. The model was evaluated

  6. Hemlock water dropwort poisoning.

    Ball, M J; Flather, M. L.; Forfar, J C

    1987-01-01

    Severe plant poisoning is relatively uncommon in adults. We report two adults who ingested hemlock water dropwort roots, having mistaken them for wild parsnip. One developed prolonged convulsions, severe metabolic acidosis and respiratory distress requiring mechanical ventilation. The toxin--oenanthotoxin--was detected in the gastric aspirate and measured by high performance liquid chromatography.

  7. Enfermedad de Von Gierke: Reporte de tres casos

    Echeverri O.

    2001-06-01

    Full Text Available La enfermedad de Von Gierke es un defecto en la glucosa 6 fosfatasa, degrada el glucógeno en el hígado, riñón e intestino. Asociada con hipoglicemia, acidosis láctica e hiperuricemia.

  8. Renal response to acute acid loading--an organ physiological approach

    Osther, P J; Engel, K; Kildeberg, P

    2004-01-01

    OBJECTIVE: In previous studies of the renal response to acute NH4Cl acidosis no correlation was found between systemic acid-base status and the traditionally used quantity, renal net acid excretion (NAE). If NAE is to be considered a physiologically meaningful quantity then this is surprising, as......-base metabolism during acid loading than previously described methods....

  9. Two cases of infectious purpura fulminans and septic shock caused by Capnocytophaga canimorsus transmitted from dogs

    Christiansen, Claus Behrend; Berg, Ronan Martin Griffen; Plovsing, Ronni R.;

    2012-01-01

    , haemolytic anaemia, metabolic acidosis, and renal failure, which may be common in C. canimorsus-associated purpura fulminans. The patients survived after treatment with broad-spectrum antibiotics and supportive intensive care. C. canimorsus should be considered as a possible cause of infectious purpura...

  10. Akut, svær leverinsufficiens forårsaget af binyretumor hos nyfødt

    Maestri Ditlevsen, Jane; Kvist, Nina; Johansen, Lars Søndergaard;

    2013-01-01

    A newborn female was hospitalized due to metabolic acidosis and conjugated hyperbilirubinaemia. Extrahepatic biliary atresia (EHBA) was suspected why a (99m)Tc-mebrofenin cholescintigraphy was performed. It showed poor hepatocyte tracer uptake and no drainage to the gut. The hepatocyte dysfunction...

  11. 78 FR 68716 - Schedules of Controlled Substances: Temporary Placement of Three Synthetic Phenethylamines Into...

    2013-11-15

    ... the Federal Register on October 10, 2013. 78 FR 61991. \\1\\ Because the Secretary of the HHS has... responsibilities under the CSA, with the concurrence of the NIDA. 50 FR 9518, Mar. 8, 1985. To make a finding that... kinase, metabolic acidosis, rhabdomyolysis, and acute kidney injury. Medical examiner and...

  12. Extracorporeal treatment for acetaminophen poisoning

    Gosselin, S; Juurlink, D N; Kielstein, J T;

    2014-01-01

    cases of APAP poisoning. However, given that APAP is dialyzable, the workgroup agreed that ECTR is suggested in patients with excessively large overdoses who display features of mitochondrial dysfunction. This is reflected by early development of altered mental status and severe metabolic acidosis prior...

  13. Is Lactate Production Related to Muscular Fatigue? A Pedagogical Proposition Using Empirical Facts

    Vaz Macedo, Denise; Lazarim, Fernanda Lorenzi; da Silva, Fernando Oliveira Catanho; Tessuti, Lucas Samuel; Hohl, Rodrigo

    2009-01-01

    The cause-effect relationship between lactic acid, acidosis, and muscle fatigue has been established in the literature. However, current experiments contradict this premise. Here, we describe an experiment developed by first-year university students planned to answer the following questions: 1) Which metabolic pathways of energy metabolism are…

  14. Preoperative prognostic factors for mortality in peptic ulcer perforation: a systematic review

    Møller, Morten Hylander; Adamsen, S.; Thomsen, R.W.;

    2010-01-01

    admission, preoperative metabolic acidosis, tachycardia, acute renal failure, low serum albumin level, high American Society of Anaesthesiologists score, and preoperative delay >24 h were associated with poor prognosis. Conclusions. In patients with PPU, a number of negative prognostic factors can be...

  15. Changes in interstitial K+ and pH during exercise: implications for blood flow regulation

    Juel, Carsten

    2007-01-01

    humans has demonstrated that blood flow is affected by changes in K+ as low as 0.1 mmol/L. The vasodilatory effect of K+ can be inhibited with simultaneous barium infusion, indicating that inward rectifier potassium (Kir)channels are involved. Acidosis has a direct effect on blood flow and an indirect...

  16. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI

    Kuteifan, K.; Gutbub, A.M.; Laplatte, G. [Service de Reanimation Medicale, Centre Hospitalier Louis Pasteur, Colmar (France); Oesterle, H.; Tajahmady, T. [Service de Neuroradiologie, Centre Hospitalier Louis Pasteur, Colmar (France)

    1998-03-01

    Methanol, a highly toxic substance, is used as an industrial solvent and in automobile antifreeze. Acute methanol poisoning produces severe metabolic acidosis and serious neurologic sequelae. We describe a 50-year-old woman with accidental methanol intoxication who was in a vegetative state. MRI showed haemorrhagic necrosis of the putamina and oedema in the deep white matter. (orig.) With 1 fig., 8 refs.

  17. Clinical Manifestation and a New "ISCU" Mutation in Iron-Sulphur Cluster Deficiency Myopathy

    Kollberg, Gittan; Tulinius, Mar; Melberg, Atle; Darin, Niklas; Andersen, Oluf; Holmgren, Daniel; Oldfors, Anders; Holme, Elisabeth

    2009-01-01

    Myopathy with deficiency of succinate dehydrogenase and aconitase is a recessively inherited disorder characterized by childhood-onset early fatigue, dyspnoea and palpitations on trivial exercise. The disease is non-progressive, but life-threatening episodes of widespread weakness, severe metabolic acidosis and rhabdomyolysis may occur. The…

  18. Lactate versus pH levels in fetal scalp blood during labor - using the Lactate Scout System

    Rørbye, Christina; Perslev, Anette; Nickelsen, Carsten

    2016-01-01

    between scalp lactate measured within 15 min prior to delivery and the umbilical cord SBE was low. CONCLUSION: Monitoring non-reassuring deliveries with scalp lactate instead of pH would have resulted in more (155 instead of 56) instrumental deliveries with no decrease in newborns with severe metabolic...... acidosis....

  19. Laktat i navlearterie- og navleveneblod hos nyfødte

    Rubak, Sune Leisgaard Mørck; Henriksen, Tine Brink

    2010-01-01

    INTRODUCTION: In theory, lactate may be used as a more precise measure of the degree of metabolic acidosis than other previous methods, thereby enabling differentiation between acute and chronic foetal hypoxia. The aim of the study was to describe lactate in arterial and venous cord blood in an...

  20. Metformin treatment is associated with a low risk of mortality in diabetic patients with heart failure: a retrospective nationwide cohort study

    Andersson, C; Olesen, JB; Hansen, PR;

    2010-01-01

    The safety of metformin in heart failure has been questioned because of a perceived risk of life-threatening lactic acidosis, though recent studies have not supported this concern. We investigated the risk of all-cause mortality associated with individual glucose-lowering treatment regimens used in...

  1. Short-term starvation with a near-fatal asthma attack induced ketoacidosis in a nondiabetic pregnant woman: A case report.

    Wei, Kuang-Yu; Chang, Shan-Yueh; Wang, Sheng-Huei; Su, Her-Young; Tsai, Chen-Liang

    2016-06-01

    Life-threatening refractory metabolic acidosis due to starvation ketoacidosis is rarely reported, even among nondiabetic pregnant women, and may be overlooked. Furthermore, stressful situations may increase the acidosis severity.In the present case, a nondiabetic multiparous woman was admitted for a near-fatal asthma attack and vomiting during the third trimester of pregnancy. She was intubated and rapidly developed high anion gap metabolic acidosis. We diagnosed the patient with starvation ketoacidosis based on vomiting with concomitant periods of stress during pregnancy and the absence of other causes of high anion gap metabolic acidosis. She responded poorly to standard treatment, although the ketoacidosis and asthma promptly resolved after an emergency caesarean section. The patient and her baby were safely discharged.Short-term starvation, if it occurs during periods of stress and medication, can result in life-threatening ketoacidosis, even among nondiabetic women during the third trimester of pregnancy. Awareness of this condition may facilitate prompt recognition and proactive treatment for dietary and stress control, and emergent interventions may also improve outcomes. PMID:27368034

  2. Incidence and Risk Factors for Delirium among Mechanically Ventilated Patients in an African Intensive Care Setting: An Observational Multicenter Study

    Arthur Kwizera

    2015-01-01

    Full Text Available Aim. Delirium is common among mechanically ventilated patients in the intensive care unit (ICU. There are little data regarding delirium among mechanically ventilated patients in Africa. We sought to determine the burden of delirium and associated factors in Uganda. Methods. We conducted a multicenter prospective study among mechanically ventilated patients in Uganda. Eligible patients were screened daily for delirium using the confusional assessment method (CAM-ICU. Comparisons were made using t-test, chi-squares, and Fisher’s exact test. Predictors were assessed using logistic regression. The level of statistical significance was set at P<0.05. Results. Of 160 patients, 81 (51% had delirium. Median time to onset of delirium was 3.7 days. At bivariate analysis, history of mental illness, sedation, multiorgan dysfunction, neurosurgery, tachypnea, low mean arterial pressure, oliguria, fevers, metabolic acidosis, respiratory acidosis, anaemia, physical restraints, marital status, and endotracheal tube use were significant predictors. At multivariable analysis, having a history of mental illness, sedation, respiratory acidosis, higher PEEP, endotracheal tubes, and anaemia predicted delirium. Conclusion. The prevalence of delirium in a young African population is lower than expected considering the high mortality. A history of mental illness, anaemia, sedation, endotracheal tube use, and respiratory acidosis were factors associated with delirium.

  3. Dietary acid load and risk of hypertension: The Rotterdam study

    Engberink, M.F.; Bakker, S.J.L.; Brink, E.J.; Baak, M.A. van; Rooij, F.J.A. van; Hofman, A.; Witteman, J.C.M.; Geleijnse, J.M.

    2012-01-01

    Background: Mild metabolic acidosis, which can be caused by diet, may result in elevated blood pressure (BP). Objective: The objective was to examine whether dietary acid load was associated with incident hypertension in a cohort of older Dutch adults from the Rotterdam Study. Design: The analyses i

  4. Association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers

    Arngrim, Nanna; Schytz, Henrik Winther; Asghar, Mohammad Sohail; Amin, Faisal Mohammad; Hougaard, Anders; Larsen, Vibeke Andrée; de Koning, Patrick J H; Larsson, Henrik Bo Wiberg; Olesen, Jes; Ashina, Messoud

    2014-01-01

    The carbonic anhydrase inhibitor acetazolamide causes extracellular acidosis and dilatation of cerebral arterioles. In this study, we tested the hypothesis that acetazolamide also may induce headache and dilatation of cranial arteries. In a randomized double-blind crossover study design, 12 young...... acetazolamide causes sensitization of cephalic perivascular nociceptors, which, in combination with vasodilatation, leads to delayed headache....

  5. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI

    Methanol, a highly toxic substance, is used as an industrial solvent and in automobile antifreeze. Acute methanol poisoning produces severe metabolic acidosis and serious neurologic sequelae. We describe a 50-year-old woman with accidental methanol intoxication who was in a vegetative state. MRI showed haemorrhagic necrosis of the putamina and oedema in the deep white matter. (orig.)

  6. Evaluation of electrolyte imbalance among tuberculosis patients receiving treatments in Southwestern Nigeria

    Adebimpe Wasiu Olalekan

    2015-09-01

    Conclusion: Hyponatraemia, hyperkalaemia, and hypochloremia characterized some of the electrolyte imbalance among TB patients receiving treatments. The raised level of bicarbonate may be attributed to overcorrection of respiratory acidosis often found in patients with tuberculosis. Monitoring electrolytes is therefore an important component of TB management.

  7. Co-Existence of Tuberous Sclerosis and the Fanconi Syndrome in Two Saudi Male Siblings: Report on Two Cases

    In this report, we present two cases of familial tuberous sclerosis co-existing with the Fanconi Syndrome. Both cases presented with history of failure to thrive and mental retardation associated with hypokalemic metabolic acidosis. To our knowledge, the association between tuberous sclerosis and the Fanconi Syndrome has not been reported previously. (author)

  8. Sammenligning af profylaktisk ephedrin- og profylaktisk phenylephrininfusion ved spinal anaestesi til kejsersnit

    Afshari, Arash; Møller, Ann M; Hangaard, Niels

    2006-01-01

    Spinal anaesthesia for caesarean delivery may be associated with hypotension and fetal acidosis. Prophylactic infusion of phenylephrine (PE) immediately after the induction of anaesthesia appears to be a more effective approach than administration of ephedrine to reduce the incidence, frequency a...

  9. Hipoglicemia neonatal: Un caso de galactosemia

    Bermúdez M.

    2001-06-01

    Full Text Available Se presenta la historia clínica de un recien nacido con un cuadro de hipoglicemia, que posteriormente desarrolla hiperbilirrubinemia conjugada, hepatomegalia, acidosis metabólica con anion gap aumentado y lactato normal e infeccion por E. coli

  10. Developmental and Reproductive Toxicology of Methanol

    Methanol is a high production volume chemical used as a feedstock for chemical syntheses and as a solvent and fuel additive. Methanol is acutely toxic to humans, causing acidosis, blindness in death at high dosages, but its developmental and reproductive toxicity in humans is poo...

  11. Conjoined hearts.

    Antonelli, D.; Shmilovitz, L; Dharan, M

    1986-01-01

    Thoracopagus twins were delivered at 37 weeks' gestation by caesarean section. Respiratory distress was present and mechanical ventilation was needed; 36 hours after delivery severe lactic acidosis developed and the twins died. The pericardial sac was common and the hearts were conjoined as a single structure with ventricular fusion.

  12. Successful emergency splenectomy during cardiac arrest due to cytomegalovirus-induced atraumatic splenic rupture

    Glesner, Matilde Kanstrup; Madsen, Kristian Rørbæk; Nielsen, Jesper Meng Rahn;

    2015-01-01

    A 27-year-old woman was admitted to the emergency department with fever and a petechial rash on suspicion of meningitis. Shortly after arriving she developed cardiac arrest. Blood work up showed severe lactate acidosis, anaemia and thrombocytopenia. A focused assessment with sonography in trauma...... essential for the management and the eventual recovery of the patient....

  13. Association between serum bicarbonate and pH with depression, cognition and sleep quality in hemodialysis patients.

    Afsar, Baris; Elsurer, Rengin

    2015-07-01

    Metabolic acidosis is a common feature in chronic renal failure patients, worsening progressively as renal function declines. There are conflicting data in hemodialysis (HD) patients with regard to acidosis, alkalosis and mortality. In HD patients, cognitive impairment, depression, sleep disorders and impaired quality of life are very common. Besides, these conditions are related with increased morbidity and mortality. However, no previous study investigated the relationship between pH, venous bicarbonate and anion gap with depression, sleep problems and cognitive function in HD patients. In this study we investigated these relationships. In total, 65 HD patients were included. The demographic parameters and laboratory parameters including bicarbonate, pH and anion gap was measured for all patients. Depressive symptoms, sleep quality and cognitive function, were measured by Beck depression inventory, The Pittsburgh Sleep Quality Index and by Mini Mental State Examination, respectively. We found that, sleep quality but not cognitive function or depression was independently related with venous pH and bicarbonate. Anion gap has no independent relationship with sleep quality, cognitive function and depression. In conclusion, metabolic acidosis and bicarbonate levels were independently related with sleep quality in HD patients. However, there was no association between metabolic acidosis and bicarbonate levels with cognitive function and depression. PMID:25894326

  14. Preoperative prognostic factors for mortality in peptic ulcer perforation: a systematic review

    Møller, Morten Hylander; Adamsen, Sven; Thomsen, Reimar Wernich; Møller, Ann Merete

    admission, preoperative metabolic acidosis, tachycardia, acute renal failure, low serum albumin level, high American Society of Anaesthesiologists score, and preoperative delay >24 h were associated with poor prognosis. Conclusions. In patients with PPU, a number of negative prognostic factors can be...

  15. Secondary Sjogren's syndrome presenting with hypokalemic periodic paralysis

    Dormohammadi Toosi, Taraneh; Naderi, Neda; Movassaghi, Shafieh; Seradj, Mehran Heydari; Khalvat, Ali; Shahbazi, Fatemeh

    2014-01-01

    Renal tubular acidosis (RTA) may develop in a large population of patients with Sjogren's syndrome (SS), but most of the subjects are asymptomatic. Here, we report a patient with known rheumatoid arthritis and symptoms of xerostomia, xerophthalmia and periodic paralysis. SS should be considered as a cause of RTA. The treatment of the underlying disorder may ameliorate the symptoms.

  16. Clinical and biochemical spectrum of hypokalemic paralysis in North: East India

    Ashok K Kayal; Munindra Goswami; Marami Das; Rahul Jain

    2013-01-01

    Background: Acute hypokalemic paralysis, characterized by acute flaccid paralysis is primarily a calcium channelopathy, but secondary causes like renal tubular acidosis (RTA), thyrotoxic periodic paralysis (TPP), primary hyperaldosteronism, Gitelman′s syndrome are also frequent. Objective: To study the etiology, varied presentations, and outcome after therapy of patients with hypokalemic paralysis. Materials And Methods: All patients who presented with acute flaccid paralysis with hypokalemia...

  17. Secondary Sjogren's syndrome presenting with hypokalemic periodic paralysis.

    Dormohammadi Toosi, Taraneh; Naderi, Neda; Movassaghi, Shafieh; Seradj, Mehran Heydari; Khalvat, Ali; Shahbazi, Fatemeh

    2014-11-01

    Renal tubular acidosis (RTA) may develop in a large population of patients with Sjogren's syndrome (SS), but most of the subjects are asymptomatic. Here, we report a patient with known rheumatoid arthritis and symptoms of xerostomia, xerophthalmia and periodic paralysis. SS should be considered as a cause of RTA. The treatment of the underlying disorder may ameliorate the symptoms. PMID:25988057

  18. Renal failure

    1997-01-01

    970363 Effect on serum PTH and 1, 25(OH)2 D3levels of rapid correction of metabolic acidosis in CRFpatients with secondary hyperparathyroidism. YUANQunsheng(袁群生), et al. Renal Div, PUMC Hosp,Beijing, 100730. Chin J Nephrol 1996; 12(6): 328-331.

  19. Diabetic Ketoacidosis in a Patient with Type 2 Diabetes After Initiation of Sodium-Glucose Cotransporter 2 Inhibitor Treatment

    Storgaard, Heidi; Bagger, Jonatan I; Knop, Filip K;

    2016-01-01

    . On admission, the primary symptoms were nausea and dizziness, and he was hypertensive (170/103) and tachycardic (119 bpm) and had mild hyperglycaemia (15.3 mmol/l), severe ketonuria and severe metabolic acidosis (pH 7.08). He responded well to infusions of insulin, glucose and saline and was discharged after...

  20. Short-term starvation with a near-fatal asthma attack induced ketoacidosis in a nondiabetic pregnant woman

    Wei, Kuang-Yu; Chang, Shan-Yueh; Wang, Sheng-Huei; Su, Her-Young; Tsai, Chen-Liang

    2016-01-01

    Abstract Life-threatening refractory metabolic acidosis due to starvation ketoacidosis is rarely reported, even among nondiabetic pregnant women, and may be overlooked. Furthermore, stressful situations may increase the acidosis severity. In the present case, a nondiabetic multiparous woman was admitted for a near-fatal asthma attack and vomiting during the third trimester of pregnancy. She was intubated and rapidly developed high anion gap metabolic acidosis. We diagnosed the patient with starvation ketoacidosis based on vomiting with concomitant periods of stress during pregnancy and the absence of other causes of high anion gap metabolic acidosis. She responded poorly to standard treatment, although the ketoacidosis and asthma promptly resolved after an emergency caesarean section. The patient and her baby were safely discharged. Short-term starvation, if it occurs during periods of stress and medication, can result in life-threatening ketoacidosis, even among nondiabetic women during the third trimester of pregnancy. Awareness of this condition may facilitate prompt recognition and proactive treatment for dietary and stress control, and emergent interventions may also improve outcomes. PMID:27368034

  1. Disease: H01348 [KEGG MEDICUS

    Full Text Available The patients present with severe neonatal lactic acidosis, hypertrophic cardiomyopathy and generalised muscu...ki-Feder E, Czermin B, Freisinger P, Sperl W Deficiency of the mitochondrial phosphate carrier presenting as myopathy and cardiomyopa...thy in a family with three affected children. Neuromuscul Disord 21:803-8 (2011) ...

  2. Cyclic vomiting syndrome masking a fatal metabolic disease.

    Fitzgerald, Marianne

    2013-05-01

    Disorders of fatty acid oxidation are rare but can be fatal. Hypoglycaemia with acidosis is a cardinal feature. Cases may present during early childhood or can be delayed into adolescence or beyond. We present a case of multiple acyl-coenzyme A dehydrogenase deficiency (MADD), an extremely rare disorder of fatty acid oxidation. Our 20-year-old patient presented with cardiovascular collapse, raised anion gap metabolic acidosis and non-ketotic hypoglycaemia. She subsequently developed multi-organ failure and sadly died. She had a previous diagnosis of cyclic vomiting syndrome (CVS) for more than 10 years, warranting frequent hospital admissions. The association between CVS and MADD has been made before though the exact relationship is unclear. All patients with persistent severe CVS should have metabolic investigations to exclude disorders of fatty acid oxidation. In case of non-ketotic hypoglycaemia with acidosis, the patient should be urgently referred to a specialist in metabolic diseases. All practitioners should be aware of these rare disorders as a cause of unexplained acidosis.

  3. Succinyl-CoA:acetoacetate transferase deficiency : identification of a new patient with a neonatal onset and review of the literature

    Niezen-Koning, K E; Wanders, R J; Ruiter, J P; Ijlst, L; Visser, G; Reitsma-Bierens, W C; Heijmans, Hugo; Reijngoud, D J; Smit, G P

    1997-01-01

    UNLABELLED: We describe the clinical symptoms and biochemical findings of a patient with succinyl-CoA:acetoacetate transferase deficiency who presented in the neonatal period and review the current literature on this subject. Our patient was initially suspected to have distal renal tubular acidosis,

  4. Resuscitation og abdominalkirurgiske aspekter ved damage control-kirurgi

    Hillingsø, Jens G; Svendsen, Lars Bo; Johansson, Pär I

    2011-01-01

    In multitrauma patients continuous bleeding is one of the major killers. Coagulation defects have been shown to be a primary event and to occur very early in multitrauma patients (acute traumatic coagulopathy). It is enhanced by acidosis, hypothermia and further coagulation disorders in the "bloody...

  5. Succinyl-CoA : acetoacetate transferase deficiency: identification of a new patient with a neonatal onset and review of the literature

    NiezenKoning, KE; Ijlst, L; Visser, G; ReitsmaBierens, WCC; Heymans, HSA; Reijngoud, DJ; Smit, GPA; Ruiter, Jos P. N.

    1997-01-01

    We describe the clinical symptoms and biochemical findings of a patient with succinyl-CoA:acetoacetate transferase deficiency who presented in the neonatal period and review the current literature on this subject. Our patient was initially suspected to have distal renal tubular acidosis, and subsequ

  6. Bicarbonate correction of ketoacidosis alters host-pathogen interactions and alleviates mucormycosis.

    Gebremariam, Teclegiorgis; Lin, Lin; Liu, Mingfu; Kontoyiannis, Dimitrios P; French, Samuel; Edwards, John E; Filler, Scott G; Ibrahim, Ashraf S

    2016-06-01

    Patients with diabetic ketoacidosis (DKA) are uniquely predisposed to mucormycosis, an angioinvasive fungal infection with high mortality. Previously, we demonstrated that Rhizopus invades the endothelium via binding of fungal CotH proteins to the host receptor GRP78. Here, we report that surface expression of GRP78 is increased in endothelial cells exposed to physiological concentrations of β-hydroxy butyrate (BHB), glucose, and iron that are similar to those found in DKA patients. Additionally, expression of R. oryzae CotH was increased within hours of incubation with DKA-associated concentrations of BHB, glucose, and iron, augmenting the ability of R. oryzae to invade and subsequently damage endothelial cells in vitro. BHB exposure also increased fungal growth and attenuated R. oryzae neutrophil-mediated damage. Further, mice given BHB developed clinical acidosis and became extremely susceptible to mucormycosis, but not aspergillosis, while sodium bicarbonate reversed this susceptibility. BHB-related acidosis exerted a direct effect on both GRP78 and CotH expression, an effect not seen with lactic acidosis. However, BHB also indirectly compromised the ability of transferrin to chelate iron, as iron chelation combined with sodium bicarbonate completely protected endothelial cells from Rhizopus-mediated invasion and damage. Our results dissect the pathogenesis of mucormycosis during ketoacidosis and reinforce the importance of careful metabolic control of the acidosis to prevent and manage this infection. PMID:27159390

  7. Effects of rapid versus slow infusion of sodium bicarbonate on cerebral hemodynamics and oxygenation in preterm infants.

    Velden, A.A.E.M. van der; Hopman, J.C.W.; Klaessens, J.H.G.M.; Feuth, A.B.; Sengers, R.C.A.; Liem, K.D.

    2006-01-01

    BACKGROUND: Sodium bicarbonate (NaHCO3) is often used for correction of metabolic acidosis in preterm infants. The effects of NaHCO3 administration on cerebral hemodynamics and oxygenation are not well known. Furthermore, there is no consensus on infusion rate of NaHCO3. OBJECTIVES: To evaluate the

  8. A Fatal, Systemic Mitochondrial Disease with Decreased Mitochondrial Enzyme Activities, Abnormal Ultrastructure of the Mitochondria and Deficiency of Heat Shock Protein 60

    Agsteribbe, Etienne; Huckriede, Anke; Veenhuis, Marten; Ruiters, Marcel H.J.; Niezen-Koning, Klaziena; Skjeldal, Ola H.; Skullerud, Kari; Gupta, Radhey S.; Hallberg, Richard; Diggelen, Otto P. van; Scholte, Hans R.

    1993-01-01

    We report on a girl presenting with facial dysmorphic features and breathing difficulties upon birth. She was hypotonic, developed a metabolic acidosis, and died two days old of heart failure. Post-mortem examination revealed abnormalities of brain, lungs, heart and liver. In cultured skin fibroblas

  9. Heliox reduces respiratory system resistance in respiratory syncytial virus induced respiratory failure

    Kneyber, Martin C. J.; van Heerde, Marc; Twisk, Jos W. R.; Plotz, Frans B.; Markhors, Dick G.

    2009-01-01

    Introduction Respiratory syncytial virus (RSV) lower respiratory tract disease is characterised by narrowing of the airways resulting in increased airway resistance, air-trapping and respiratory acidosis. These problems might be overcome using helium-oxygen gas mixture. However, the effect of mechan

  10. Outcomes of acute exacerbations in COPD in relation to pre-hospital oxygen therapy

    Ringbaek, Thomas J; Terkelsen, Jakob; Lange, Peter

    2015-01-01

    . METHODS: In an audit of 405 consecutive patients with AECOPD arriving by ambulance to Hvidovre Hospital, details of transit time, oxygen administration, saturation, and arterial blood gases were registered. Outcomes were respiratory acidosis, need of supported ventilation, length of hospitalisation, and...

  11. Feedlot therapeutics.

    Apley, M D; Fajt, V R

    1998-07-01

    This article discusses therapeutic approaches to conditions commonly encountered in feedlots. Challenges discussed include bovine respiratory complex, tracheal edema, atypical interstitial pneumonia, footrot, toe abscesses, mycoplasma arthritis, cardiovascular disease, lactic acidosis, bloat, coccidiosis, central nervous system diseases, abscesses and cellulitis, pregnancy management and abortion, and ocular disease. PMID:9704416

  12. Greystones Nursing Home, Church Road, Greystones, Wicklow.

    Fitzgerald, Marianne

    2013-05-01

    Disorders of fatty acid oxidation are rare but can be fatal. Hypoglycaemia with acidosis is a cardinal feature. Cases may present during early childhood or can be delayed into adolescence or beyond. We present a case of multiple acyl-coenzyme A dehydrogenase deficiency (MADD), an extremely rare disorder of fatty acid oxidation. Our 20-year-old patient presented with cardiovascular collapse, raised anion gap metabolic acidosis and non-ketotic hypoglycaemia. She subsequently developed multi-organ failure and sadly died. She had a previous diagnosis of cyclic vomiting syndrome (CVS) for more than 10 years, warranting frequent hospital admissions. The association between CVS and MADD has been made before though the exact relationship is unclear. All patients with persistent severe CVS should have metabolic investigations to exclude disorders of fatty acid oxidation. In case of non-ketotic hypoglycaemia with acidosis, the patient should be urgently referred to a specialist in metabolic diseases. All practitioners should be aware of these rare disorders as a cause of unexplained acidosis.

  13. A Rare Case of β-Ketothiolase Deficiency

    B. Modh

    2015-06-01

    Full Text Available We are reporting a case of β-ketothiolase deficiency, a rare disorder of amino acid metabolism. A 10 month old child presented with complaints of vomiting, convulsions, fever and altered sensorium that on investigations showed metabolic acidosis, hyperammonemia and ketosis. Gas chromatography/ mass spectroscopic examination was suggestive of β-ketothiolase deficiency.

  14. NUTRITION AND HEALTH OF HIGH-PRODUCTIVE COWS Питание и здоровье высокопродуктивных коров

    Ryadchikov V. G.

    2012-05-01

    Full Text Available It this article, the situation in dairy practice with nutrition factors caused metabolic diseases such as ketosis, acidosis, lameness and a decline in fertility is shown. The article has the proposes on the nutrition of highly productive cows in transition period

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

    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.

  16. Is calcitonin an active hormone in the onset and prevention of hypocalcemia in dairy cattle?

    Rodríguez, E M; Bach, A; Devant, M; Aris, A

    2016-04-01

    The objective of this study was to assess the potential importance of calcitonin (CALC) in the onset of subclinical hypocalcemia (experiment 1) and in the physiological mechanisms underlying the prevention of bovine hypocalcemia under metabolic acidosis (experiments 2 and 3). In experiment 1, 15 Holstein cows naturally incurring subclinical hypocalcemia during the first 5d postpartum were classified as low subclinical hypocalcemia (LSH) when blood Ca concentrations were between 7.5 and 8.5mg/dL, or as high subclinical hypocalcemia (HSH) when blood Ca concentrations were between 6.0 and 7.6mg/dL. Blood samples were taken daily from d -5 to 5 relative to parturition to determine concentrations of parathyroid hormone (PTH), CALC, and 1,25(OH)2D3. In experiment 2, 24 Holstein bulls (497±69kg of body weight and 342±10.5d of age) were assigned to 2 treatments (metabolic acidosis or control). Metabolic acidosis was induced by an oral administration of ammonium chloride (2.5mEq/d) during 10 d, and animals were slaughtered thereafter. Blood samples were collected before slaughter to determine CALC, PTH, 1,25(OH)2D3, and samples of urine, kidney, parathyroid, and thyroid glands were obtained immediately after slaughter to determine expression of several genes in these tissues. Last, in experiment 3, we tested the activity of CALC under metabolic acidosis in vitro using breast cancer cell (T47D) cultures. Although PTH tended to be greater in HSH than in LSH, the levels of 1,25(OH)2D3 were lower in HSH cows (experiment 1). Blood CALC concentration was not affected by the severity of subclinical hypocalcemia, but it was influenced by days from calving (experiment 1). The expression of PTH receptor (PTHR) in the kidney was increased under metabolic acidosis (experiment 2). Furthermore, the activity of CALC was impaired under acidic blood pH (experiment 3). In conclusion, the CALC rise in HSH cows after calving impaired the recovery of blood Ca concentrations because the PTHR

  17. Acid-base equilibrium during capnoretroperitoneoscopic nephrectomy in patients with end-stage renal failure: a preliminary report.

    Demian, A D; Esmail, O M; Atallah, M M

    2000-04-01

    We have studied the acid-base equilibrium in 12 patients with end-stage renal failure (ESRF) during capnoretroperitoneoscopic nephrectomy. Bupivacaine (12 mL, 0.375%) and morphine (2mg) were given in the lumbar epidural space, and fentanyl (0.5 microg kg(-1)) and midazolam (50 microg kg(-1)) were given intravenously. Anaesthesia was induced by thiopental, maintained with halothane carried by oxygen enriched air (inspired oxygen fraction = 0.35), and ventilation was achieved with a tidal volume of 10 mL kg(-1) at a rate of 12 min(-1). This procedure resulted in a mild degree of respiratory acidosis that was cleared within 60 min. We conclude that capnoretroperitoneoscopic nephrectomy can be performed in patients with end-stage renal failure with minimal transient respiratory acidosis that can be avoided by increased ventilation. PMID:10866009

  18. Cyanide poisoning after bitter almond ingestion

    Y Mouaffak

    2013-01-01

    Full Text Available Plants are responsible for 5% poisoning recorded by Poison Control Centers. Among all known toxic plants, some present a real danger if ingested. We report the case of a five years old child, who presented, after ten bitter almonds ingestion, consciousness disorders progressing to coma with generalized tonic-clonic seizures, miosis and metabolic acidosis. Bitter almonds and nuclei of stone fruits or other rosaceae (apricot, peach, plum contain cyanogenic glycosides, amygdalin, that yields hydrogen cyanide when metabolized in the body. Swallowing six to ten bitter almonds may cause serious poisoning, while the ingestion of fifty could kill a man. The binding of cyanide ions on cytochrome oxidase lead to a non hypoxemic hypoxia by blocking the cellular respiratory chain. Therapeutic measures include, oxygen support, correction of acidosis and cyanide antidote by hydroxocobalamin in case of serious poisoning.

  19. 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

    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.

  20. Recovery by the Norway lobster Nephrops norvegicus (L.) from the physiological stresses of trawling: Influence of season and live-storage position

    Lund, H. S.; Wang, T.; Chang, E. S.;

    2009-01-01

    -base status. In winter, a potential metabolic lactic acidosis was compensated by a marked respiratory alkalosis, with significantly increased haemolymph pH and decreased CO2 total content and partial pressure. These effects disappeared gradually over 96 h. Summer lobsters showed combined metabolic and...... summer, respectively. The recovery of specific physiological and metabolic variables from the intense stresses associated with capture (trawling and air-exposure during sorting) was followed in seawater at 5 °C in winter or 18 °C in summer. Recovery was compared in lobsters held individually in two...... respiratory acidosis at 4 h, although this had recovered to control values in the small number of survivors sampled at 24 h. The capture stresses elicited very high haemolymph crustacean hyperglycaemic hormone (CHH) titres, significantly higher in summer than in winter. In winter, CHH titre had declined...

  1. Development and characterization of a nonprimate animal model of methanol-induced neurotoxicity

    Eells, J.T.; Salzman, M.M.; Lewandowski, M.F. [Medical Coll. of Wisconsin, Milwaukee, WI (United States); Murray, T.G. [Univ. of Miami School of Medicine, Miami, FL (United States). Bascom Palmer Eye Inst.

    1996-12-31

    Humans and nonhuman primates are uniquely sensitive to the toxic effects of methanol. The toxic syndrome in these species is characterized by formic acidemia, metabolic acidosis and blindness or serious visual impairment. Nonprimate species are normally resistant to the accumulation of formate and associated metabolic and visual toxicity. The authors have developed a nonprimate model of methanol toxicity using rates in which formate oxidation has been selectively inhibited. Methanol-intoxicated rats developed formic acidemia, metabolic acidosis and visual toxicity analogous to the human methanol poisoning syndrome. Visual dysfunction was manifested as reductions in the flash evoked cortical potential and electroretinogram which occurred coincident with blood formate accumulation. Histopathologic studies revealed mitochondrial disruption and vacuolation in the retinal pigment epithelium, photoreceptor inner segments and optic nerve. The establishment of this nonprimate animal model of methanol intoxication will facilitate research into the mechanistic aspects of methanol toxicity as well as the development and testing of treatments for human methanol poisoning.

  2. Euglycemic Diabetic Ketoacidosis in a Patient with Cocaine Intoxication.

    Abu-Abed Abdin, Asma; Hamza, Muhammad; Khan, Muhammad S; Ahmed, Awab

    2016-01-01

    Diabetic ketoacidosis (DKA) is characterized by elevated anion gap metabolic acidosis, hyperglycemia, and elevated ketones in urine and blood. Hyperglycemia is a key component of DKA; however, a subset of DKA patients can present with near-normal blood glucose, an entity described as "euglycemic DKA." This rare phenomenon is thought to be due to starvation and food restriction in insulin dependent diabetic patients. Cocaine abuse is considered a trigger for development of DKA. Cocaine also has anorexic effects. We describe an interesting case of euglycemic DKA in a middle-aged diabetic female presenting with elevated anion gap metabolic acidosis, with near-normal blood glucose, in the settings of noncompliance to insulin and cocaine abuse. We have postulated that cocaine abuse was implicated in the pathophysiology of euglycemic DKA in this case. This case highlights complex physiological interplay between type-1 diabetes, noncompliance to insulin, and cocaine abuse leading to DKA, with starvation physiology causing development of euglycemic DKA. PMID:27579186

  3. Recurrent Attacks of Hypokalemic Quadriparesis: An Unusual Presentation of Primary Sjögren Syndrome.

    Seirafian, Shiva; Shafie, Mohammad; Abedini, Amin; Pakzad, Bahram; Roomizadeh, Peyman

    2016-01-01

    We herein report the case of a 64-year old woman with recurrent attacks of hypokalemic quadriparesis which resulted from distal renal tubular acidosis (dRTA) secondary to Sjögren syndrome. The patient presented with sudden onset quadriparesis. A physical examination showed symmetric weakness of all four limbs. Severe hypokalemia (1.8 mEq/L), accompanied by normal anion gap metabolic acidosis, a positive urine anion gap and an inappropriately high urine pH pointed toward the diagnosis of dRTA. Further investigations disclosed primary Sjögren syndrome, which had not previously been recognized. On the basis of the current report and a review of the literature we suggest investigating the possibility of Sjögren syndrome in all patients with clinically unexplained dRTA. PMID:27374687

  4. Glycolysis in energy metabolism during seizures

    Heng Yang; Jiongxing Wu; Ren Guo; Yufen Peng; Wen Zheng; Ding Liu; Zhi Song

    2013-01-01

    Studies have shown that glycolysis increases during seizures, and that the glycolytic metabolite lactic acid can be used as an energy source. However, how lactic acid provides energy for seizures and how it can participate in the termination of seizures remains unclear. We reviewed possible mechanisms of glycolysis involved in seizure onset. Results showed that lactic acid was involved in seizure onset and provided energy at early stages. As seizures progress, lactic acid reduces the pH of tissue and induces metabolic acidosis, which terminates the seizure. The specific mechanism of lactic acid-induced acidosis involves several aspects, which include lactic acid-induced inhibition of the glycolytic enzyme 6-diphosphate kinase-1, inhibition of the N-methyl-D-aspartate receptor, activation of the acid-sensitive 1A ion channel, strengthening of the receptive mechanism of the inhibitory neurotransmitter γ-aminobutyric acid, and changes in the intra- and extracellular environment.

  5. Cetrimide-chlorhexidine-induced multiorgan failure in surgery of pulmonary hydatid cyst.

    Tripathy, Swagata; Sasmal, Prakash; Rao, P Bhaskar; Mishra, Tushar S; Nayak, Sukdev

    2016-01-01

    Savlon (0.5% cetrimide/0.05% chlorhexidine) is used as a scolicidal during surgery of hydatid cysts. It is considered a safe and effective agent. However, there are no recommendations for the appropriate concentration or dosage of these agents. Previously reported to cause severe metabolic acidosis, its effects on the pulmonary system have not been explored. We present a case of acute lung injury and respiratory distress along with acute cardiopulmonary distress, severe metabolic acidosis, and renal failure following its use during surgical removal of pulmonary hydatid cyst. The agent may act as a chemical sclerosant causing pulmonary parenchymal damage through bronchial openings present in the pericyst. Till safe dose limits are known, use of this agent should be limited, especially in large or multiple cyst surgery. PMID:27397471

  6. Unmeasured anions and mortality in critically ill patients in 2016.

    Kotake, Yoshifumi

    2016-01-01

    The presence of acid-base disturbances, especially metabolic acidosis may negatively affect the outcome of critically ill patients. Lactic acidosis is the most frequent etiology and has largest impact on the prognosis. Since lactate measurement might not have always been available at bedside, it had been regarded as one of the unmeasured anions. Therefore, anion gap and strong ion gap has been used to as a surrogate of lactate concentration. From this perspective, the relationship between either anion gap or strong ion gap and mortality has been explored. Then, lactate became routinely measurable at bedside and the direct comparison between directly measured lactate and these surrogate parameters can be possible. Currently available evidence suggests that directly measured lactate has larger prognostic ability for mortality than albumin-corrected anion gap and strong ion gap without lactate. In this commentary, the rationale and possible clinical implications of these findings are discussed. PMID:27429758

  7. Metabolik Asidozda Arteriyal, Serebro-Spinal pH ilişkisi ve NaHCO3 Tedavisinde Cevabı

    KAPICIOĞLU, S.; GÜRÇAY, A.; TANYERİ, F.

    2009-01-01

    SUMMARY The relationship of arterial and cerobro-spinal fluid pH in metabolic aci¬dosis and its response to NaHCO3 therapy Blood and CSF pH ieveis are measured in 16 patients with metabolic acidosis, and 8 patients with normal acid-base balance. In normal patients CSF pH was 7.39 + 0.05, arterial pH was 7.40 ""+0.03. In metabolic acidosis these measurements were 7.32 + 0.11 and 7.22"+" 0.10 respectively. Arterial pH rose as CSF pH fell 2 and 4 hours after NaHCOa infusion and CSF pH st...

  8. Recurrent Hypokalemic Periodic Paralysis Unmasks Sjogren Syndrome without Sicca Symptoms.

    Hung, Yao-Min; Huang, Neng-Chyan; Wann, Shue-Ren; Chang, Yun-Te; Wang, Jyh-Seng

    2015-04-01

    Hypokalemic Periodic Paralysis (HPP) may occur as a rare complication of Sjogren Syndrome (SS) and Renal Tubular Acidosis (RTA). A 64-year male patient came with HPP, and was later diagnosed with distal RTA. The patient, who had no xerostomia and xerophthalmia, was diagnosed with primary SS from serologic and histologic findings of minor salivary gland biopsy. The patient recovered after potassium replacement therapy. Renal biopsy was also performed and revealed evidence of tubulointerstitial nephritis. Corticosteroids were administered and there was no recurrence of HPP during a 4-year follow-up period. The case highlights the significance of acute hypokalemia management in emergency department as it can unmask SS even if the SS is not associated with sicca symptoms. Hypokalemic paralysis associated with normal anion gap metabolic acidosis should prompt toward the diagnosis of SS. PMID:25933458

  9. Teaching acid/base physiology in the laboratory

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

    2010-01-01

    Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory...... 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...

  10. Hashimoto Thyroiditis and Nephrocalcinosis in a Child with Down Syndrome

    Spahiu, Lidvana; Jashari, Haki; Mulliqi-Kotori, Vjosa; Elezi-Rugova, Blerta; Merovci, Besart

    2016-01-01

    Introduction: Hypothyroidism has been reported to affect renal function and structure. However, the association of hypothyroidism with distal renal tubular acidosis (dRTA) is rarely reported in children. Case Presentation: We present a 6-year-boy with Down syndrome admitted in our department due to vomiting, weakness, polyuria, polydipsia, irritability and weight loss in the last few weeks. Investigations revealed features of hypokalemia, metabolic acidosis and alkaline urine consistent with dTRA. Abdominal ultrasound found nephrocalcinosis. In addition, Antithyroid peroxidase antibodies were positive, suggesting an autoimmune background for the pathogenesis of the tubular dysfunction. Treatment for dRTA and hypothyroidism was started and symptomatic improve was noticed. Conclusion: dRTA should be excluded in children with autoimmune disorders who develop weakness, polyuria, polydipsia or growth failure. Early diagnosis would reduce long-term complications. PMID:27147809

  11. Euglycemic Diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SGLT2) inhibitor Canagliflozin.

    Bader, Nimrah; Mirza, Lubna

    2016-01-01

    We are reporting a timely case of atypical euglycemic diabetic ketoacidosis in a type 1 diabetic patient treated with sodium-glucose cotransporter-2 (SGLT-2) inhibitor canagliflozin. The clinical history, physical examination findings and laboratory values are described. Other causes of acidosis such as salicylate toxicity or alcohol intoxication were excluded. Ketoacidosis resolved after increasing dextrose and insulin doses supporting the hypothesis that SGLT-2 inhibitors may lead to hypoinsulinemia. Euglycemic ketoacidosis did not recur in our patient after discontinuing canagliflozin. We recommend reserving SGLT2 inhibitor therapy to type 2 diabetics, discontinuing medication and treating patients presenting with ketoacidosis due to SGLT-2 inhibitors with higher concentrations of dextrose with appropriate doses of insulin to help resolve acidosis. PMID:27375734

  12. Refractory cardiopulmonary failure after glyphosate surfactant intoxication: a case report

    Chang Chia-Chu

    2009-01-01

    Full Text Available Abstract Background Glyphosate is an herbicide considered to be of low toxicity to humans because its effects are specific to plants. However, fatal reactions to glyphosate have been reported after the ingestion of large amounts. Pulmonary edema, shock, and arrhythmia were the reported causes of mortality. Case presentation We present the case of a 57-year-old woman who was admitted to the emergency department unconsciousness after ingestion of glyphosate surfactant in a suicide attempt. Metabolic acidosis, refractory respiratory failure, and shock developed during hospitalization. Despite aggressive supportive care, the patient died in the hospital. Conclusion The toxicokinetics of glyphosate surfactant is complicated. Respiratory failure, metabolic acidosis, tachycardia, elevated creatinine, and hyperkalemia are poor prognostic factors if presented. Physicians should consider using hemodialysis early to improve the outcome of patients with glyphosate surfactant intoxication.

  13. A young man with polyuria and lethargy

    Salman Imtiaz

    2011-01-01

    Full Text Available 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.

  14. Effect of diet on maintenance of acid-basal balance in blood of dairy cows

    Gaál T.

    2003-01-01

    Full Text Available High-performance breeds of ruminants often exhibit production disorders which can be accompanied by a disturbed acid-basal balance. Most of the disorders in the acid-basal balance are closely related to digressions in the diet norms of these animals. A deficiency or surplus of energy equally cause disorders in the acid-basal status of the organism. Metabolic acidosis is the most frequent of the four types of basic disorders in the acid-basal balance in ruminants. It appears as a consequence of rumen acidosis, ketosis, or diarrhea. Acute disorders in the acid-basal balance are far more dangerous than chronic ones. Therapy of the basic diseases is generally sufficient compensation for the effects of the acid-basal disorders, but in certain cases it is necessary to perform alkalization, that is, acidification of the rumen content using the necessary preparations.

  15. Využití psychosociálních služeb na hemodialyzačních střediscích

    HACKLOVÁ, Lucie

    2009-01-01

    Chronic disorder of kidneys is a gradual progression from the state of health to the state of a disease, resulting in permanent failure of excretory, regulatory, and hormonal (metabolic) functions of kidneys. During a kidney failure water and electrolyte imbalance, retention of catabolites, and metabolic acidosis occur; there is a shortage of substances produced in kidneys. A complex metabolic disorder occurs, whose clinic corelate is a uremic syndrom. Conservative treatment consists in adjus...

  16. Piperazine side-effects in a patient with pre-existing renal insufficiency

    Majid Malaki

    2014-01-01

    Piperazine as an antihelminth has many adverse effects, especially on patients with renal insufficiency. We report the use of piperazine in a girl with a moderately severe kidney disease due to Biedl Bardet syndrome. She developed coma and acute kidney injury due to acute interstitial nephritis (AIN), anemia and thrombocytopenia. The presence of fever, proteinuria, acidosis, anemia, sterile pyuria and non-oliguric renal failure strongly suggested AIN. Her problems abated mostly by discontinui...

  17. Acute isoniazid intoxication: case report

    Dilek Altun; Halil Cetingok; Gulay AsIk Eren; Zafer Cukurova; Oya Hergunsel

    2015-01-01

    Isoniazid is a bactericidal antituberculosis drug, used commonly for treatment and prophylaxis of tuberculosis. Acute isoniazid intoxication is characterized by a clinical triad consisting of metabolic acidosis with a high anion gap resistant to treatment with sodium bicarbonate, seizures which may be fatal and refractory to standard anticonvulsant therapy, and coma. Pyridoxine, in a dose equivalent to the amount of isoniasid ingested, is the only effective antidote. Here, we reported a 14 ye...

  18. Design of liposome-based pH sensitive nanoSPIN probes: nano-sized particles with incorporated nitroxides

    Woldman, Yakov Y.; Semenov, Sergey V.; Bobko, Andrey A.; Kirilyuk, Igor A.; Polienko, Julya F.; Voinov, Maxim A.; Bagryanskaya, Elena G.; Khramtsov, Valery V.

    2009-01-01

    Liposome-based nanoSized Particles with Incorporated Nitroxides, or nanoSPINs, were designed for EPR applications as pH probes in biological systems. Phospholipid membrane of the liposomes with incorporated gramicidin A showed selective permeability to a small analyte, H+, while protecting entrapped sensing nitroxide from biological reductants. An application of the pH-sensitive nanoSPIN in an ischemia model in rat heart homogenate allows for monitoring ischemia-induced acidosis while protect...

  19. Enhancement of Radiotherapeutic Efficacy by Paclitaxel-Loaded pH-Sensitive Block Copolymer Micelles

    Seong-Yun Jeong; Doo Sung Lee; Si Yeol Song; Heon Joo Park; Dong-Hoon Jin; Hye Kyung Chung; Jinhyang Choi; Jaesook Park; Joohee Jung; Sung-Jin Park; Min Sang Kim; Eun Kyung Choi

    2012-01-01

    Radiotherapy (RT) is a major modality for cancer treatment, but its efficacy is often compromised by the resistance caused by tumor-specific microenvironment including acidosis and hypoxia. For an effective RT, concurrent administration of radiosensitizer with RT has been emphasized. However, most anticancer agents enhancing radiotherapeutic efficacy have obstacles such as poor solubility and severe toxicity. Paclitaxel (PTX), a well-known radiosensitizer, is insoluble in water and needs toxi...

  20. 瘤胃中乳酸的代谢及其调控机制%Advances in the metabolism and regulation of lactic acids in the rumen

    陈连民; 王洪荣

    2016-01-01

    有关瘤胃酸中毒发生机制研究表明,瘤胃乳酸的累积可能对酸中毒诱导起重要作用,而高精料日粮下瘤胃乳酸累积主要取决于瘤胃乳酸产生菌和乳酸利用菌间的平衡程度。本文综述了瘤胃微生物对乳酸的代谢机制,包括主要乳酸产生菌[溶纤维丁酸弧菌(Butyrivibriofibrisolvens)、牛链球菌(Streptococcus bovis)、乳酸杆菌(Lactobacillus)]和主要乳酸利用菌[反刍兽新月单胞菌(Selenomonus ruminantium)、埃氏巨型球菌(Megasphaera elsdenii)],并简要概述了酸中毒的调控方法,旨在为反刍动物瘤胃酸中毒的乳酸中毒机制深入解析提供参考。%Reviews of the ruminant lactic acidosis indicated that accumulation of lactic acids in the rumen may play an important role in inducing ruminal lactic acidosis,while rumen lactic acids accumulation mainly depends on the degree of balance of rumen producing and utilizing bacteria in feeding high concentrate diets.In this pa-per,advances in lactic acids metabolism associated rumen bacteria (Butyrivibriofibrisovens,Streptococcus bo-vis,Lactobacillus,Selenomonus ruminantium and Megasphaera elsdenii)were discussed,prevention strate-gies of ruminal acidosis were discussed in purpose to provide reference for further research of lactic acids rumen acidosis mechanism.

  1. Hair dye poisoning and the developing world

    Sampathkumar Krishnaswamy; Yesudas Sooraj

    2009-01-01

    Hair dye poisoning has been emerging as one of the important causes of intentional self harm in the developing world. Hair dyes contain paraphenylene-diamine and a host of other chemicals that can cause rhabdomyolysis, laryngeal edema, severe metabolic acidosis and acute renal failure. Intervention at the right time has been shown to improve the outcome. In this article, we review the various manifestations, clinical features and treatment modalities for hair dye poisoning.

  2. Diabetic ketoacidosis associated with atypical antipsychotic drug, clozapine treatment: Report of a case and review of literature

    Pillai L

    2006-01-01

    Full Text Available Atypical antipsychotic drugs are associated with metabolic disturbances like weight gain, type 2 diabetes hyperglycaemia and dyslipedemia, which can result in serious health risk in patients. Diabetic ketoacidosis resulting in serious metabolic acidosis, occurring in a schizophrenic patient on treatment with clozapine is being reported to draw attention this association. Frequent monitoring of the blood sugar and lipids is advised before and during therapy with atypical antipsychotic drugs.

  3. Growth Hormone Therapy in Children with Chronic Renal Failure

    Cayir, Atilla; Kosan, Celalettin

    2014-01-01

    Growth is impaired in a chronic renal failure. Anemia, acidosis, reduced intake of calories and protein, decreased synthesis of vitamin D and increased parathyroid hormone levels, hyperphosphatemia, renal osteodystrophy and changes in growth hormone-insulin-like growth factor and the gonadotropin-gonadal axis are implicated in this study. Growth is adversely affected by immunosuppressives and corticosteroids after kidney transplantation. Treating metabolic disorders using the recombinant huma...

  4. Neem oil poisoning: Case report of an adult with toxic encephalopathy

    Mishra, Ajay; Dave, Nikhil

    2013-01-01

    Neem oil has widespread use in Indian subcontinent due to its many bioactive properties. Azadirachtin, an active ingredient, is implicated in causing the effects seen in neem oil poisoning. Neem oil poisoning is rare in adults. This report highlights the toxicity associated with neem oil poisoning in an elderly male. The patient presented with vomiting, seizures, metabolic acidosis, and toxic encephalopathy. The patient recovered completely with symptomatic treatment.

  5. Neem oil poisoning: Case report of an adult with toxic encephalopathy.

    Mishra, Ajay; Dave, Nikhil

    2013-09-01

    Neem oil has widespread use in Indian subcontinent due to its many bioactive properties. Azadirachtin, an active ingredient, is implicated in causing the effects seen in neem oil poisoning. Neem oil poisoning is rare in adults. This report highlights the toxicity associated with neem oil poisoning in an elderly male. The patient presented with vomiting, seizures, metabolic acidosis, and toxic encephalopathy. The patient recovered completely with symptomatic treatment. PMID:24339648

  6. Acute Tubuler Necrosis Related to Rhabdomyolysis

    Fatma Sarı DOĞAN

    2014-05-01

    Full Text Available Rhabdomyolysis is a clinical and laboratory syndrome due to traumatic or non-traumatic injury that leads muscle cell contents participation into circulation. Dehydration and acidosis may cause myoglobinuric acute renal failure in patient with rhabdomyolysis. This case presents a 27-year-old male referred to emergency unit with weakness and abdominal ache who has a story of urine decrease and trauma exposure. Diagnosis of rhabdomyolysis in this case highlights the importance of anamnesis in early diagnosis and treatment.

  7. A critical appraisal of the evidence for using cardiotocography plus ECG ST interval analysis for fetal surveillance in labor. Part I: The randomized controlled trials

    Olofsson, Per; Ayres-de-Campos, Diogo; Kessler, Jörg; Tendal, Britta; Yli, Branislava Markovic; Devoe, Lawrence

    2014-01-01

    We reappraised the five randomized controlled trials that compared cardiotocography plus ECG ST interval analysis (CTG+ST) vs. cardiotocography. The numbers enrolled ranged from 5681 (Dutch randomized controlled trial) to 799 (French randomized controlled trial). The Swedish randomized controlled trial (n = 5049) was the only trial adequately powered to show a difference in metabolic acidosis, and the Plymouth randomized controlled trial (n = 2434) was only powered to show a difference in ope...

  8. ST analysis of the fetal ECG : towards evidence based fetal surveillance

    J.H. Becker

    2012-01-01

    It was the aim of this thesis to perform a meta-analysis of published trial on FECG monitoring during labor, to assess its effects on fetal outcome, on the use of FBS, and on instrumental and operative interventions. Furthermore we conducted secondary studies of published data sets to address thus far unresolved issues, such as: are the consensus-based recommendations for additional fetal information effective in preventing fetal acidosis; what is the association between the baseline T/QRS of...

  9. Hair dye poisoning and the developing world

    Sampathkumar Krishnaswamy

    2009-01-01

    Full Text Available Hair dye poisoning has been emerging as one of the important causes of intentional self harm in the developing world. Hair dyes contain paraphenylene-diamine and a host of other chemicals that can cause rhabdomyolysis, laryngeal edema, severe metabolic acidosis and acute renal failure. Intervention at the right time has been shown to improve the outcome. In this article, we review the various manifestations, clinical features and treatment modalities for hair dye poisoning.

  10. Optic neuropathy in a patient with pyruvate dehydrogenase deficiency

    Small, Juan E. [Massachusetts General Hospital and Harvard Medical School, Department of Radiology, Boston, MA (United States); Gonzalez, Guido E. [Massachusetts Eye and Ear Infirmary and Harvard Medical School, Department of Radiology, Boston, MA (United States); Clinica Alemana de Santiago, Departmento de Imagenes, Santiago (Chile); Nagao, Karina E.; Walton, David S. [Massachusetts Eye and Ear Infirmary and Harvard Medical School, Department of Ophthalmology, Boston, MA (United States); Caruso, Paul A. [Massachusetts Eye and Ear Infirmary and Harvard Medical School, Department of Radiology, Boston, MA (United States)

    2009-10-15

    Pyruvate dehydrogenase (PDH) deficiency is a genetic disorder of mitochondrial metabolism. The clinical manifestations range from severe neonatal lactic acidosis to chronic neurodegeneration. Optic neuropathy is an uncommon clinical sequela and the imaging findings of optic neuropathy in these patients have not previously been described. We present a patient with PDH deficiency with bilateral decreased vision in whom MRI demonstrated bilateral optic neuropathy and chiasmopathy. (orig.)

  11. The effect of pH and ADP on ammonia affinity for human glutamate dehydrogenases

    Zaganas, Ioannis; Pajecka, Kamilla; Nielsen, Camilla Wendel;

    2013-01-01

    Glutamate dehydrogenase (GDH) uses ammonia to reversibly convert α-ketoglutarate to glutamate using NADP(H) and NAD(H) as cofactors. While GDH in most mammals is encoded by a single GLUD1 gene, humans and other primates have acquired a GLUD2 gene with distinct tissue expression profile. The two h...... of the kidney during systemic acidosis. The reverse could apply for conditions of local or systemic hyperammonemia or alkalosis....

  12. Alternative management of diabetic ketoacidosis in a Brazilian pediatric emergency department

    Savoldelli Roberta D

    2010-06-01

    Full Text Available Abstract DKA is a severe metabolic derangement characterized by dehydration, loss of electrolytes, hyperglycemia, hyperketonemia, acidosis and progressive loss of consciousness that results from severe insulin deficiency combined with the effects of increased levels of counterregulatory hormones (catecholamines, glucagon, cortisol, growth hormone. The biochemical criteria for diagnosis are: blood glucose > 200 mg/dl, venous pH 3 mmol/L and presence of ketonuria. A patient with DKA must be managed in an emergency ward by an experienced staff or in an intensive care unit (ICU, in order to provide an intensive monitoring of the vital and neurological signs, and of the patient's clinical and biochemical response to treatment. DKA treatment guidelines include: restoration of circulating volume and electrolyte replacement; correction of insulin deficiency aiming at the resolution of metabolic acidosis and ketosis; reduction of risk of cerebral edema; avoidance of other complications of therapy (hypoglycemia, hypokalemia, hyperkalemia, hyperchloremic acidosis; identification and treatment of precipitating events. In Brazil, there are few pediatric ICU beds in public hospitals, so an alternative protocol was designed to abbreviate the time on intravenous infusion lines in order to facilitate DKA management in general emergency wards. The main differences between this protocol and the international guidelines are: intravenous fluid will be stopped when oral fluids are well tolerated and total deficit will be replaced orally; if potassium analysis still indicate need for replacement, it will be given orally; subcutaneous rapid-acting insulin analog is administered at 0.15 U/kg dose every 2-3 hours until resolution of metabolic acidosis; approximately 12 hours after treatment initiation, intermediate-acting (NPH insulin is initiated at the dose of 0.6-1 U/kg/day, and it will be lowered to 0.4-0.7 U/kg/day at discharge from hospital.

  13. Hepatotoxicity due to zinc phosphide poisoning in two patients: role of N-acetylcysteine.

    Oghabian, Zohreh; Afshar, Arefeh; Rahimi, Hamid Reza

    2016-08-01

    Zinc phosphide (Zn3P2/ZnP) is used as a rodenticide. The most common signs of toxicity are nausea, vomiting, hypotension, and metabolic acidosis; patients presenting such signs are referred to the emergency department (ED) of the hospitals. Therefore, this study aimed to report two cases of hepatotoxicity following accidental and intentional ZnP poisoning and successful management with N-acetylcysteine (NAC). PMID:27525081

  14. Systemic physiology and neuroapoptotic profiles in young and adult rats exposed to surgery

    Ibrahim, Rami Mossad; Krammer, Caspar Weel; Hansen, Tom Giedsing;

    2015-01-01

    experimental groups receiving dexmedetomidine, while propofol administration was associated with increased systemic lactate levels and metabolic acidosis. A substantial difference in anaesthesia/surgery-induced neuroapoptosis was found between young and adult rats in several brain regions. Combination of...... one of four anaesthetics regimens: (i) sevoflurane/dexmedetomidine, (ii) sevoflurane/fentanyl; (iii) propofol/dexmedetomidine, and (iv) propofol/fentanyl. Animals underwent a dorsal skin flap procedure while physiologic, metabolic and biochemical parameters were closely monitored. Neuroapoptotic...

  15. Bench-to-bedside review: Glucose production from the kidney

    Cano, Noël,

    2002-01-01

    Data obtained from net organ balance studies of glucose production lead to the classic view according to which glucose homeostasis is mainly ensured by the liver, and renal glucose production only plays a significant role during acidosis and prolonged starvation. Renal glucose release and uptake, as well as the participation of gluconeogenic substrates in renal gluconeogenesis, were recently re-evaluated using systemic and renal arteriovenous balance of substrates in combination with deuterat...

  16. MITOCHIP Assessment of Differential Gene Expression in the Skeletal Muscle of Ant1 Knockout Mice: Coordinate Regulation of OXPHOS, Antioxidant, and Apoptotic Genes

    Subramaniam, Vaidya; Golik, Pawel; Murdock, Deborah G.; Levy, Shawn,; Kerstann, Keith W.; Coskun, Pinar E.; Melkonian, Goarik A.; Wallace, Douglas C.

    2008-01-01

    Genetic inactivation of the nuclear-encoded mitochondrial heart-muscle adenine nucleotide translocator-1 (ANT1), which exports mitochondrial ATP to the cytosol in both humans (ANT1−/−) and mice (Ant1−/−), results in lactic acidosis and mitochondrial cardiomyopathy and myopathy, the latter involving hyper-proliferation of mitochondria, induction of oxidative phosphorylation (OXPHOS) enzymes, increased reactive oxygen species (ROS), and excessive mtDNA damage. To understand these manifestations...

  17. Urosepsis in infants with vesicoureteral reflux masquerading as the salt-losing type of congenital adrenal hyperplasia

    Vaid, Y.N.; Lebowitz, R.L.

    1989-08-01

    Three male infants with vomiting, dehydration, hyponatremia, hyperkalemia and metabolic acidosis were found to have vesicoureteral reflux (VUR) and urinary tract infection. Two were initially thought to have the salt-losing form of congenital adrenal hyperplasia. Although prompt diagnosis of this potentially fatal condition is critical, its mimicry by urosepsis in infants with VUR is actually more common. Infection probably causes unresponsiveness of the distal renal tubules to aldoterone. (orig.).

  18. DETERMINATION OF ANTIBACTERIAL ACTIVITY OF PUNICA GRANATUM FRUIT

    P. P. Lasure*, N. M. Munot and S. S. Lawande

    2012-01-01

    Punica granatum L. belongs to the family Punicaceae, which is originating from the Middle East, extending throughout the Mediterranean, eastward to China and India. Punica granatum has been used extensively as a traditional medicine in many countries for the treatment of dysentery, diarrhea, helminthiasis, acidosis, hemorrhage and respiratory pathologies. In addition, P. granatum is reported to have antioxidant, anti-atherosclerotic and antiviral properties. The dried pomegranate peels (20gms...

  19. Hyaline membrane disease (HMD): the role of the perinatal pathologist

    Giorgia Locci; Vassilios Fanos; Clara Gerosa; Gavino Faa

    2014-01-01

    Hyaline membrane disease (HMD), the pathologic correlate of respiratory distress syndrome (RDS) of the newborn, is an acute lung disease of premature infant caused by inadequate amounts of surfactant. Decreased surfactant results in insufficient surface tension in the alveolus during expiration, leading to atelectasis, decreased gas exchange, severe hypoxia and acidosis. HMD predominantly occurs in infants younger than 32 weeks of gestation and weighing less than 1,200 g. In the interpretatio...

  20. Rhabdomyolysis of the head and neck: computed tomography and magnetic resonance imaging findings

    Mian, AZ; Saito, N; Sakai, O

    2011-01-01

    Rhabdomyolysis is rare in the head and neck. Early diagnosis and treatment is essential to prevent serious complications such as hyperkalaemia, acidosis, acute renal failure and disseminated intravascular coagulation. We present a case of rhabdomyolysis of the head and neck. CT and MRI findings supported the diagnosis of rhabdomyolysis with the patient's clinical and laboratory findings. While imaging is not crucial, it can aid in the detection of rhabdomyolysis and narrow the differential di...