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Sample records for acidosis

  1. Metabolic acidosis

    Science.gov (United States)

    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

    OpenAIRE

    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. Proximal renal tubular acidosis

    Science.gov (United States)

    Renal tubular acidosis - proximal; Type II RTA; RTA - proximal; Renal tubular acidosis type II ... are neutralized by alkaline substances, mainly bicarbonate. Proximal renal tubular acidosis (Type II RTA) occurs when bicarbonate ...

  4. Distal renal tubular acidosis

    Science.gov (United States)

    Renal tubular acidosis - distal; Renal tubular acidosis type I; Type I RTA; RTA - distal; Classical RTA ... blood and excreting it into the urine. Distal renal tubular acidosis (Type I RTA) is caused by ...

  5. Acidosis and Urinary Calcium Excretion

    DEFF Research Database (Denmark)

    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 inhibition of calcium transport processes within the renal tubule. The mechanisms whereby acid alters the integrity and stability of bone have been examined extensively in the published literature. Here, after briefly reviewing this literature, we consider the effects of acid on calcium transport...

  6. Renal tubular acidosis type 4 in pregnancy.

    Science.gov (United States)

    Jakes, Adam Daniel; Baynes, Kevin; Nelson-Piercy, Catherine

    2016-03-17

    We describe the clinical course of renal tubular acidosis (RTA) type 4 in pregnancy, which has not been previously published. Renal tubular acidosis type 4 is a condition associated with increased urinary ammonia secondary to hypoaldosteronism or pseudohypoaldosteronism. Pregnancy may worsen the hyperkalaemia and acidosis of renal tubular acidosis type 4, possibly through an antialdosterone effect. We advise regular monitoring of potassium and pH throughout pregnancy to ensure safe levels are maintained.

  7. Acidosis activates complement system in vitro

    Directory of Open Access Journals (Sweden)

    Michael Emeis

    1998-01-01

    Full Text Available We investigated the in vitro effect of different form s of acidosis (pH 7.0 on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 μ mol/ml blood or lactic acid (5.5 μ mol/ml to heparin blood (N=12 caused significant activation of C3a and C5a compared to control (both p=0.002. Respiratory acidosis activated C3a (p=0.007 and C5a (p=0.003 compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5.

  8. Acidosis activates complement system in vitro.

    Science.gov (United States)

    Emeis, M; Sonntag, J; Willam, C; Strauss, E; Walka, M M; Obladen, M

    1998-01-01

    We investigated the in vitro effect of different forms of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 micromol/ml blood) or lactic acid (5.5 micromol/ml) to heparin blood (N=12) caused significant activation of C3a and C5a compared to control (both p=0.002). Respiratory acidosis activated C3a (p=0.007) and C5a (p=0.003) compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5. PMID:9927235

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

    NARCIS (Netherlands)

    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

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

    OpenAIRE

    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 ...

  11. Acidosis inhibits mineralization in human osteoblasts.

    Science.gov (United States)

    Takeuchi, Shoko; Hirukawa, Koji; Togari, Akifumi

    2013-09-01

    Osteoblasts and osteoclasts maintain bone volume. Acidosis affects the function of these cells including mineral metabolism. We examined the effect of acidosis on the expression of transcription factors and mineralization in human osteoblasts in vitro. Human osteoblasts (SaM-1 cells) derived from the ulnar periosteum were cultured with α-MEM containing 50 μg/ml ascorbic acid and 5 mM β-glycerophosphate (calcifying medium). Acidosis was induced by incubating the SaM-1 cells in 10 % CO₂ (pH approximately 7.0). Mineralization, which was augmented by the calcifying medium, was completely inhibited by acidosis. Acidosis depressed c-Jun mRNA and increased osteoprotegerin (OPG) production in a time-dependent manner. Depressing c-Jun mRNA expression using siRNA increased OPG production and inhibited mineralization. In addition, depressing OPG mRNA expression with siRNA enhanced mineralization in a dose-dependent manner. Acidosis or the OPG protein strongly inhibited mineralization in osteoblasts from neonatal mice. The present study was the first to demonstrate that acidosis inhibited mineralization, depressed c-Jun mRNA expression, and induced OPG production in human osteoblasts. These results suggest that OPG is involved in mineralization via c-Jun in human osteoblasts.

  12. Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

    OpenAIRE

    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 ...

  13. Moduretic-induced metabolic acidosis and hyperkalaemia.

    OpenAIRE

    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.

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

    Directory of Open Access Journals (Sweden)

    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. Severe metabolic acidosis following assault chemical burn

    Directory of Open Access Journals (Sweden)

    Sophie De Roock

    2012-01-01

    Full Text Available Assault chemical burns are uncommon in northern Europe. Besides local toxicity, systemic manifestations are possible after strong acid exposure. A 40-year-old woman was admitted 1 h after a criminal assault with sulfuric acid. The total burned surface area was 35%, third degree. Injury was due to sulfuric acid (measured pH 0.9 obtained from a car battery. Immediate complications were obstructive dyspnea and metabolic acidosis. The admission arterial pH was 6.92, with total bicarbonate 8.6 mEq/l and base deficit 23.4 mEq/l. The correction of metabolic acidosis was achieved after several hours by the administration of bicarbonate and lactate buffers. The patient developed several burns-related complications (sepsis and acute renal failure. Cutaneous projections of strong acids may cause severe metabolic acidosis, particularly when copious irrigation and clothes removal cannot be immediately performed at the scene.

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

    Science.gov (United States)

    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.

    Science.gov (United States)

    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. Trauma triggering thyrotoxic crisis with lactic acidosis

    Directory of Open Access Journals (Sweden)

    Jennifer S Prosser

    2015-01-01

    Full Text Available Thyrotoxic crisis (TC is defined as a life-threatening exacerbation of the hyperthyroid state that causes multiple autonomic and metabolic disturbances. It is considered to be an endocrine emergency that must be urgently diagnosed and treated. We describe a case of TC precipitated by trauma with a resultant lactic acidosis. The patient is a 24-year-old male with a history of hyperthyroidism who presented to the emergency department following a motor vehicle accident. The patient was initially tachycardic and hypertensive, however, was afebrile. Initial laboratory analysis showed an anion gap of 26, lactic acid 7.6, free T4 5.61 and thyroid stimulating hormone < 0.015. A diagnosis of TC was made, and he was treated with intravenous fluids, propranolol, and methimazole with improvement of tachycardia and lactic acidosis. We discuss the features of this case, which reviews the presentations of TC as well as its metabolic sequelae.

  19. Trauma triggering thyrotoxic crisis with lactic acidosis.

    Science.gov (United States)

    Prosser, Jennifer S; Quan, Dan K

    2015-01-01

    Thyrotoxic crisis (TC) is defined as a life-threatening exacerbation of the hyperthyroid state that causes multiple autonomic and metabolic disturbances. It is considered to be an endocrine emergency that must be urgently diagnosed and treated. We describe a case of TC precipitated by trauma with a resultant lactic acidosis. The patient is a 24-year-old male with a history of hyperthyroidism who presented to the emergency department following a motor vehicle accident. The patient was initially tachycardic and hypertensive, however, was afebrile. Initial laboratory analysis showed an anion gap of 26, lactic acid 7.6, free T4 5.61 and thyroid stimulating hormone < 0.015. A diagnosis of TC was made, and he was treated with intravenous fluids, propranolol, and methimazole with improvement of tachycardia and lactic acidosis. We discuss the features of this case, which reviews the presentations of TC as well as its metabolic sequelae.

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

    Directory of Open Access Journals (Sweden)

    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 and Calcium Nephrolithiasis

    Science.gov (United States)

    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.

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

    OpenAIRE

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    DEFF Research Database (Denmark)

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

    2000-01-01

    in tailbeat frequencies, aerobic scope or maximum sustainable swimming speed. The results indicate that the eel is extremely tolerant of hypercapnic acidosis. Acute, severe acidosis and hypoxaemia had no effect on CO or whole animal O2 uptake; chronic acidosis and hypoxaemia had no effect on the ability.......5 ± 2.2 vol%, significantly lower than in the control animals, where pHa was 7.89 ± 0.04 and ca,O2 11.6 ± 1.5 vol%. Exercise performance was studied in a swimming respirometer. Stepwise increases in swimming speed caused similar, exponential increases in O2 uptake in all groups, with no differences...

  5. Distal renal tubular acidosis in recurrent renal stone formers

    DEFF Research Database (Denmark)

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

    1989-01-01

    Renal acidification ability was examined in 90 recurrent renal stone formers, using fasting morning urinary pH levels followed by a short ammonium chloride loading test in subjects with pH levels above 6.0. Fifteen patients (16.6%) revealed a distal renal tubular acidification defect: one patient...... (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...... 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...

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

    Science.gov (United States)

    ... 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 ...

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

    Science.gov (United States)

    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

  8. A distal renal tubular acidosis showing hyperammonemia and hyperlactacidemia

    OpenAIRE

    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...

  9. Metformin-induced lactic acidosis: a case series

    OpenAIRE

    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 ...

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

    Science.gov (United States)

    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

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

    Science.gov (United States)

    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

  12. Metabolic Acidosis with Ophthalmic Dorzolamide in a Neonate.

    Science.gov (United States)

    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

  13. Type B Lactic Acidosis Associated With Venlafaxine Overdose.

    Science.gov (United States)

    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

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

    NARCIS (Netherlands)

    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)

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

    Science.gov (United States)

    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

  16. [5-0xoproline (pyroglutamic acid) acidosis and acetaminophen- a differential diagnosis in high anion gap metabolic acidosis].

    Science.gov (United States)

    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

  17. [5-0xoproline (pyroglutamic acid) acidosis and acetaminophen- a differential diagnosis in high anion gap metabolic acidosis].

    Science.gov (United States)

    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.

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

    Science.gov (United States)

    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

  19. Cerebrovascular response to acute metabolic acidosis in humans.

    NARCIS (Netherlands)

    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

  20. Metformin-induced lactic acidosis: a case series

    Directory of Open Access Journals (Sweden)

    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

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

    Science.gov (United States)

    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

  2. A distal renal tubular acidosis showing hyperammonemia and hyperlactacidemia

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    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.

  3. Metformin-Associated Acute Kidney Injury and Lactic Acidosis

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  6. Blood Parameters Modification at Different Ruminal Acidosis Conditions

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    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.

  7. Complement and contact activation in term neonates after fetal acidosis

    Science.gov (United States)

    Sonntag, J.; Wagner, M.; Strauss, E.; Obladen, M.

    1998-01-01

    AIMS—To evaluate complement and contact activation after fetal acidosis.
METHODS—Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay.
RESULTS—Median complement function (46 vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 µg/l), C5a (5.0 vs 0.6 µg/l), and factor XIIa (3.2 vs 1.3 µg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor.
CONCLUSIONS—Complement and contact activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.

 PMID:9577283

  8. In-vitro activation of complement system by lactic acidosis in newborn and adults

    Directory of Open Access Journals (Sweden)

    Friederike Hecke

    2001-01-01

    Full Text Available Introduction: Complement activation occurs secondary to a variety of external stimuli. Lactic acidosis has been previously shown to activate the complement factors C3a and C5a. In the present investigation we examined the differential effect of lactic acidosis on anaphylatoxin levels in cord and adult blood. Furthermore we aimed to determine if the entire complement cascade could be activated by lactic acidosis.

  9. Acidosis slows electrical conduction through the atrio-ventricular node

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    Ashley Muir Nisbet

    2014-06-01

    Full Text Available Acidosis affects the mechanical and electrical activity of mammalian hearts but comparatively little is known about its effects on the function of the atrio-ventricular node (AVN. In this study, the electrical activity of the epicardial surface of the left ventricle of isolated Langendorff-perfused rabbit hearts was examined using optical methods. Perfusion with hypercapnic Tyrode’s solution (20% CO2, pH 6.7 increased the time of earliest activation (Tact from 100.5+7.9 to 166.1+7.2ms (n=8 at a pacing cycle length (PCL of 300ms (37oC. Tact increased at shorter PCL, and the hypercapnic solution prolonged Tact further: at 150ms PCL, Tact was prolonged from 131.0+5.2 to 174.9+16.3ms. 2:1 AVN block was common at shorter cycle lengths. Atrial and ventricular conduction times were not significantly affected by the hypercapnic solution suggesting that the increased delay originated in the AVN. Isolated right atrial preparations were superfused with Tyrode’s solutions at pH 7.4 (control, 6.8 and 6.3. Low pH prolonged the atrial-Hisian (AH interval, the effective and functional refractory periods and Wenckebach cycle length significantly. Complete AVN block occurred in 6 out of 9 preparations. Optical imaging of conduction at the AV junction revealed increased conduction delay in the region of the AVN, with less marked effects in atrial and ventricular tissue. Thus acidosis can dramatically prolong the AVN delay, and in combination with short cycle lengths, this can cause partial or complete AVN block and is therefore implicated in the development of brady-arrhythmias in conditions of local or systemic acidosis.

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

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    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.

  11. Renal histology and immunopathology in distal renal tubular acidosis.

    Science.gov (United States)

    Feest, T G; Lockwood, C M; Morley, A R; Uff, J S

    1978-11-01

    Renal biospy studies are reported from 10 patients with distal renal tubular acidosis (DRTA). On the biopsies from 6 patients who had associated immunological abnormalities immunofluorescent studies for immunoglobulins, complement, and fibrin were performed. Interstitial cellular infiltration and fibrosis were common findings in patients with and without immunological abnormalities, and were usually associated with nephrocalcinosis and/or recurrent urinary infection. No immune deposits were demonstrated in association with the renal tubules. This study shows that DRTA in immunologically abnormal patients is not caused by tubular deposition of antibody or immune complexes. The possibility of cell mediated immune damage is discussed.

  12. LACTIC ACIDOSIS: A RARE MANIFESTATION OF SYNTHETIC MARIJUANA INTOXICATION.

    Science.gov (United States)

    Antill, T; Jakkoju, A; Dieguez, J; Laskhmiprasad, L

    2015-01-01

    Synthetic cannabinoids are designer drugs that mimic the effect of cannabis, which has become popular with young drug users. These drugs have a similar chemical structure and pharmacologic effects as marijuana, but seem to be more potent. These substances have been banned by the US Drug Enforcement Agency in 2010. Prior to 2010, these drugs were perceived as "safer" by the general population. Synthetic cannabinoids cause effects similar to marijuana making the subjects euphoric. However, they act as full, rather than partial, agonist at the receptor sites causing more severe side effects such as severe agitation, seizures, acute renal failure, and lactic acidosis. PMID:27159480

  13. A Fatal Case of Metformin-associated Lactic Acidosis.

    Science.gov (United States)

    Ozeki, Toshikazu; Kawato, Rui; Watanabe, Mitsuru; Minatoguchi, Shun; Murai, Yukari; Ryuge, Akihiro; Takasugi, Koji; Hamada, Takuya; Oyama, Yukako; Nomura, Atsushi; Tomino, Tatsuhito; Shimizu, Hideaki; Fujita, Yoshiro

    2016-01-01

    A 72-year-old woman with a history of type 2 diabetes mellitus was brought to the ER with metformin-associated lactic acidosis. She received continuous hemofiltration and hemodialysis, but the laboratory analyses showed no improvement. She died 11 hours after admission. Metformin is minimally bound to proteins and is readily dialyzable, but a prolonged period of dialysis is required, because metformin has a very large distribution volume and is distributed to multiple compartments. The peak blood metformin level was 432 mg/L in this case, which is one of the highest metformin concentrations ever reported, and eight hours of hemodialysis were not sufficient to reduce the serum level.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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.

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

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    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.

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

    NARCIS (Netherlands)

    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

  18. Metformin and lactic acidosis : cause or coincidence? A review of case reports

    NARCIS (Netherlands)

    Stades, AME; Heikens, JT; Erkelens, DW; Holleman, F; Hoekstra, JBL

    2004-01-01

    Objective. Metformin has been associated with the serious side-effect lactic acidosis. However, it remains unclear whether the use of metformin was a cause or a coincidence in lactic acidosis. Design. A literature search of the Index Medicus (1959-66) and of the databases Embase, Medline, Medline Ex

  19. Ruminal Acidosis in Feedlot: From Aetiology to Prevention

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    Joaquín Hernández

    2014-01-01

    Full Text Available Acute ruminal acidosis is a metabolic status defined by decreased blood pH and bicarbonate, caused by overproduction of ruminal D-lactate. It will appear when animals ingest excessive amount of nonstructural carbohydrates with low neutral detergent fiber. Animals will show ruminal hypotony/atony with hydrorumen and a typical parakeratosis-rumenitis liver abscess complex, associated with a plethora of systemic manifestations such as diarrhea and dehydration, liver abscesses, infections of the lung, the heart, and/or the kidney, and laminitis, as well as neurologic symptoms due to both cerebrocortical necrosis and the direct effect of D-lactate on neurons. In feedlots, warning signs include decrease in chewing activity, weight, and dry matter intake and increase in laminitis and diarrhea prevalence. The prognosis is quite variable. Treatment will be based on the control of systemic acidosis and dehydration. Prevention is the most important tool and will require normalization of ruminal pH and microbiota. Appropriate feeding strategies are essential and involve changing the dietary composition to increase neutral detergent fiber content and greater particle size and length. Appropriate grain processing can control the fermentation rate while additives such as prebiotics or probiotics can help to stabilize the ruminal environment. Immunization against producers of D-lactate is being explored.

  20. Ruminal acidosis in feedlot: from aetiology to prevention.

    Science.gov (United States)

    Hernández, Joaquín; Benedito, José Luis; Abuelo, Angel; Castillo, Cristina

    2014-01-01

    Acute ruminal acidosis is a metabolic status defined by decreased blood pH and bicarbonate, caused by overproduction of ruminal D-lactate. It will appear when animals ingest excessive amount of nonstructural carbohydrates with low neutral detergent fiber. Animals will show ruminal hypotony/atony with hydrorumen and a typical parakeratosis-rumenitis liver abscess complex, associated with a plethora of systemic manifestations such as diarrhea and dehydration, liver abscesses, infections of the lung, the heart, and/or the kidney, and laminitis, as well as neurologic symptoms due to both cerebrocortical necrosis and the direct effect of D-lactate on neurons. In feedlots, warning signs include decrease in chewing activity, weight, and dry matter intake and increase in laminitis and diarrhea prevalence. The prognosis is quite variable. Treatment will be based on the control of systemic acidosis and dehydration. Prevention is the most important tool and will require normalization of ruminal pH and microbiota. Appropriate feeding strategies are essential and involve changing the dietary composition to increase neutral detergent fiber content and greater particle size and length. Appropriate grain processing can control the fermentation rate while additives such as prebiotics or probiotics can help to stabilize the ruminal environment. Immunization against producers of D-lactate is being explored.

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

    OpenAIRE

    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...

  2. Acidosis láctica grave asociada a intoxicación por metformina Severe lactic acidosis associated to metformin intoxication

    Directory of Open Access Journals (Sweden)

    M. S. Holanda Peña

    2007-02-01

    Full Text Available La metformina es una biguanida ampliamente utilizada en el tratamiento de la diabetes mellitus tipo II. Entre los efectos secundarios derivados de su empleo destaca por su baja frecuencia de presentación pero potencial gravedad la acidosis láctica. El diagnóstico de la misma se basa generalmente en la coexistencia de la acidosis láctica en un paciente en tratamiento con metformina con uno o mas factores de riesgo para la presentación de la misma. El desarrollo de acidosis láctica en relación con el tratamiento con metformina conlleva una mortalidad que oscila entre 50-80%.Metformin is a biguanide extensively used in the treatment of type II diabetes mellitus. Between the nocive effects of the metformin emphasizes tha lactic acidosis because of its low frecuency but potential severity. The diagnosis of the poisoning due to metformin is based on the coexistence of lactic acidosis and one or more of the risk factors. The development of lactic acidosis in metformin poisoning is associated to a range of 50-80% of mortality.

  3. Screening renal stone formers for distal renal tubular acidosis

    DEFF Research Database (Denmark)

    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...

  4. Acute starvation in pregnancy: a cause of severe metabolic acidosis.

    Science.gov (United States)

    Patel, A; Felstead, D; Doraiswami, M; Stocks, G M; Waheed, U

    2011-07-01

    We report a case of starvation-induced metabolic ketoacidosis in a previously healthy 29-year-old, nulliparous woman at 32 weeks of gestation. She was admitted to hospital with mild preeclampsia associated with persistent nausea and vomiting that progressed to severe preeclampsia requiring urgent control of hypertension before caesarean delivery. Prolonged and severe vomiting limited oral caloric intake and led to starvation ketoacidosis, characterised by ketonuria and a raised anion gap metabolic acidosis that required intensive care support. Despite significant metabolic derangement the patient appeared clinically well. Intravascular volume was replenished. Fluid restriction used as part of our preeclampsia treatment regimen delayed the therapeutic administration of sufficient dextrose, which rapidly corrected her metabolic derangement when commenced after delivery. Electrolyte supplementation was given to prevent re-feeding syndrome. Both mother and baby were discharged without sequelae.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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.

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

    OpenAIRE

    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.

  8. Acidosis-induced p38 MAPK activation and its implication in regulation of cardiac contractility

    Institute of Scientific and Technical Information of China (English)

    Ming ZHENG; Rong HOU; Rui-ping XIAO

    2004-01-01

    AIM: To determine the possible role of pH in mediating activation of p38 mitogen-activated protein kinase (MAPK) and the consequent function of activated p38 MAPK in regulating cardiac contractility. METHODS: Adult rat cardiomyocytes were isolated and cultured. Low pH media was used to induce intracellular acidosis and contraction of single cardiomyocyte was measured. RESULTS: Phosphorylation of p38 MAPK was increased during ischemia, and pHi was decreased. Intracellular acidosis activated p38 MAPK to a similar level as ischemia. Inhibition of p38 MAPK activation by SB203580, a specific inhibitor of p38 MAPK, reversed acidosis-mediated reduction of myocyte contractility. CONCLUSION: In adult rat cardiomyocytes, intracellular acidification activated p38 MAPK and decreased cardiac contractility. Pretreatment of cardiomyocytes with SB203580 completely blocked p38 MAPK activation and partially reversed acidosis-mediated decline of cardiac contractility.

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

    Science.gov (United States)

    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

  10. Medullary nephrocalcinosis, distal renal tubular acidosis and polycythaemia in a patient with nephrotic syndrome

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    Karunarathne Suneth

    2012-07-01

    Full Text Available Abstract Background Medullary nephrocalcinosis and distal renal tubular acidosis are closely associated and each can lead to the other. These clinical entities are rare in patients with nephrotic syndrome and polycythaemia is an unusual finding in such patients. We describe the presence of medullary nephrocalcinosis, distal renal tubular acidosis and polycythaemia in a patient with nephrotic syndrome due to minimal change disease. Proposed mechanisms of polycythaemia in patients with nephrotic syndrome and distal renal tubular acidosis include, increased erythropoietin production and secretion of interleukin 8 which in turn stimulate erythropoiesis. Case presentation A 22 year old Sri Lankan Sinhala male with nephrotic syndrome due to minimal change disease was investigated for incidentally detected polycythaemia. Investigations revealed the presence of renal tubular acidosis type I and medullary nephrocalcinosis. Despite extensive investigation, a definite cause for polycythaemia was not found in this patient. Treatment with potassium and bicarbonate supplementation with potassium citrate led to correction of acidosis thereby avoiding the progression of nephrocalcinosis and harmful effects of chronic acidosis. Conclusion The constellation of clinical and biochemical findings in this patient is unique but the pathogenesis of erythrocytosis is not clearly explained. The proposed mechanisms for erythrocytosis in other patients with proteinuria include increased erythropoietin secretion due to renal hypoxia and increased secretion of interleukin 8 from the kidney. This case illustrates that there may exist hitherto unknown connections between tubular and glomerular dysfunction in patients with nephrotic syndrome.

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

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    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.

  12. 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.

    Science.gov (United States)

    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

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

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    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

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

    Directory of Open Access Journals (Sweden)

    Maria José Rodriguez Cabalgante

    2012-12-01

    Full Text Available 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. Change (Δ of intracellular calcium concentration, basal and after Angiotensin II (10-6M exposition, were measured to evaluate cellular performance. EMT was evaluated by the expression of α-smooth muscle actin (α-SMA and E-cadherin by immunocytochemistry and/or Western blot. TGF-β1 secretion was determined by ELISA in cell supernatant. RESULTS: At pH 7.0 HK2 cells significantly reduced E-cadherin and increased α-SMA expression (EMT. Supernatant TGF-β1 levels were higher than in control group. Calcium citrate decreased acidosis induced EMT and improved cells performance, without reduction of TGF-β production. CONCLUSIONS: Acidosis induces EMT and secretion of TGF-β1 in tubular proximal cells in culture and citrate improves cellular performance and ameliorates acidosis induced EMT.

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

    Directory of Open Access Journals (Sweden)

    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.

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

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    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.

  17. In vitro activation of complement and contact system by lactic acidosis.

    Science.gov (United States)

    Sonntag, J; Emeis, M; Strauss, E; Obladen, M

    1998-01-01

    The activation of complement and contact systems occurs in reperfusion injuries with initial tissue hypoxia, and lactic acidosis such as mycardial infarction and birth asphyxia. The aim of our experiment was the formal proof of activation by sole lactic acidosis. Lactic acid was added to blood and plasma samples from 10 healthy volunteers. C5a and factor XIIa were measured by EIA after incubation at 37 degrees C for 1 h. Both concentrations increased (P < 0.0001 by Friedman analysis) in blood and plasma samples with increasing amount of added lactic acid. Lactic acidosis can activate C5 from the complement system and factor XII from the contact system directly, even in the absence of cellular components. PMID:9839699

  18. in vitro activation of complement and contact system by lactic acidosis

    Directory of Open Access Journals (Sweden)

    J. Sonntag

    1998-01-01

    Full Text Available The activation of complement and contact systems occurs in reperfusion injuries with initial tissue hypoxia, and lactic acidosis such as mycardial infarction and birth asphyxia. The aim of our experiment was the formal proof of activation by sole lactic acidosis. Lactic acid was added to blood and plasma samples from 10 healthy volunteers. C5a and factor XIIa were measured by EIA after incubation at 37°C for 1 h. Both concentrations increased (P<0.0001 by Friedman analysis in blood and plasma samples with increasing amount of added lactic acid. Lactic acidosis can activate C5 from the complement system and factor XII from the contact system directly, even in the absence of cellular components.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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 ...

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

    Science.gov (United States)

    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

  2. Activation of GPR4 by acidosis increases endothelial cell adhesion through the cAMP/Epac pathway.

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    Aishe Chen

    Full Text Available Endothelium-leukocyte interaction is critical for inflammatory responses. Whereas the tissue microenvironments are often acidic at inflammatory sites, the mechanisms by which cells respond to acidosis are not well understood. Using molecular, cellular and biochemical approaches, we demonstrate that activation of GPR4, a proton-sensing G protein-coupled receptor, by isocapnic acidosis increases the adhesiveness of human umbilical vein endothelial cells (HUVECs that express GPR4 endogenously. Acidosis in combination with GPR4 overexpression further augments HUVEC adhesion with U937 monocytes. In contrast, overexpression of a G protein signaling-defective DRY motif mutant (R115A of GPR4 does not elicit any increase of HUVEC adhesion, indicating the requirement of G protein signaling. Downregulation of GPR4 expression by RNA interference reduces the acidosis-induced HUVEC adhesion. To delineate downstream pathways, we show that inhibition of adenylate cyclase by inhibitors, 2',5'-dideoxyadenosine (DDA or SQ 22536, attenuates acidosis/GPR4-induced HUVEC adhesion. Consistently, treatment with a cAMP analog or a G(i signaling inhibitor increases HUVEC adhesiveness, suggesting a role of the G(s/cAMP signaling in this process. We further show that the cAMP downstream effector Epac is important for acidosis/GPR4-induced cell adhesion. Moreover, activation of GPR4 by acidosis increases the expression of vascular adhesion molecules E-selectin, VCAM-1 and ICAM-1, which are functionally involved in acidosis/GPR4-mediated HUVEC adhesion. Similarly, hypercapnic acidosis can also activate GPR4 to stimulate HUVEC adhesion molecule expression and adhesiveness. These results suggest that acidosis/GPR4 signaling regulates endothelial cell adhesion mainly through the G(s/cAMP/Epac pathway and may play a role in the inflammatory response of vascular endothelial cells.

  3. In-vitro activation of complement system by lactic acidosis in newborn and adults.

    Science.gov (United States)

    Hecke, F; Hoehn, T; Strauss, E; Obladen, M; Sonntag, J

    2001-01-01

    INTRODUCTION: Complement activation occurs secondary to a variety of external stimuli. Lactic acidosis has been previously shown to activate the complement factors C3a and C5a. In the present investigation we examined the differential effect of lactic acidosis on anaphylatoxin levels in cord and adult blood. Furthermore we aimed to determine if the entire complement cascade could be activated by lactic acidosis. METHODS: Cord and adult blood samples (n = 20 each) were collected and incubated for one hour in either untreated condition or with the addition of lactate in two concentrations (5.5 mmol/l vs. 22 mmol/l). Following incubation, levels of C3a, C5a and sC5b-9, and blood gas parameters were determined. RESULTS: Anaphylatoxin (C3a and C5a) and sC5b-9 levels increased with the addition of lactate in a dose-dependent manner in cord and adult blood (C3a: 1 h, 5.5 mmo/l, 22 mmol/l: 418/498/622 microg/l in cord blood; 1010/1056/1381 microg/l in adult blood, p<0,05; similar results were found for C5a and sC5b-9). CONCLUSION: Lactic acidosis leads to an activation of the entire complement system in neonates and in adults. This activation is dose-dependent and more pronounced in adults as compared to neonates. PMID:11324901

  4. Indicators of induced subacute ruminal acidosis (SARA) in Danish Holstein cows

    DEFF Research Database (Denmark)

    Danscher, Anne Mette; Li, Shucong; Andersen, Pia H.;

    2015-01-01

    BACKGROUND: The prevalence of subacute ruminal acidosis (SARA) in dairy cows is high with large impact on economy and welfare. Its current field diagnosis is based on point ruminal pH measurements by oral probe or rumenocentesis. These techniques are invasive and inaccurate, and better markers...

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

    DEFF Research Database (Denmark)

    Andersen, NN; Ladefoged, NN

    1991-01-01

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

    NARCIS (Netherlands)

    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

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

    Science.gov (United States)

    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

  8. Severe lactic acidosis associated with juice of the mangosteen fruit Garcinia mangostana.

    Science.gov (United States)

    Wong, Leslie P; Klemmer, Philip J

    2008-05-01

    The tropical mangosteen fruit has long been prized in Southeast Asia for its traditional healing properties. Mangosteen fruit juice is now available in the United States and marketed for its purported health benefits. We describe a case of severe lactic acidosis associated with the use of mangosteen juice as a dietary supplement.

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    F.H.D. González

    2010-01-01

    Full Text Available La acidosis ruminal es un trastorno frecuente en cabras como consecuencia de errores en el manejo alimentario en animales no adaptados a dietas que contienen carbohidratos fácilmente fermentables. La forma subaguda de la enfermedad es de difícil diagnóstico toda vez que no muestra evidencia de signos clínicos claros y los parámetros ácido-básicos pueden permanecer en el rango normal. El presente estudio tuvo por objetivo probar la hipótesis de que la haptoglobina y la proteína amilóide sérica A, las dos proteínas de fase aguda más importantes en rumiantes, pueden ser útiles como marcadores de acidosis subaguda en cabras. Se indujo acidosis ruminal a seis cabras de la raza Murciano-Granadina, no adaptadas al consumo de concentrado, mediante el suministro de una dieta con 60% de concentrado y 40% de heno de alfalfa durante 5 días. Dos cabras fueron sometidas a fistulación ruminal para comprobar el efecto del tratamiento sobre el pH del rumen. A todos los animales se les tomaron muestras de sangre y orina el día anterior a la inducción, durante el período de inducción y hasta 18 días después de la inducción (período de recuperación. El pH ruminal cayó a menos de 5,5 durante el período de inducción de acidosis en las cabras fistuladas, mientras que la mitad de las cabras tuvieron diarrea al tercer día de la inducción de acidosis. Los parámetros gasométricos indicaron que los mecanismos compensatorios fueron eficientes para mantener el equilibrio ácido-básico. La haptoglobina sérica presentó un aumento moderado durante el período de inducción de acidosis, mientras que la amilóide sérica A no presentó cambios. Los resultados sugieren que la haptoglobina puede utilizarse como un potencial indicador de acidosis ruminal en cabras.

  11. Starvation Ketoacidosis as a Cause of Unexplained Metabolic Acidosis in the Perioperative Period

    Science.gov (United States)

    Mostert, Monique; Bonavia, Anthony

    2016-01-01

    Patient: Female, 24 Final Diagnosis: Starvation ketoacidosis Symptoms: None Medication: — Clinical Procedure: Lumbar laminectomy Specialty: Orthopedics and Traumatology Objective: Unusual clinical course Background: Besides providing anesthesia for surgery, the anesthesiologist’s role is to optimize the patient for surgery and for post-surgical recovery. This involves timely identification and treatment of medical comorbidities and abnormal laboratory values that could complicate the patient’s perioperative course. There are several potential causes of anion and non-anion gap metabolic acidosis in surgical patients, most of which could profoundly affect a patient’s surgical outcome. Thus, the presence of an acute acid-base disturbance requires a thorough workup, the results of which will influence the patient’s anesthetic management. Case Report: An otherwise-healthy 24-year-old female presented for elective spine surgery and was found to have metabolic acidosis, hypotension, and polyuria intraoperatively. Common causes of acute metabolic acidosis were investigated and systematically ruled out, including lactic acidosis, diabetic ketoacidosis, drug-induced ketoacidosis, ingestion of toxic alcohols (e.g., methanol, ethylene glycol), uremia, and acute renal failure. Laboratory workup was remarkable only for elevated serum and urinary ketone levels, believed to be secondary to starvation ketoacidosis. Due to the patient’s unexplained acid-base disturbance, she was kept intubated postoperatively to allow for further workup and management. Conclusions: Starvation ketoacidosis is not widely recognized as a perioperative entity, and it is not well described in the medical literature. Lack of anesthesiologist awareness about this disorder may complicate the differential diagnosis for acute intraoperative metabolic acidosis and lead to a prolonged postoperative stay and an increase in hospital costs. The short- and long-term implications of perioperative

  12. Acidosis downregulates platelet haemostatic functions and promotes neutrophil proinflammatory responses mediated by platelets.

    Science.gov (United States)

    Etulain, Julia; Negrotto, Soledad; Carestia, Agostina; Pozner, Roberto Gabriel; Romaniuk, María Albertina; D'Atri, Lina Paola; Klement, Giannoula Lakka; Schattner, Mirta

    2012-01-01

    Acidosis is one of the hallmarks of tissue injury such as trauma, infection, inflammation, and tumour growth. Although platelets participate in the pathophysiology of all these processes, the impact of acidosis on platelet biology has not been studied outside of the quality control of laboratory aggregation assays or platelet transfusion optimization. Herein, we evaluate the effect of physiologically relevant changes in extracellular acidosis on the biological function of platelets, placing particular emphasis on haemostatic and secretory functions. Platelet haemostatic responses such as adhesion, spreading, activation of αIIbβ3 integrin, ATP release, aggregation, thromboxane B2 generation, clot retraction and procoagulant activity including phosphatidilserine exposure and microparticle formation, showed a statistically significant inhibition of thrombin-induced changes at pH of 7.0 and 6.5 compared to the physiological pH (7.4). The release of alpha granule content was differentially regulated by acidosis. At low pH, thrombin or collagen-induced secretion of vascular endothelial growth factor and endostatin were dramatically reduced. The release of von Willebrand factor and stromal derived factor-1α followed a similar, albeit less dramatic pattern. In contrast, the induction of CD40L was not changed by low pH, and P-selectin exposure was significantly increased. While the generation of mixed platelet-leukocyte aggregates and the increased chemotaxis of neutrophils mediated by platelets were further augmented under acidic conditions in a P-selectin dependent manner, the increased neutrophil survival was independent of P-selectin expression. In conclusion, our results indicate that extracellular acidosis downregulates most of the haemostatic platelet functions, and promotes those involved in amplifying the neutrophil-mediated inflammatory response.

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

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    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

  14. A case of quadriparesis due to renal tubular acidosis accompanied by vitamin D deficiency in Sjogren's syndrome

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    Can Huzmeli

    2016-08-01

    Full Text Available Renal tubular acidosis (RTA is metabolic acidosis disorder with a normal anion gap that occurs resulting from bicarbonate reabsorption or disorder in the hydrogen excretion from the kidney. A variety of tests are required to be administered in a stepwise fashion for the diagnosis and characterization of RTA. Correct diagnosis involves careful evaluation, including exclusion of other entities causing acidosis. The patients were treated with potassium and bicarbonate supplementation. A fifty-one years old female patient presented to the emergency department with quadriparesis dependent on hypokalemia and vitamin D deficiency, was diagnosed with distal renal tubular acidosis (dRTA combined with Sjogrens Syndrome (SS. We submitted this case in order to draw attention to the presentation of the RTA with SS. [Int J Res Med Sci 2016; 4(8.000: 3625-3628

  15. Acidosis activation of the proton-sensing GPR4 receptor stimulates vascular endothelial cell inflammatory responses revealed by transcriptome analysis.

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    Lixue Dong

    Full Text Available Acidic tissue microenvironment commonly exists in inflammatory diseases, tumors, ischemic organs, sickle cell disease, and many other pathological conditions due to hypoxia, glycolytic cell metabolism and deficient blood perfusion. However, the molecular mechanisms by which cells sense and respond to the acidic microenvironment are not well understood. GPR4 is a proton-sensing receptor expressed in endothelial cells and other cell types. The receptor is fully activated by acidic extracellular pH but exhibits lesser activity at the physiological pH 7.4 and minimal activity at more alkaline pH. To delineate the function and signaling pathways of GPR4 activation by acidosis in endothelial cells, we compared the global gene expression of the acidosis response in primary human umbilical vein endothelial cells (HUVEC with varying level of GPR4. The results demonstrated that acidosis activation of GPR4 in HUVEC substantially increased the expression of a number of inflammatory genes such as chemokines, cytokines, adhesion molecules, NF-κB pathway genes, and prostaglandin-endoperoxidase synthase 2 (PTGS2 or COX-2 and stress response genes such as ATF3 and DDIT3 (CHOP. Similar GPR4-mediated acidosis induction of the inflammatory genes was also noted in other types of endothelial cells including human lung microvascular endothelial cells and pulmonary artery endothelial cells. Further analyses indicated that the NF-κB pathway was important for the acidosis/GPR4-induced inflammatory gene expression. Moreover, acidosis activation of GPR4 increased the adhesion of HUVEC to U937 monocytic cells under a flow condition. Importantly, treatment with a recently identified GPR4 antagonist significantly reduced the acidosis/GPR4-mediated endothelial cell inflammatory response. Taken together, these results show that activation of GPR4 by acidosis stimulates the expression of a wide range of inflammatory genes in endothelial cells. Such inflammatory response can be

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

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    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.

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

    Science.gov (United States)

    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

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

    DEFF Research Database (Denmark)

    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...... of the disease. bovine, subacute ruminal acidosis, fecal microbiome, biological marker Host publication information...... in the 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...... 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 markers...

  19. Hypernatraemic dehydration in infants in Kuwait with special reference to therapy of associated metabolic acidosis.

    Science.gov (United States)

    John, A I; Fedeczko, D; Fernando, N P

    1984-12-01

    Over a period of 16 months 510 children with diarrhoea were admitted to the Al-Adan Hospital, Kuwait, of whom 26 (5.1%) developed hypernatraemic dehydration. Prominent clinical features included vomiting (92.3%), fever (84.6%) and convulsions (19.2%). The majority were below six months of age with a mean age of 3.1 months. The sex distribution was equal. Twenty infants (77%) had severe metabolic acidosis and were treated with a combination of sodium bicarbonate and 5% glucose in water until the acidosis was corrected after which a solution of sodium chloride replaced the use of sodium bicarbonate. The sodium concentration of the intravenous fluid varied from 15 to 30 mmol/l and was given at a rate of 100 to 120 ml/kg/day. One infant died. The 25 survivors, (96.15%), which included three who developed convulsions during treatment, recovered without any neurologic sequelae.

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

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    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.

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

    OpenAIRE

    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...

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

    OpenAIRE

    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 ...

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

    Directory of Open Access Journals (Sweden)

    Maneksh Delinda

    2010-01-01

    Full Text Available 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 and respiratory movements were recorded. Either aqueous extract of C. collinus or control solution was administered intraperitoneally. Serial measurements of blood gases, electrolytes and urinary pH were made. Isolated brush border and basolateral membranes from rat kidney were incubated with C. collinus extract and reduction in ATPase activity was assessed. Venous blood samples from human volunteers and rats were incubated with an acetone extract of C. collinus and plasma potassium was estimated as an assay for sodium-potassium pump activity. Results : The mortality was 100% in tests and 17% in controls. Terminal event in test animals was respiratory arrest. Controls had metabolic acidosis, respiratory compensation , acidic urine and hyperkalemia. Test animals showed respiratory acidosis, alkaline urine and low blood potassium as compared to controls. C. collinus extract inhibited ATPase activity in rat kidney. Plasma K + did not increase in human blood incubated with C. collinus extract. Conclusions and Implications : Active principles of C. collinus inhibit proton pumps in the renal brush border, resulting in type I DRTA in rats. There is no inhibition of sodium-potassium pump activity. Test animals develop respiratory acidosis, and the immediate cause of death is respiratory arrest.

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

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    Fareed B. Kamar

    2015-01-01

    Full Text Available 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.

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

    Science.gov (United States)

    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.

  6. Relationship between rickets and incomplete distal renal tubular acidosis in children

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    Oduwole Abiola O

    2010-08-01

    Full Text Available Abstract Background In the Sub Saharan Africa Rickets has now been established to be due primarily to calcium deficiency and sometimes in combination with vitamin D deficiency. The main thrust of management is calcium supplementation with or without vitamin D. An observation was made that some children with nutritional rickets do not respond to this management modality. The recently reported high prevalence of Incomplete Distal Renal Tubular Acidosis (idRTA in adults with osteoporosis as brought to fore the possibility of this being a possible cause of calcium wastage and therefore the poor response in these group of children with rickets. Aim To determine the prevalence of idRTA amongst a cohort of subjects with rickets To show a relationship between rickets and incomplete distal renal acidosis To determine the response of children with rickets and idRTA to addition of Shohl's solution to therapy Methodology Two separate cohorts of children with rickets performed the ammonium chloride loading test to detect those with incomplete renal tubular acidosis. Following identification for idRTA, Shohl's solution was added to therapy of calcium and vitamin D supplementation and their response compared to those without idRTA on calcium and vitamin D supplementation solely. Results 50 children with rickets aged from two to six years of age and composed of 29 females and 21males were investigated. Incomplete renal tubular acidosis was found in 38% of them. Prevalence of idRTA was highest amongst those aged 3-6 years of age. Those with idRTA had worse limb deformities, biochemical and radiological parameters than those who hadn't. Rate of response on those with idRTA treated with Shohl's solution was at par with those without idRTA. Conclusion Incomplete idRTA exist amongst children with rickets and should be looked out for in severe rickets and older children. Treatment of idRTA will lead to optimal response and healing of rickets.

  7. Metabolic acidosis and changes in water and electrolyte balance after maximal exercise.

    Science.gov (United States)

    Sejersted, O M; Medbø, J I; Hermansen, L

    1982-01-01

    The purpose of this investigation was to study lactate production and the consequent changes in acid-base status, and in water and electrolyte balance, in response to 1 min of maximal exercise in sprint- and endurance-trained subjects. So far, the results from only two subjects (one sprinter and one marathon runner) have been analysed. The rate of lactate production was higher in the sprinter than in the marathon runner, as shown by peak blood lactate concentrations of 20.8 and 13.3 mM for the two subjects, respectively. Arterial blood pH fell from 7.43 to 7.14 in the sprinter and from 7.44 to 7.23 for the marathon runner. The metabolic acidosis was partly compensated for by a lowering of arterial CO2 tension by 0.0775 kPa per 1 mM drop in base excess. In each subject large changes in water and electrolyte balance occurred. Haematocrit increased dramatically in both subjects, and the calculated decrease in plasma volume was 20% for the marathon runner and 30% for the sprinter. In each subject sodium was removed from the circulation in amounts sufficient to keep the plasma sodium concentration constant. Plasma potassium concentration was unrelated to the state of acidosis, being 2.5 mM above the resting concentration immediately after maximal exercise, and dropping by 3 mM in the subsequent 2-3 min of recovery during prevailing acidosis. The degree of lactic acidosis was large in both subjects, although more severe in the sprinter than in the endurance runner. However, buffer capacity and compensatory mechanisms were largely similar in both subjects.

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

    OpenAIRE

    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 ...

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

    DEFF Research Database (Denmark)

    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 7.50). Induction...... of hypercapnic acidosis (10% CO2) or normocapnic acidosis (15 mmol/L HCO3-) caused significant inhibition of smooth muscle tension, and both conditions reduced pHi as well as pHo. N-Nitro-L-arginine significantly inhibited the relaxation to hypercapnic acidosis but had no significant effect on relaxation...... to normocapnic acidosis. Predominant extracellular acidosis, induced by reducing [HCO3-] from 25 to 9 mmol/L and CO2 from 5% to 2.5%, also caused inhibition of tension in steady state. By contrast, predominant intracellular acidosis, induced by increasing [HCO3-] from 25 to 65 mmol/L and CO2 from 5% to 15...

  10. Lactic Acidosis Induced by Linezolid Mimics Symptoms of an Acute Intracranial Bleed: A Case Report and Literature Review

    Science.gov (United States)

    Zuccarini, Nichole Suzzanne; Yousuf, Tariq; Wozniczka, Daniel; Rauf, Anis Abdul

    2016-01-01

    Lactic acidosis is common and most often associated with disturbed acid-base balance. Rarely, it can be a life-threatening medication side effect. Hence, determining the etiology of lactic acidosis early in patients is paramount in choosing the correct therapeutic intervention. Although lactic acidosis as an adverse drug reaction of linezolid is a well-recognized and documented clinical entity, the occurrence of such mimicking an acute intracranial bleed has not been reported to our knowledge. The following case is presented as an example of such an occurrence. A 67-year-old woman presented to the emergency department for lethargy, nausea and syncope. The head CT did not demonstrate any bleeding or mass effect, but lab results were significant for elevated lactic acid. The patient recently underwent left total hip replacement surgery, which was complicated by a methicillin-resistant Staphylococcus aureus (MRSA) infection. She received 6 weeks of oral linezolid therapy. And upon learning that key part of her history, the linezolid was discontinued. Her lactic acid rapidly normalized and she was discharged home. Several publications demonstrate that linezolid induces lactic acidosis by disrupting crucial mitochondrial functions. It is essential that clinicians are aware that linezolid can cause lactic acidosis. And, the important reminder is that adverse drug reactions can often mimic common diseases. If it is not recognized early, ominous clinical consequences may occur. In conclusion, linezolid should be suspected and included in the differential diagnosis if lactic acidosis exists with an uncommon clinical picture. PMID:27635182

  11. Acidosis láctica secundaria a terapia antirretroviral en pacientes con VIH/sida

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    Benhard Hasbum-Fernández

    2006-06-01

    Full Text Available La acidosis láctica es una complicación infrecuente de la terapia antirretroviral para VIH. Su aparición se ha relacionado con la administración de análogos nucleósidos de la transcriptasa inversa, en especial estavudina y didanosina. Se presentan los 2 casos que se manejaron en el año 2005 en el Servicio de Medicina del Hospital México. En ambos el desenlace fue fatal, aún cuando se utilizaron todas las medidas terapéuticas recomendadas.Lactic acidosis is a rare complication of antiretroviral treatment for HIV. Its occurrence has been related to the use of transcriptase reverse nucleoside analogues, especially estavudine and didanosine. We present here 2 cases of HIV patients who suffered lactic acidosis and were treated at the Internal Medicine Department of the Hospital Mexico, San Jose, Costa Rica. Both cases had a fatal evolution, despite that both received all the therapeutic measures recommended in the literature.

  12. Proximal tubule-specific glutamine synthetase deletion alters basal and acidosis-stimulated ammonia metabolism.

    Science.gov (United States)

    Lee, Hyun-Wook; Osis, Gunars; Handlogten, Mary E; Lamers, Wouter H; Chaudhry, Farrukh A; Verlander, Jill W; Weiner, I David

    2016-06-01

    Glutamine synthetase (GS) catalyzes the recycling of NH4 (+) with glutamate to form glutamine. GS is highly expressed in the renal proximal tubule (PT), suggesting ammonia recycling via GS could decrease net ammoniagenesis and thereby limit ammonia available for net acid excretion. The purpose of the present study was to determine the role of PT GS in ammonia metabolism under basal conditions and during metabolic acidosis. We generated mice with PT-specific GS deletion (PT-GS-KO) using Cre-loxP techniques. Under basal conditions, PT-GS-KO increased urinary ammonia excretion significantly. Increased ammonia excretion occurred despite decreased expression of key proteins involved in renal ammonia generation. After the induction of metabolic acidosis, the ability to increase ammonia excretion was impaired significantly by PT-GS-KO. The blunted increase in ammonia excretion occurred despite greater expression of multiple components of ammonia generation, including SN1 (Slc38a3), phosphate-dependent glutaminase, phosphoenolpyruvate carboxykinase, and Na(+)-coupled electrogenic bicarbonate cotransporter. We conclude that 1) GS-mediated ammonia recycling in the PT contributes to both basal and acidosis-stimulated ammonia metabolism and 2) adaptive changes in other proteins involved in ammonia metabolism occur in response to PT-GS-KO and cause an underestimation of the role of PT GS expression.

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

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    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. The effect of acidosis on the interval-force relation and mechanical restitution in ferret papillary muscle.

    Science.gov (United States)

    McCall, E; Orchard, C H

    1991-01-01

    1. The effect of a respiratory acidosis on the interval-force relation and on mechanical restitution was investigated in ferret papillary muscles. 2. Acidosis (pH 6.85) decreased developed force over a range of stimulation frequencies (1.0.06 Hz); the percentage decrease was greatest at the lowest stimulation frequencies. Qualitatively similar effects of acidosis on developed force were observed in the presence of the sarcoplasmic reticulum (SR) inhibitor ryanodine. 3. Mechanical restitution curves were constructed by interpolating extra-systoles at different test intervals following a train of steady-state beats. Mechanical restitution in ferret papillary muscle was triphasic: an initial, rapid, exponential increase in force with test intervals to 2 s, a further increase with test intervals between 60 and 90 s and then a slow decline, with a plateau at about 30 min (0.33 Hz, 30 degrees C). 4. Acidosis slowed the initial phase of mechanical restitution. The degree of slowing depended on the steady-state stimulation frequency, being greatest at low frequencies. 5. Inhibition of the SR abolished the initial phase of mechanical restitution, suggesting that this phase depends on Ca2+ release from the SR. 6. The strength of the first contraction after the extra-systole varied inversely with the size of the extra-systole under all conditions studied. 7. It is concluded that acidosis may inhibit the SR by altering the time required for Ca2+ recycling between contractions. This effect may alter Ca2+ release from the SR during acidosis, and may underlie the mechanical alternans (the alternation of small and large contractions) that can occur during acidosis.

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

  19. Coma, metabolic acidosis, and methemoglobinemia in a patient with acetaminophen toxicity.

    Science.gov (United States)

    Kanji, Hussein D; Mithani, Shazma; Boucher, Paul; Dias, Valerian C; Yarema, Mark C

    2013-01-01

    We present a case of early coma, metabolic acidosis and methemoglobinemia after substantial acetaminophen toxicity in the absence of hepatic failure. A 77-year-old female presented to the emergency department with a decreased level of consciousness. She was found unresponsive by a family member in her bed, and was reported to be acting normally when she was last seen eight hours earlier. Laboratory results on arrival were: pH 7.19, sodium 139 mmol/L, chloride 106 mmol/L, potassium 3.3 mmol/L, CO2 8 mmol/L, and an anion gap of 25. Both venous lactate (10.2 mmol/L) and methemoglobin (9.4 %) were elevated. The patient's acetaminophen concentration was markedly elevated at 7138 µmol/L (1078 µg/ml). Hepatic enzymes and coagulation tests were normal [alanine transaminase (ALT) 8 U/L, international normalized ratio (INR) 1.0]. Intravenous N-acetylcysteine (NAC) was initiated at a dose of 150 mg/kg over 15 minutes, followed by 50 mg/kg over the next four hours, followed by 100 mg/kg over the next 16 hours. Twenty-four hours after admission, the anion gap metabolic acidosis had resolved, and the methemoglobin was 2.1%. Aminotransferases peaked at 44 U/L and INR peaked at 1.9. A urine 5-oxoproline assay performed five days after admission was negative, suggesting no evidence of a 5-oxoprolinase deficiency. We describe the pathophysiology and discuss the literature on acetaminophen-induced coma and metabolic acidosis in the absence of hepatic injury; and propose mechanisms for associated methemoglobinemia. 

  20. Metformin-associated lactic acidosis: Current perspectives on causes and risk.

    Science.gov (United States)

    DeFronzo, Ralph; Fleming, G Alexander; Chen, Kim; Bicsak, Thomas A

    2016-02-01

    Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the results of future studies. This literature-based review provides an update on the impact of renal function and other conditions on metformin plasma levels and the risk of MALA in patients with type 2 diabetes.

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

    OpenAIRE

    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...

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

    DEFF Research Database (Denmark)

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

    1993-01-01

    Indomethacin is known to attenuate quite markedly the increase in CBF during hypercapnia. Hypercapnia is, in all likelihood, mediated by the acid shift at the level of the smooth muscle cells of the cerebral arterioles. We therefore investigated the effect of indomethacin on the CBF increase caused...... 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...

  3. Acidosis láctica secundaria a terapia antirretroviral en pacientes con VIH/sida

    Directory of Open Access Journals (Sweden)

    Benhard Hasbum-Fernández

    2006-06-01

    Full Text Available La acidosis láctica es una complicación infrecuente de la terapia antirretroviral para VIH. Su aparición se ha relacionado con la administración de análogos nucleósidos de la transcriptasa inversa, en especial estavudina y didanosina. Se presentan los 2 casos que se manejaron en el año 2005 en el Servicio de Medicina del Hospital México. En ambos el desenlace fue fatal, aún cuando se utilizaron todas las medidas terapéuticas recomendadas.

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

    OpenAIRE

    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...

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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...

  7. A Case of Myopathy, Encephalopathy, Lactic Acidosis and Stroke-Like Episodes (MELAS) Syndrome with Intracardiac Thrombus [corrected].

    Science.gov (United States)

    Joo, Jung-Chul; Seol, Myung Do; Yoon, Jin Won; Lee, Young Soo; Kim, Dong-Keun; Choi, Yong Hoon; Ahn, Hyo Seong; Cho, Wook Hyun

    2013-03-01

    Myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a multisystem clinical syndrome manifested by mitochondrial myopathy, encephalopathy, lactic acidosis and recurrent stroke-like episodes. A 27-year-old female with MELAS syndrome presented with cerebral infarction. Echocardiography revealed a thrombus attached to the apex of the hypertrophied left ventricle, with decreased systolic function. The embolism of the intracardiac thrombus might have been the cause of stroke. There should be more consideration given to the increased possibility of intracardiac thrombus formation when a MELAS patient with cardiac involvement is encountered.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  12. Refeeding syndrome as an unusual cause of anion gap metabolic acidosis.

    Science.gov (United States)

    Singla, Manish; Perry, Alexandra; Lavery, Eric

    2012-11-01

    Refeeding syndrome is characterized by hypophosphatemia in the setting of malnutrition. It is commonly seen in patients with anorexia, alcoholism, or malignancy, and it is often a missed diagnosis. Because of the potential morbidity associated with missing the diagnosis of refeeding syndrome, it is important to monitor for this disease in any malnourished patient. We present a case of a 49-year-old male with chronic alcohol abuse who presented for alcohol detoxification and was found to have low phosphate, potassium, and magnesium on presentation, in addition to an elevated anion gap of unclear etiology. After extensive workup to evaluate the cause of his elevated anion gap and worsening of his electrolyte abnormalities despite replenishment, it was felt his symptoms were a result of refeeding syndrome. After oral intake was held and aggressive electrolyte replenishment was performed for 24 hours, the patient's anion gap closed and his electrolyte levels stabilized. This case demonstrates a unique presentation of refeeding syndrome given the patient's profound metabolic acidosis that provided a clue toward his eventual diagnosis. The standard workup for an anion gap metabolic acidosis was negative, and it was not until his refeeding syndrome had been treated that the anion gap closed.

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

    International Nuclear Information System (INIS)

    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

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

  16. Local anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite

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    Takahiro Ueno

    2008-11-01

    Full Text Available Takahiro Ueno1, Hironori Tsuchiya2, Maki Mizogami1, Ko Takakura11Department of Anesthesiology, Asahi University School of Dentistry, Mizuho, Gifu, Japan; 2Department of Dental Basic Education, Asahi University School of Dentistry, Mizuho, Gifu, JapanAbstract: The presence of inflammation decreases local anesthetic efficacy, especially in dental anesthesia. Although inflammatory acidosis is most frequently cited as the cause of such clinical phenomena, this has not been experimentally proved. We verified the acidosis mechanism by studying the drug and membrane lipid interaction under acidic conditions together with proposing an alternative hypothesis. Liposomes and nerve cell model membranes consisting of phospholipids and cholesterol were treated at different pH with lidocaine, prilocaine and bupivacaine (0.05%–0.2%, w/v. Their membrane-interactive potencies were compared by the induced-changes in membrane fluidity. Local anesthetics fluidized phosphatidylcholine membranes with the potency being significantly lower at pH 6.4 than at pH 7.4 (p < 0.01, supporting the acidosis theory. However, they greatly fluidized nerve cell model membranes even at pH 6.4 corresponding to inflamed tissues, challenging the conventional mechanism. Local anesthetics acted on phosphatidylserine liposomes, as well as nerve cell model membranes, at pH 6.4 with almost the same potency as that at pH 7.4, but not on phosphatidylcholine, phosphatidylethanolamine and sphingomyelin liposomes. Since the positively charged anesthetic molecules are able to interact with nerve cell membranes by ion-paring with anionic components like phosphatidylserine, tissue acidosis is not essentially responsible for the local anesthetic failure associated with inflammation. The effects of local anesthetics on nerve cell model membranes were inhibited by treating with peroxynitrite (50 μM, suggesting that inflammatory cells producing peroxynitrite may affect local anesthesia

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

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    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  1. An autopsy case of death due to metabolic acidosis after citric acid ingestion.

    Science.gov (United States)

    Ikeda, Tomoya; Usui, Akihito; Matsumura, Takashi; Aramaki, Tomomi; Hosoya, Tadashi; Igari, Yui; Ohuchi, Tsukasa; Hayashizaki, Yoshie; Usui, Kiyotaka; Funayama, Masato

    2015-11-01

    A man in his 40s was found unconscious on a sofa in a communal residence for people with various disabilities. He appeared to have drunk 800 ml of undiluted citric acid from a commercial plastic bottle. The instructions on the label of the beverage specified that the beverage be diluted 20- to 30-fold before consumption. The patient was admitted to an emergency hospital with severe metabolic acidosis (pH, 6.70; HCO3(-), 3.6 mEq/L) and a low ionized calcium level (0.73 mmol/L). Although ionized calcium and catecholamines were continuously administered intravenously to correct the acidosis, the state of acidemia and low blood pressure did not improve, and he died 20 h later. Citric acid concentrations in the patient's serum drawn shortly after treatment in the hospital and from the heart at autopsy were 80.6 mg/ml and 39.8 mg/dl, respectively (normal range: 1.3-2.6 mg/dl). Autopsy revealed black discoloration of the mucosal surface of the esophagus. Microscopically, degenerated epithelium and neutrophilic infiltration in the muscle layer were observed. In daily life, drinking a large amount of concentrated citric acid beverage is rare as a cause of lethal poisoning. However, persons with mental disorders such as dementia may mistakenly drink detergent or concentrated fluids, as in our case. Family members or facility staff in the home or nursing facility must bear in mind that they should not leave such bottles in places where they are easily accessible to mentally handicapped persons.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    OpenAIRE

    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...

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

    OpenAIRE

    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...

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

    DEFF Research Database (Denmark)

    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...

  8. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome mimicking herpes simplex encephalitis on imaging studies.

    Science.gov (United States)

    Gieraerts, Christopher; Demaerel, Philippe; Van Damme, Philip; Wilms, Guido

    2013-01-01

    We present a case in which mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome mimicked the clinical and radiological signs of herpes simplex encephalitis. In a patient with subacute encephalopathy, on computed tomography and magnetic resonance imaging, lesions were present in both temporal lobes extending to both insular regions with sparing of the lentiform nuclei and in both posterior straight and cingulate gyri. Final diagnosis of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome was based on biochemical investigations on cerebrospinal fluid, electromyogram, muscle biopsy, and genetic analysis. On diffusion-weighted imaging, diffusion restriction was present in some parts of the lesions but not throughout the entire lesions. We suggest that this could be an important sign in the differential diagnosis with herpes simplex encephalitis.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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.

  11. Complex III deficiency due to an in-frame MT-CYB deletion presenting as ketotic hypoglycemia and lactic acidosis

    Directory of Open Access Journals (Sweden)

    Mari Mori

    2015-09-01

    Full Text Available Complex III deficiency due to a MT-CYB mutation has been reported in patients with myopathy. Here, we describe a 15-year-old boy who presented with metabolic acidosis, ketotic hypoglycemia and carnitine deficiency. Electron transport chain analysis and mitochondrial DNA sequencing on muscle tissue lead to the eventual diagnosis of complex III deficiency. This case demonstrates the critical role of muscle biopsies in a myopathy work-up, and the clinical efficacy of supplement therapy.

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

    Science.gov (United States)

    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

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

    Science.gov (United States)

    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.

  14. Low-flow CO2 removal integrated into a renal-replacement circuit can reduce acidosis and decrease vasopressor requirements

    Science.gov (United States)

    2013-01-01

    Introduction Lung-protective ventilation in patients with ARDS and multiorgan failure, including renal failure, is often paralleled with a combined respiratory and metabolic acidosis. We assessed the effectiveness of a hollow-fiber gas exchanger integrated into a conventional renal-replacement circuit on CO2 removal, acidosis, and hemodynamics. Methods In ten ventilated critically ill patients with ARDS and AKI undergoing renal- and respiratory-replacement therapy, effects of low-flow CO2 removal on respiratory acidosis compensation were tested by using a hollow-fiber gas exchanger added to the renal-replacement circuit. This was an observational study on safety, CO2-removal capacity, effects on pH, ventilator settings, and hemodynamics. Results CO2 elimination in the low-flow circuit was safe and was well tolerated by all patients. After 4 hours of treatment, a mean reduction of 17.3 mm Hg (−28.1%) pCO2 was observed, in line with an increase in pH. In hemodynamically instable patients, low-flow CO2 elimination was paralleled by hemodynamic improvement, with an average reduction of vasopressors of 65% in five of six catecholamine-dependent patients during the first 24 hours. Conclusions Because no further catheters are needed, besides those for renal replacement, the implementation of a hollow-fiber gas exchanger in a renal circuit could be an attractive therapeutic tool with only a little additional trauma for patients with mild to moderate ARDS undergoing invasive ventilation with concomitant respiratory acidosis, as long as no severe oxygenation defects indicate ECMO therapy. PMID:23883472

  15. Computed tomography and angiography in MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes). Report of 3 cases

    Energy Technology Data Exchange (ETDEWEB)

    Hasuo, K.; Tamura, S.; Yasumori, K.; Uchino, A.; Masuda, K.; Goda, S.; Ishimoto, S.; Kamikaseda, K.; Wakuta, Y.; Kishi, M.

    1987-07-01

    Among mitochondrial encephalomyopathies, MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, Pavlakis et al., 1983) is recognized as a distinct syndrome characterized by generalized convulsions and recurrrent stroke-like episodes. The neuroradiological findings of three patients with MELAS are reported here. Retrospective review shows that MELAS should be included in the differential diagnosis of infarct-like lesions of the cerebrum.

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  19. Pathophysiological evaluation of subacute ruminal acidosis (SARA) by continuous ruminal pH monitoring

    Science.gov (United States)

    2016-01-01

    Abstract Evaluation of the radio‐transmission pH‐measurement system for monitoring the ruminal pH and subacute ruminal acidosis (SARA) in cattle is described. This is done in order to reveal the possible application of this system for detection and pathophysiological research of SARA by continuous ruminal pH measurement. The possibility of using this system for assessment of the ruminal pH in SARA cattle, and the presence of negative correlation between the ruminal pH and ruminal temperature in heathy and SARA cattle were determined. In addition, the 16S rRNA gene pyrosequencing analysis showed that the ruminal microbial community was simpler in SARA cattle, and the bacterial numbers in SARA cattle were lower than those in healthy hay‐fed cattle. Concentrate feeding might have reduced the diversity of the ruminal microbial community. Changes in the ruminal microbial community of SARA cattle might be related to the changes in ruminal pH followed by the decrease in the number of some bacteria. Continuous monitoring of the ruminal pH using the radio‐transmission pH‐measurement system would be applied for detection and prevention of SARA in the field and pathophysiological research of SARA, including ruminal zymology and bacteriology, which have been determined previously by sampling of the ruminal fluid and measuring of ruminal pH. PMID:26279060

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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. Methods: Sixteen professional male road cyclists (mean (SD) age 26 (1) years) performed a ramp test on a cycle ergometer (workload increases of 5 W/12 s, averaging 25 W/min). Heart rate (HR), gas exchange parameters, and blood variables (lactate, pH, P50 of the oxyhaemoglobin dissociation curve, and K+) were measured during the tests. Results: A HRDP was shown in 56% of subjects at about 88% of their maximal HR (HRDP group; n = 9) but was linear in the rest (No-HRDP group; n = 7). In the HRDP group, the slope of the HR-workload regression line above the HRDP correlated inversely with levels of K+ at the maximal power output (r = -0.67; p<0.05). Conclusions: The HRDP phenomenon is associated, at least partly, with exercise induced hyperkalaemia. PMID:11916893

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

    DEFF Research Database (Denmark)

    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...

  3. The role of dietary acid load and mild metabolic acidosis in insulin resistance in humans.

    Science.gov (United States)

    Williams, Rebecca S; Kozan, Pinar; Samocha-Bonet, Dorit

    2016-05-01

    Type 2 diabetes is increasingly being recognised as a global health crisis (World Health Organisation). Insulin resistance is closely associated with obesity and precedes the development of type 2 diabetes. However, there is now increasing evidence to suggest that diet itself may independently be associated with type 2 diabetes risk. A diet with a high acid load (or high potential renal net acid load, PRAL) can result in a decrease in pH towards the lower end of the normal physiological range, which may in turn lead to the development of insulin resistance. Conversely, reducing dietary acid load (the so called 'alkaline diet') may be protective and prevent the onset of type 2 diabetes. Here, we explore the influence of dietary acid load on the development of mild metabolic acidosis and induction of insulin resistance. Whilst large prospective cohort studies link high dietary acid load or low serum bicarbonate with the development of type 2 diabetes, the effect of a diet with a low acid (or high alkaline) load remains unclear. Further interventional studies are required to investigate the influence of dietary composition on the body's acid/base balance, insulin resistance and incidence of type 2 diabetes. PMID:26363101

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

    Directory of Open Access Journals (Sweden)

    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.

  5. Treatment options for mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome.

    Science.gov (United States)

    Santa, Kristin M

    2010-11-01

    Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a rare neurodegenerative disease caused by the decreased ability of cells to produce sufficient energy in the form of adenosine 5'-triphosphate. Although it is one of the most common maternally inherited mitochondrial disorders, its exact incidence is unknown. Caused most frequently by an A-to-G point mutation at the 3243 position in the mitochondrial DNA, MELAS syndrome has a broad range of clinical manifestations and a highly variable course. The classic neurologic characteristics include encephalopathy, seizures, and stroke-like episodes. In addition to its neurologic manifestations, MELAS syndrome exhibits multisystem effects including cardiac conduction defects, diabetes mellitus, short stature, myopathy, and gastrointestinal disturbances. Unfortunately, no consensus guidelines outlining standard drug regimens exist for this syndrome. Many of the accepted therapies used in treating MELAS syndrome have been identified through a small number of clinical trials or isolated case reports. Currently, the drugs most often used include antioxidants and various vitamins aimed at minimizing the demands on the mitochondria and supporting and maximizing their function. Some of the most frequently prescribed agents include coenzyme Q(10), l-arginine, B vitamins, and levocarnitine. Although articles describing MELAS syndrome are available, few specifically target education for clinical pharmacists. This article will provide pharmacists with a practical resource to enhance their understanding of MELAS syndrome in order to provide safe and effective pharmaceutical care.

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

    Directory of Open Access Journals (Sweden)

    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

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

    Institute of Scientific and Technical Information of China (English)

    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.

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

    Institute of Scientific and Technical Information of China (English)

    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.

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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...

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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.

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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

  19. Seizure-induced damage to substantia nigra and globus pallidus is accompanied by pronounced intra- and extracellular acidosis

    Energy Technology Data Exchange (ETDEWEB)

    Inamura, K.; Smith, M.L.; Hansen, A.J.; Siesjoe, B.K. (Univ. of Lund (Sweden))

    1989-12-01

    Status epilepticus of greater than 30-min duration in rats gives rise to a conspicuous lesion in the substantia nigra pars reticulata (SNPR) and globus pallidus (GP). The objective of the present study was to explore whether the lesion, which encompasses necrosis of both neurons and glial cells, is related to intra- and extracellular acidosis. Using the flurothyl model previously described to produce seizures, we assessed regional pH values with the autoradiographic 5,5-dimethyl(2-14C)oxazolidine-2,4-dione technique. Regional pH values were assessed in animals with continuous seizures for 20 and 60 min, as well as in those allowed to recover for 30 and 120 min after seizure periods of 20 or 60 min. In additional animals, changes in extracellular fluid pH (pHe) were measured with ion-selective microelectrodes, and extracellular fluid (ECF) volume was calculated from the diffusion profile for electrophoretically administered tetramethylammonium. In structures such as the neocortex and the hippocampus, which show intense metabolic activation during seizures, status epilepticus of 20- and 60-min duration was accompanied by a reduction of the composite tissue pH (pHt) of 0.2-0.3 unit. Recovery of pHt was observed upon termination of seizures. In SNPR and in GP, the acidosis was marked to excessive after 20 and 60 min of seizures (delta pHt approximately 0.6 after 60 min).

  20. pHj, contractility and Ca-balance under hypercapnic acidosis in the myocardium of different vertebrate species

    DEFF Research Database (Denmark)

    Gesser, H; Bonefeld-Jørgensen, Eva Cecilie

    1982-01-01

    The influence of hypercapnic acidosis upon the heart was examined in four vertebrate species. The CO2 in the tissue bath was increased from 2.7 to 15% at 12 degrees C for flounder (Platichthys flesus) and cod (Gadus morhua) and from 3 to 13% at 22 degrees C for turtle (Pseudemys scripta) and rain......The influence of hypercapnic acidosis upon the heart was examined in four vertebrate species. The CO2 in the tissue bath was increased from 2.7 to 15% at 12 degrees C for flounder (Platichthys flesus) and cod (Gadus morhua) and from 3 to 13% at 22 degrees C for turtle (Pseudemys scripta......) and rainbow trout (Salmo gairdneri). During hypercapnia, as previously described, there was a decline and recovery of contractility in heart strips of flounder and turtle, and a sustained decrease in cod and rainbow trout. At high CO2 the increase in contractile force following increases in the extracellular...... concentration of hydrogen ions was larger in the turtle than in the trout myocardium. Intracellular Ca-activity, measured by efflux of 45Ca from preloaded heart strips, was unaffected by high CO2 in trout, but was raised in the other three species. Thus the ability to counteract the negative inotropic effect...

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  3. Comparison of end-tidal carbon dioxide and arterial blood bicarbonate levels in patients with metabolic acidosis referred to emergency medicine

    Science.gov (United States)

    Taghizadieh, Ali; Pouraghaei, Mahboub; Moharamzadeh, Payman; Ala, Alireza; Rahmani, Farzad; Basiri Sofiani, Karim

    2016-01-01

    Introduction: The routine and gold standard method to diagnose of acid – base disturbance is arterial blood gas (ABG) sampling. Capnography could be used to measure the end-tidal carbon dioxide (ETCO2) levels and ETco2 has a close correlation with the PaCo2. The aim of this study was comparison the ETco2 and arterial blood bicarbonate levels in patients with metabolic acidosis. Methods: In a descriptive-analytical study that performed in Emergency Department of Emam Reza Medical Research and Training Hospital of Tabriz on patients with metabolic acidosis, ETco2 level and blood bicarbonate levels in 262 patients were evaluated. Results: Mean of ETco2 and Hco3 levels in patients with metabolic acidosis were 22.29 ± 4.15 and 12.78 ± 3.83, respectively. In all patients, the significant direct linear relationship was found between ETco2 with Hco3 (r = 0.553, P < 0.001). We had 4 groups of patients with metabolic acidosis, also there is a significant direct linear relationship between the ETCo2 and the Hco3 level of arterial blood in patients with renal failure (P < 0.001 and r = 0.551), sepsis (P < 0.001 and r = 0.431), drug toxicity (P < 0.001 and r = 0.856), and ketoacidosis (DKA) (P < 0.001 and r = 0.559). Conclusion: According to the results of this study, capnography can be used for primary diagnosis of metabolic acidosis in spontaneously breathing patients who referred to the emergency wards, however, the ABG must be considered as the gold standard tool for diagnosis and guiding the treatment. PMID:27777693

  4. Clinical, pathological and genetic study of a kindred of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes

    Institute of Scientific and Technical Information of China (English)

    FENG Yan-qing; GUO Ning; HUANG Fan; LI Ling; YAO Xiao-li; LI Xun-hua; ZHANG Cheng; LIANG Xiu-ling

    2005-01-01

    @@ The first description of a syndrome including stroke-like episodes, lactic acidaemia, and ragged red fibres, was reported by Shapira et al in 1975.1 Pavlakis et al2 described further cases, introduced the acronym MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes), and suggested that this represented a distinct mitochondrial disease phenotype. In 1990, Goto et al3 identified A3243G mutation in the transfer RNA (tRNA) leucine (UUR) gene in some patients with MELAS. Although this mutation has now been established to be the commonest mtDNA defect it is often misdiagnosed. Here we report a kindred of MELAS including a mother and a son. Clinical, pathological and genetic studies are proceeding.

  5. [A case of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episode/Leigh overlap syndrome].

    Science.gov (United States)

    Matsui, Jun; Takano, Tomoyuki; Ryujin, Fukiko; Anzai, Yuko; Yoshioka, Seiichiro; Takeuchi, Yoshihiro; Goto, Yuichi

    2014-09-01

    We experienced a case in which mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) was identified as complications following the onset of Leigh syndrome along with a 10191 T>C mutation of the mitochondrial gene. The case pertains to a 26-year-old woman. The disease appeared when she was 11 years old due to divergent strabismus, at which point a diagnosis of juvenile Leigh syndrome was made. Many infraction images not conforming to the vessel region were observed upon a brain MRI which was performed at 26 years of age, thus leading to her being diagnosed with MELAS as a complication. Upoon bibliographical consideration, it was speculated that the clinical features of MELAS/Leigh overlap syndrome clearly differ from Leigh syndrome in terms of age of onset, symptoms, and prognosis. Pleiotropic genetic factors including heteroplasmy were presumed to be involved in the diverse phenotype of overlap syndrome.

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

    Institute of Scientific and Technical Information of China (English)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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.

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

    LENUS (Irish Health Repository)

    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.

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

    OpenAIRE

    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...

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

    OpenAIRE

    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...

  14. Atypical Strokes in a Young African American Male: A Case of Mitochondrial Encephalopathy Lactic Acidosis and Stroke-Like Episodes (MELAS Syndrome

    Directory of Open Access Journals (Sweden)

    Jully M. Sanchez

    2011-01-01

    Full Text Available Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS syndrome is a rare but important cause of stroke-like symptoms which can often be missed Thambisetty and Newman 2004. We describe a case of a young male presenting with stroke-like episodes, later diagnosed with MELAS in an attempt to improve the understanding about diagnosing MELAS in the appropriate clinical context.

  15. Differential impacts of elevated CO2 and acidosis on the energy budget of gill and liver cells from Atlantic cod, Gadus morhua.

    Science.gov (United States)

    Stapp, L S; Kreiss, C M; Pörtner, H O; Lannig, G

    2015-09-01

    Ocean acidification impacts fish and other marine species through increased seawater PCO2 levels (hypercapnia). Knowledge of the physiological mechanisms mediating effects in various tissues of fish is incomplete. Here we tested the effects of extracellular hypercapnia and acidosis on energy metabolism of gill and liver cells of Atlantic cod. Exposure media mimicked blood conditions in vivo, either during normo- or hypercapnia and at control or acidic extracellular pH (pHe). We determined metabolic rate and energy expenditure for protein biosynthesis, Na(+)/K(+)-ATPase and H(+)-ATPase and considered nutrition status by measurements of metabolic rate and protein biosynthesis in media with and without free amino acids (FAA). Addition of FAA stimulated hepatic but not branchial oxygen consumption. Normo- and hypercapnic acidosis as well as hypercapnia at control pHe depressed metabolic stimulation of hepatocytes. In gill cells, acidosis depressed respiration independent of PCO2 and FAA levels. For both cell types, depressed respiration was not correlated with the same reduction in energy allocated to protein biosynthesis or Na(+)/K(+)-ATPase. Hepatic energy expenditure for protein synthesis and Na(+)/K(+)-ATPase was even elevated at acidic compared to control pHe suggesting increased costs for ion regulation and cellular reorganization. Hypercapnia at control pHe strongly reduced oxygen demand of branchial Na(+)/K(+)-ATPase with a similar trend for H(+)-ATPase. We conclude that extracellular acidosis triggers metabolic depression in gill and metabolically stimulated liver cells. Additionally, hypercapnia itself seems to limit capacities for metabolic usage of amino acids in liver cells while it decreases the use and costs of ion regulatory ATPases in gill cells.

  16. 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

    OpenAIRE

    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 ...

  17. 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

    Institute of Scientific and Technical Information of China (English)

    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。

  18. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  19. Severe Encephalopathy, Lactic Acidosis, Vegetative Instability and Neuropathy with 5-Fluorouracil Treatment – Pyrimidine Degradation Defect or Beriberi

    Directory of Open Access Journals (Sweden)

    A. Rosen

    2011-08-01

    Full Text Available We present the case of a 19-year-old female with nasopharyngeal carcinoma, who received two courses of chemotherapy with 5-fluorouracil (5-FU in combination with folic acid and cisplatin. Upon developing esophageal strictures in the course of her radiotherapy, she required total parenteral nutrition. In the course of therapy, the patient developed severe multisystem failure with encephalopathy, lactic acidosis, vegetative instability and neuropathy. The treatment with 5-FU can lead to severe toxicity due to enzyme deficiencies in the degradation of pyrimidines, but it can also lead to thiamine deficiency with the classic symptoms of beriberi. Beriberi is a rare disorder, usually attributed to malnutrition or alcoholism. 5-FU has been shown to induce thiamine depletion. Reduced food intake or total parenteral nutrition devoid of vitamin supplements may aggravate symptoms. We were unable to find a genetic cause for increased 5-FU toxicity in our patient, ruling out deficiencies of dihydropyrimidine dehydrogenase, dihydropyrimidinase or β-ureidopropionase and double-strand break repair deficits. We come to the conclusion that, even without any definable enzyme deficiency, treatment with 5-FU can lead to high toxicity due to thiamine deficiency if vitamin supplementation is not undertaken.

  20. Acidosis Mediates the Switching of Gs-PKA and Gi-PKCε Dependence in Prolonged Hyperalgesia Induced by Inflammation.

    Directory of Open Access Journals (Sweden)

    Wei-Yu Huang

    Full Text Available Chronic inflammatory pain, when not effectively treated, is a costly health problem and has a harmful effect on all aspects of health-related quality of life. Previous studies suggested that in male Sprague Dawley rats, prostaglandin E2 (PGE2-induced short-term hyperalgesia depends on protein kinase A (PKA activity, whereas long-lasting hyperalgesia induced by PGE2 with carrageenan pre-injection, requires protein kinase Cε (PKCε. However, the mechanism underlying the kinase switch with short- to long-term hyperalgesia remains unclear. In this study, we used the inflammatory agents carrageenan or complete Freund's adjuvant (CFA to induce long-term hyperalgesia, and examined PKA and PKCε dependence and switching time. Hyperalgesia induced by both agents depended on PKA/PKCε and Gs/Gi-proteins, and the switching time from PKA to PKCε and from Gs to Gi was about 3 to 4 h after inflammation induction. Among the single inflammatory mediators tested, PGE2 and 5-HT induced transient hyperalgesia, which depended on PKA and PKCε, respectively. Only acidic solution-induced hyperalgesia required Gs-PKA and Gi-PKCε, and the switch time for kinase dependency matched inflammatory hyperalgesia, in approximately 2 to 4 h. Thus, acidosis in inflamed tissues may be a decisive factor to regulate switching of PKA and PKCε dependence via proton-sensing G-protein-coupled receptors.

  1. A single nucleotide polymorphism in kidney anion exchanger 1 gene is associated with incomplete type 1 renal tubular acidosis

    Science.gov (United States)

    Takeuchi, Takumi; Hattori-Kato, Mami; Okuno, Yumiko; Kanatani, Atsushi; Zaitsu, Masayoshi; Mikami, Koji

    2016-01-01

    Various conditions including distal renal tubular acidosis (dRTA) can induce stone formation in the kidney. dRTA is characterized by an impairment of urine acidification in the distal nephron. dRTA is caused by variations in genes functioning in intercalated cells including SLC4A1/AE1/Band3 transcribing two kinds of mRNAs encoding the Cl−/HCO3− exchanger in erythrocytes and that expressed in α-intercalated cells (kAE1). With the acid-loading test, 25% of urolithiasis patients were diagnosed with incomplete dRTA. In erythroid intron 3 containing the promoter region of kAE1, rs999716 SNP showed a significantly higher minor allele A frequency in incomplete dRTA compared with non-dRTA patients. The promoter regions of the kAE1 gene with the minor allele A at rs999716 downstream of the TATA box showed reduced promoter activities compared that with the major allele G. Patients with the A allele at rs999716 may express less kAE1 mRNA and protein in the intercalated cells, developing incomplete dRTA. PMID:27767102

  2. Differing effects of 2 active dried yeast (Saccharomyces cerevisiae) strains on ruminal acidosis and methane production in nonlactating dairy cows.

    Science.gov (United States)

    Chung, Y-H; Walker, N D; McGinn, S M; Beauchemin, K A

    2011-05-01

    different strains of S. cerevisiae fed as active dried yeasts vary in their ability to modify the rumen fermentative pattern in nonlactating dairy cows. Because strain 2 tended (when compared with strain 1) to lower CH(4) emissions but increase the risk of acidosis, it may be prudent to further evaluate this strain in cattle fed high-forage diets, for which the risk of acidosis is low but CH(4) emissions are high.

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    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

  5. Liquid extracorporeal carbon dioxide removal: use of THAM (tris-hydroxymethyl aminomethane) coupled to hemofiltration to control hypercapnic acidosis in a porcine model of protective mechanical ventilation

    Science.gov (United States)

    Tapia, Pablo; Lillo, Felipe; Soto, Dagoberto; Escobar, Leslie; Simon, Felipe; Hernández, Karina; Alegría, Leyla; Bruhn, Alejandro

    2016-01-01

    A promising approach to facilitate protective mechanical ventilation is the use of extracorporeal CO2 removal techniques. Several strategies based on membrane gas exchangers have been developed. However, these techniques are still poorly available. The goal of this study was to assess the efficacy and safety of THAM infusion coupled to hemofiltration for the management of hypercapnic acidosis. A severe respiratory acidosis was induced in seven anesthetized pigs. Five of them were treated with THAM 8-mmol·kg-1·h-1 coupled to hemofiltration (THAM+HF group) at 100 mL·kg-1·h-1. After 18-hours of treatment the THAM infusion was stopped but hemofiltration was kept on until 24-hours. The 2 other animals were treated with THAM but without hemofiltration. After 1-hour of treatment in THAM+HF, PaCO2 rapidly decreased from a median of 89.0 (IQR) (80.0, 98.0) to 71.3 (65.8, 82.0) mmHg (P<0.05), while pH increased from 7.12 (7.01, 7.15) to 7.29 (7.27, 7.30) (P<0.05). Thereafter PaCO2 remained stable between 60-70 mmHg, while pH increased above 7.4. After stopping THAM at 18 hours of treatment a profound rebound effect was observed with severe hypercapnic acidosis. The most important side effect we observed was hyperosmolality, which reached a maximum of 330 (328, 332) mOsm·kg H2O-1 at T18. The animals treated only with THAM developed severe hypercapnia, despite the fact that pH returned to normal values, and died after 12 hours. Control-group had an uneven evolution until the end of the experiment. A combined treatment with THAM coupled to hemofiltration may be an effective treatment to control severe hypercapnic acidosis. PMID:27648139

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

    OpenAIRE

    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...

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

    OpenAIRE

    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...

  8. Estimation of the true incidence of lactic acidosis within the Lighthouse Clinic cohort, and the likely magnitude of missed diagnoses in the region

    Directory of Open Access Journals (Sweden)

    Colin Speight

    2014-11-01

    Full Text Available Introduction: Lactic acidosis is one of the most serious side effects associated with ART, most commonly associated with stavudine. Clinical features are non-specific and specialist laboratory capabilities are essential to confirm the diagnosis, making under-diagnosis likely in resource-constrained settings. Lighthouse Trust is a tertiary referral ART centre with over 23,500 patients on ART. The adjacent University of North Carolina Project laboratory, also serving Kamuzu Central Hospital, has been the only site processing lactate tests in Central Zone for many years. Our objective was to quantify the true incidence within our cohort, and estimate the likely degree of historical missed diagnoses from less central ART clinics. Methods: All high lactate results between June 2010 and June 2013 were treated as cases, and cross referenced with the Lighthouse database. Patients transferring in to Lighthouse within one month prior to diagnosis were assumed to have been referred due to their lactic acidosis, and moved to the Central Zone cohort to avoid referral bias. Routinely collected quarterly ART cohort data for both Lighthouse and the entire Central Zone were analyzed. Results: Over the three-year period, from within the Lighthouse cohort, there were 138 cases: 74% were female, median duration on ART was 14 months (IQR 10–26, and 98.5% were attributable to stavudine (only two cases to zidovudine. Over this period, the average number of patients taking stavudine at Lighthouse was 10,960 (3,600 on zidovudine. For the whole Central Zone (minus Lighthouse patients there were 61,000 on stavudine (4,830 on zidovudine, yet only 124 cases of lactic acidosis were apparently diagnosed from within this cohort. Conclusions: Although cases may, of course, also have been missed at Lighthouse, as a tertiary referral centre the rate observed is likely to be closer to the true incidence. Over the three years, with 138 cases from the 10,960 patients taking

  9. Liquid extracorporeal carbon dioxide removal: use of THAM (tris-hydroxymethyl aminomethane) coupled to hemofiltration to control hypercapnic acidosis in a porcine model of protective mechanical ventilation.

    Science.gov (United States)

    Tapia, Pablo; Lillo, Felipe; Soto, Dagoberto; Escobar, Leslie; Simon, Felipe; Hernández, Karina; Alegría, Leyla; Bruhn, Alejandro

    2016-01-01

    A promising approach to facilitate protective mechanical ventilation is the use of extracorporeal CO2 removal techniques. Several strategies based on membrane gas exchangers have been developed. However, these techniques are still poorly available. The goal of this study was to assess the efficacy and safety of THAM infusion coupled to hemofiltration for the management of hypercapnic acidosis. A severe respiratory acidosis was induced in seven anesthetized pigs. Five of them were treated with THAM 8-mmol·kg(-1)·h(-1) coupled to hemofiltration (THAM+HF group) at 100 mL·kg(-1)·h(-1). After 18-hours of treatment the THAM infusion was stopped but hemofiltration was kept on until 24-hours. The 2 other animals were treated with THAM but without hemofiltration. After 1-hour of treatment in THAM+HF, PaCO2 rapidly decreased from a median of 89.0 (IQR) (80.0, 98.0) to 71.3 (65.8, 82.0) mmHg (P<0.05), while pH increased from 7.12 (7.01, 7.15) to 7.29 (7.27, 7.30) (P<0.05). Thereafter PaCO2 remained stable between 60-70 mmHg, while pH increased above 7.4. After stopping THAM at 18 hours of treatment a profound rebound effect was observed with severe hypercapnic acidosis. The most important side effect we observed was hyperosmolality, which reached a maximum of 330 (328, 332) mOsm·kg H2O(-1) at T18. The animals treated only with THAM developed severe hypercapnia, despite the fact that pH returned to normal values, and died after 12 hours. Control-group had an uneven evolution until the end of the experiment. A combined treatment with THAM coupled to hemofiltration may be an effective treatment to control severe hypercapnic acidosis. PMID:27648139

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

    Science.gov (United States)

    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

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

    Science.gov (United States)

    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.

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

    Science.gov (United States)

    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

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

    Institute of Scientific and Technical Information of China (English)

    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

    Institute of Scientific and Technical Information of China (English)

    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. Expression of Glutamine Transporter Slc38a3 (SNAT3 During Acidosis is Mediated by a Different Mechanism than Tissue-Specific Expression

    Directory of Open Access Journals (Sweden)

    Sarojini Balkrishna

    2014-05-01

    Full Text Available Background: Despite homeostatic pH regulation, systemic and cellular pH changes take place and strongly influence metabolic processes. Transcription of the glutamine transporter SNAT3 (Slc38a3 for instance is highly up-regulated in the kidney during metabolic acidosis to provide glutamine for ammonia production. Methods: Slc38a3 promoter activity and messenger RNA stability were measured in cultured cells in response to different extracellular pH values. Results: Up-regulation of SNAT3 mRNA was mediated both by the stabilization of its mRNA and by the up-regulation of gene transcription. Stabilisation of the mRNA involved a pH-response element, while enhanced transcription made use of a second pH-sensitive Sp1 binding site in addition to a constitutive Sp1 binding site. Transcriptional regulation dominated the early response to acidosis, while mRNA stability was more important for chronic adaptation. Tissue-specific expression of SNAT3, by contrast, appeared to be controlled by promoter methylation and histone modifications. Conclusions: Regulation of SNAT3 gene expression by extracellular pH involves post-transcriptional and transcriptional mechanisms, the latter being distinct from the mechanisms that control the tissue-specific expression of the gene.

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

    Science.gov (United States)

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

    Institute of Scientific and Technical Information of China (English)

    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

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

    Science.gov (United States)

    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

  19. Interaction between bunk management and monensin concentration on finishing performance, feeding behavior, and ruminal metabolism during an acidosis challenge with feedlot cattle.

    Science.gov (United States)

    Erickson, G E; Milton, C T; Fanning, K C; Cooper, R J; Swingle, R S; Parrott, J C; Vogel, G; Klopfenstein, T J

    2003-11-01

    Two commercial feedlot experiments and a metabolism study were conducted to evaluate the effects of monensin concentrations and bunk management strategies on performance, feed intake, and ruminal metabolism. In the feedlot experiments, 1,793 and 1,615 steers were used in Exp. 1 and 2, respectively, in 18 pens for each experiment (six pens/treatment). Three treatments were evaluated: 1) ad libitum bunk management with 28.6 mg/kg monensin and clean bunk management strategies with either 2) 28.6 or 3) 36.3 mg/kg monensin. In both experiments, 54 to 59% of the clean bunk pens were clean at targeted clean time, or 2200, compared with 24 to 28% of the ad libitum pens. However, only 13% of the pens were clean by 2000 in Exp. 1 (summer), whereas 44% of the pens in Exp. 2 (winter) were clean by 2000. In Exp. 1, bunk management and monensin concentration did not affect carcass-adjusted performance. In Exp. 2, steers fed ad libitum had greater DMI (P 0.13) similar to that of clean bunk-fed steers. Monensin concentration had no effect on carcass-adjusted performance (P > 0.20) in either experiment. A metabolism experiment was conducted with eight fistulated steers in a replicated 4 x 4 Latin square acidosis challenge experiment. An acidosis challenge was imposed by feeding 125% of the previous day's DMI, 4 h later than normal. Treatments consisted of monensin concentrations (mg/kg) of 0, 36.7, 48.9, or 36.7 until challenged and switched to 48.9 on the challenge day and 4 d following. Each replicate of the Latin square was managed with separate bunk management strategies (clean bunk or ad libitum). Feeding any concentration of monensin increased number of meals and decreased DMI rate (%/h) (P < 0.12) for the 4 d following the acidosis challenge. Meal size, pH change, and pH variance were lower (P < 0.10) for steers fed monensin with clean bunk management. However, no monensin effect was observed for steers fed ad libitum. Bunk management strategy has the potential to decrease

  20. Mutation-free baby born from a mitochondrial encephalopathy, lactic acidosis and stroke-like syndrome carrier after blastocyst trophectoderm preimplantation genetic diagnosis.

    Science.gov (United States)

    Heindryckx, Björn; Neupane, Jitesh; Vandewoestyne, Mado; Christodoulou, Christodoulos; Jackers, Yens; Gerris, Jan; Van den Abbeel, Etienne; Van Coster, Rudy; Deforce, Dieter; De Sutter, Petra

    2014-09-01

    To investigate the applicability of preimplantation genetic diagnosis (PGD), we used trophectoderm (TE) biopsy to determine the mutation load in a 35-year-old female with mitochondrial encephalopathy, lactic acidosis and stroke-like syndrome (MELAS). Transfer of a mutation-free blastocyst gave birth to a healthy boy with undetectable mutation in any of the analyzed tissues. We found strong correlation among TE cells (r=0.90) within blastocysts and also between cytoplasmic fragments and TE (r=0.95). This is the first case of mutation-free baby born from a MELAS patient after TE biopsy and supports the applicability of blastocyst PGD for patients with mtDNA disorders to establish healthy offspring.

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

    Directory of Open Access Journals (Sweden)

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

    Energy Technology Data Exchange (ETDEWEB)

    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.)

  3. The effects of active dried and killed dried yeast on subacute ruminal acidosis, ruminal fermentation, and nutrient digestibility in beef heifers.

    Science.gov (United States)

    Vyas, D; Uwizeye, A; Mohammed, R; Yang, W Z; Walker, N D; Beauchemin, K A

    2014-02-01

    The study addressed the importance of yeast (Saccharomyces cerevisiae) viability for reducing the incidence of subacute ruminal acidosis (SARA) and improving total tract nutrient digestibility in beef heifers. Six ruminally cannulated beef heifers (680 ± 50 kg BW) were used in a replicated 3 × 3 Latin square design and were fed a diet consisting of 40% barley silage, 10% chopped grass hay, and 50% barley grain-based concentrate (DM basis). Treatments were 1) no yeast (Control), 2) active dried yeast (ADY; 4 g providing 10(10) cfu/g; AB Vista, Marlborough, UK), and 3) killed dried yeast (KDY; 4 g autoclaved ADY). The treatments were directly dosed via the ruminal cannula daily at the time of feeding. The periods consisted of 2 wk of adaptation (d 1 to 14) and 7 d of measurements (d 15 to 21). Ruminal pH was continuously measured (d 15 to 21) using an indwelling system. Ruminal contents were sampled on d 15 and 17 at 0, 3, 6, 9, and 12 h after feeding. Total tract nutrient digestibility was measured using an external marker (YbCl3) from d 15 to 19. No treatment difference was observed for DMI (P = 0.86). Yeast supplementation (ADY and KDY) tended to increase total tract digestibility of starch (P = 0.07) whereas no effects were observed on digestibility of other nutrients. Both ADY and KDY elevated minimum (P yeast supplementation was effective in reducing time that ruminal pH was below 5.8 (P 0.10); however, the proportion of Ruminococcus flavefaciens in solid fraction of digesta was greater with KDY (P = 0.05). The study demonstrates the positive effects of yeast, irrespective of its viability, in reducing the severity of SARA. However, further studies are required to evaluate the importance of yeast viability for other dietary conditions, particularly when the risk of acidosis is high.

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

    Energy Technology Data Exchange (ETDEWEB)

    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.)

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

    Science.gov (United States)

    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

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

    Science.gov (United States)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

  8. 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.

    OpenAIRE

    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 ...

  9. [A case of rhabdomyolysis after status epilepticus without stroke-like episodes in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes].

    Science.gov (United States)

    Yokoyama, Jun; Yamaguchi, Hiroo; Shigeto, Hiroshi; Uchiumi, Takeshi; Murai, Hiroyuki; Kira, Jun-ichi

    2016-01-01

    A 24-year-old man was referred to our hospital emergency department due to a sudden onset of convulsions after drinking. On arrival he presented status epilepticus and was managed by artificial ventilation. He had no brainstem signs or meningeal irritation. Head MRI showed an old infarction-like lesion in the left occipital lobe, but no abnormal signals on diffusion-weighted images. The patient showed acute rhabdomyolysis (CK 18,000 IU/l) and renal failure, and hemodialysis was started. On 18 day after admission, he was transferred to our department with mild proximal limb muscle weakness and bilateral sensorineural hearing impairment. Electroencephalography demonstrated diffuse intermittent slow wave activities. We suspected a mitochondrial disease because of a significant increase in the lactate/pyruvate ratio (24.1) in the spinal fluid, and identified A3243G mutations in mitochondrial DNA (heteroplasmy 20%) in peripheral white blood cells. We diagnosed his illness as mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). This is a rare case presenting an acute onset of rhabdomyolysis following alcohol intake related to A3243G mitochondrial mutation without preceding stroke-like episodes. PMID:26960270

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

    Institute of Scientific and Technical Information of China (English)

    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. A new disease-related mutation for mitochondrial encephalopathy lactic acidosis and strokelike episodes (MELAS) syndrome affects the ND4 subunit of the respiratory complex I

    Energy Technology Data Exchange (ETDEWEB)

    Lertrit, P.; Noer, A.S.; Kapsa, R.; Marzuki, S. (Monash Univ., Clayton, Victoria (Australia)); Jean-Francois, M.J.B.; Thyagarajan, D.; Byrne, E. (St. Vincent' s Hospital, Fitzroy, Victoria (Australia)); Dennett, X. (Univ. of Melbourne, Parkville, Victoria (Australia)); Lethlean, K. (Prince Henry Hospital, Sydney (Australia))

    1992-09-01

    The molecular lesions in two patients exhibiting classical clinical manifestations of MELAS (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) syndrome have been investigated. A recently reported disease-related A[yields]G base substitution at nt 3243 of the mtDNA, in the DHU loop of tRNA[sup Leu], was detected by restriction-enzyme analysis of the relevant PCR-amplified segment of the mtDNA of one patient but was not observed, by either restriction-enzyme analysis or nucleotide sequencing, in the other. To define the molecular lesion in the patient who does not have the A[yields]G base substitution at nt 3243, the total mitochondrial genome of the patient has been sequenced. An A[yields]G base substitution at nt 11084, leading to a Thr-to-Ala amino acid replacement in the ND4 subunit of the respiratory complex I, is suggested to be a disease-related mutation. 49 refs., 7 figs., 1 tab.

  12. Rumen microbial abundance and fermentation profile during severe subacute ruminal acidosis and its modulation by plant derived alkaloids in vitro.

    Science.gov (United States)

    Mickdam, Elsayed; Khiaosa-Ard, Ratchaneewan; Metzler-Zebeli, Barbara U; Klevenhusen, Fenja; Chizzola, Remigius; Zebeli, Qendrim

    2016-06-01

    Rumen microbiota have important metabolic functions for the host animal. This study aimed at characterizing changes in rumen microbial abundances and fermentation profiles using a severe subacute ruminal acidosis (SARA) in vitro model, and to evaluate a potential modulatory role of plant derived alkaloids (PDA), containing quaternary benzophenanthridine and protopine alkaloids, of which sanguinarine and chelerythrine were the major bioactive compounds. Induction of severe SARA strongly affected the rumen microbial composition and fermentation variables without suppressing the abundance of total bacteria. Protozoa and fungi were more sensitive to the low ruminal pH condition than bacteria. Induction of severe SARA clearly depressed degradation of fiber (P methanogenic 16S rRNA gene abundance was not affected. According to principal component analysis, Methanobrevibacter spp. correlated to methane concentration. Addition of PDA modulated ruminal fermentation under normal conditions such as enhanced (P < 0.05) concentration of total SCFA, propionate and valerate, and increased (P < 0.05) degradation of crude protein compared with the unsupplemented control diet. Our results indicate strong shifts in the microbial community during severe SARA compared to normal conditions. Supplementation of PDA positively modulates ruminal fermentation under normal ruminal pH conditions. PMID:26868619

  13. 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

    Directory of Open Access Journals (Sweden)

    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

  14. 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

    Institute of Scientific and Technical Information of China (English)

    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

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

    Directory of Open Access Journals (Sweden)

    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

  16. 肾小管性酸中毒骨骼并发症的临床分析%Clinical analysis of bone complications in renal tubular acidosis

    Institute of Scientific and Technical Information of China (English)

    马毓华; 谢静远; 张春丽; 李晓; 沈平雁; 任红; 陈楠

    2013-01-01

    Objectives This study aims to investigate the features of bone complications secondary to renal tubular acidosis(RTA) and to further discuss the differences and characteristics of clinical manifestations between patients with primary RTA (PRTA) or RTA Secondary to Sj? gren's syndrome (SRTA) patients.Methods We retrospectively recruited 109 SRTA patients and 144 PRTA patients who admitted to our clinical center during 1996 and 2010.Baseline demographic,clinical features,laboratory examinations,outcomes and isotope bone density examination were collected and analyzed.Results The study included 144 PRTA and 109 SRTA patients.In PRTA group,there were 63 men and 81 women,the average age was 38 years; In SRTA group,there were 10 men and 99 women,the average age was 42 years..Within the PRTA group,bone pain and joint pain occured in 22 cases (15.3%),reduced bone mass was observed in 3 cases (2.1%),osteoporosis was found in 17 cases (11.8%).While in SRTA group,25 patients (22.9%) were reported to have bone pain and joint pain,and reduced bone mass was found in 10 cases (9.2%),9 cases (8.3%) of the patients had osteoporosis.Accordingly,more patients with bone disease were detected in SRTA group than in PRTA group (37.6% vs 24.3%,p < 0.05).The isotope bone density with lumbar spine T value of 9 PRTA patients is more than the SRTA patients.Additionally,SRTA patients had a lower lumber spine T value than PRTA patients (-0.53 ± 0.97 vs-1.65 ± 1.29,P < 0.05) by isotope bone density test which indicated a higher frequency and more severe bone disease occurred in RTA patients with Sj? gren 's syndrome than primary RTA patients.Conclusions Sjgren's syndrome is the most common cause of secondary RTA,the incidence and severity of bone disease was higher in RTA patients secondary to Sj? gren's syndrome than primary RTA patients,which aroused early diagnosis and clinical attentions.%目的 总结肾小管酸中毒(Renal Tubular Acidosis,RTA)骨骼并发症的特

  17. 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

    Directory of Open Access Journals (Sweden)

    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

  18. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  19. 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

    Institute of Scientific and Technical Information of China (English)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  1. 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

    Institute of Scientific and Technical Information of China (English)

    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

  2. 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

    Institute of Scientific and Technical Information of China (English)

    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

  3. 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

    Institute of Scientific and Technical Information of China (English)

    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

  4. 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

    Directory of Open Access Journals (Sweden)

    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

  5. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  6. 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

    Institute of Scientific and Technical Information of China (English)

    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。

  7. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  8. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  9. 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

    Institute of Scientific and Technical Information of China (English)

    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

  10. 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

    Institute of Scientific and Technical Information of China (English)

    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

  11. 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

    Directory of Open Access Journals (Sweden)

    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."""

  12. 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

    Institute of Scientific and Technical Information of China (English)

    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

  13. 两种连续肾脏替代纠正乳酸酸中毒的临床观察%Clinical investigation of continuous venous-venous hemofiltration and continuous venous-venous hemodialysis on lactic acidosis

    Institute of Scientific and Technical Information of China (English)

    彭绵; 方伟强; 蔡举瑜; 简小莉

    2014-01-01

    Objective To investigate the effect of continuous venous-venous hemofiltration (CVVH) and continuous venous-venous hemodialysis (CVVHD) on patients with lactic acidosis.Methods A total of 137 cases with lactic acidosis were included in this prospective randomized control study.lhe patients were collected from the University of Hong Kong-shenzhen Hospitall and the First Affiliated Hospital of Shantou University Medical College from April 2009 to April 2013.Inclusion criteria were patients with lactic acidosis.Exclusion criteria were patients with end-stage malignancy or terminal stage of illnesses.The patients were randomly divided into two groups:CVVH group and CVVHD group,and patients of both group were intervened with conventional treatments as well.For each group,the lactic acid and blood gas analysis were tested before CRRT,and at 4 hours,8 hours,12 hours,24 hours,and 48 hours of CRRT.The patients' mortality and length of ICU stay time were analysed and recorded.Statistical analysis was performed using SPSS 15.0software.Results When the length of time for treatment was the same,the efficacy between CVVH group and CVVHD group showed no difference in blood lactic acid level [4 h:(11.65 ± 3.39) mmol/L vs.(11.12±2.65) mmol/L; 8 h:(8.78±2.35) mmol/L vs.(8.59±2.09) mmol/L; 12 h:(6.91 ±1.67)mmol/Lvs.(6.74±1.76) mmol/L;24h:(1.66±0.39) mmol/Lvs.(1.51±0.30) mmol/L; 48 h:(0.95 ±0.24) mmol/L vs.(0.66 ±0.20) mmol/L,P > 0.05) and pH value [4 h:(6.93 ±0.14) vs.(7.05±0.09);8h:(7.04±0.10)vs.(7.12±0.05); 12h:(7.13±0.07)vs.(7.20±0.04);24h:(7.30±0.03) vs.(7.38±0.04); 48h:(7.41 ±0.03) vs.(7.46±0.02),P> 0.05].There are also no difference in the hospital mortality (11.4% vs.10.4%,P=0.854) and length ofICU stay time [(9.5 ±2.4) d vs.(8.8 ± 2.9) d,P =0.329].Conclusions Both CVVH and CVVHD can effectively correct hyperlactemia,enhance acid-base balance,contributing no differences in length of ICU stay time and patients' hospital mortality.%目的 比较持

  14. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  15. Brain carbonic acid acidosis after acetazolamide

    DEFF Research Database (Denmark)

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

    1975-01-01

    of the carbonic anhydrase inhibition on the brain tissue. As a further support for this conclusion was considered the finding of a prolonged response time of brain pH to HCO3-minus i.v. to CO2-minus inhalation, and to hyperventilation after the acetazolamide inhibtion. No changes in brain extracelllular potassium......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...

  16. Topiramate and Metabolic Acidosis in Infants

    Directory of Open Access Journals (Sweden)

    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.

  17. 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

    Directory of Open Access Journals (Sweden)

    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

  18. 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

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    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.

  19. 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

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    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

  20. 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

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    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。

  1. 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

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    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.

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

    NARCIS (Netherlands)

    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

  3. Unmeasured anions account for most of the metabolic acidosis in patients with hyperlactatemia Ânions não mensuráveis são responsáveis pela maior parte da acidose metabólica de pacientes com hiperlactatemia

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    Alexandre Toledo Maciel

    2007-02-01

    Full Text Available PURPOSE: To characterize the different components of metabolic acidosis in patients with hyperlactatemia in order to determine the degree to which lactate is responsible for the acidosis and the relevance that this might have in the outcome of these patients. METHODS: Arterial blood gas, arterial lactate, Na+, K+, Ca2+, Mg2+, Cl-, phosphate, albumin, and creatinine were measured on admission to make a diagnosis of the acid-base disturbances present. Intensive Care Unit and in-hospital mortality were also recorded. RESULTS: A total of 58 patients with hyperlactatemia were included. They usually had a mild acidemia (pH 7.31 ± 0.12 and a significantly high Standard Base Deficit (7.6 ± 6.7 mEq/L. In addition to lactate (4.3 ± 2.3 mEq/L, chloride (106.9 ± 9.5 mEq/L and unmeasured anions (8.6 ± 5.0 mEq/L accounted for the metabolic acidosis. Unmeasured anions were primarily responsible for the acidosis in both Intensive Care Unit survivors and nonsurvivors (44.7% ± 26.0% and 46.0% ± 17.5%, respectively, P = 0.871. Lactate contributed in similar percentages to the acidosis in both groups (23.0% ± 11.8% and 24.2% ± 9.7% in Intensive Care Unit survivors and nonsurvivors, respectively; P = 0.753. Correlation between Standard Base Deficit and lactate was found only in Intensive Care Unit nonsurvivors (r = 0.662, P OBJETIVO: Caracterizar os diferentes componentes da acidose metabólica de pacientes com hiperlactatemia de modo a verificar o quanto o lactato é responsável pela acidose e a relevância que isso possa ter no prognóstico desses pacientes. MÉTODOS: Gasometria arterial com dosagem de lactato, Na+, K+, Ca2+, Mg2+, Cl-, fosfato, albumina e creatinina séricas foram coletados no momento da admissão para fazer o diagnóstico dos possíveis distúrbios ácido-básicos presentes. Mortalidade na UTI e mortalidade hospitalar foram avaliadas. RESULTADOS: Um total de 58 pacientes com hiperlactatemia foram incluídos. Eles tinham na média uma

  4. 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

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    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

  5. 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

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    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.

  6. 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

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    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.

  7. 儿童线粒体脑肌病伴高乳酸血症和卒中样发作综合征2例报告%Children with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome:two cases report

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    唐志慧; 罗强

    2015-01-01

    ObjectiveTo discuss the clinical features, diagnosis and treatment of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome in children.Methods The clinical features and treatment process of two children with MELAS were retrospectively analyzed.ResultsThe main clinical features of MELAS were stroke-like epi-sodes, seizure, visual anomaly and lactic acidosis. Cephalic MRI ifndings performed during episode periods were in accord with the typical radiographic features of MELAS. Gene testing on the two children and their mothers showed the point mutation of A3243G in mitochondrial genome. The symptoms were improved signiifcantly after energy supply and corticosteroid treatment. Conclusions MELAS syndrome is easy to be misdiagnosed due to the varied clinical features. The diagnosis depends on the musclebiopsy and gene testing. Corticosteroid therapy is effective for MELAS syndrome.%目的:探讨线粒体脑肌病伴高乳酸血症和卒中样发作综合征(MELAS)的诊断与治疗。方法回顾性分析2例MELAS患儿的临床特征及诊疗过程。结果2例患儿主要临床表现为卒中样发作、抽搐、视物模糊、高乳酸血症;发作期头颅磁共振成像结果符合典型的MELAS综合征影像学表现;基因测序存在mtDNA的A3243G点突变;改善供能及皮质激素治疗后症状明显改善。结论 MELAS临床症状复杂多样,血乳酸及头颅磁共振成像检查有助临床诊断,确诊需要肌肉活检或基因检测,皮质激素治疗有效。

  8. 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

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    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

  9. 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

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    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

  10. Subdiaphragmatic venous stasis and tissular hypoperfusion as sources of metabolic acidosis during passive portal-jugular and caval-jugular bypasses in dogs Estase venosa subdiafragmática e hipoperfusão tissular como fontes de acidose metabólica durante desvios porta-jugular e cava-jugular passivos em cães

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    Antônio Roberto de Barros Coelho

    2000-06-01

    Full Text Available Subdiafragmatic venous decompression during anhepatic stage of canine orthotopic liver transplantation attenuates portal and caval blood stasis and minimize hipoperfusion and metabolic acidosis observed with occlusion of portal and caval veins. During two hours, six dogs submitted to portal-jugular and caval-jugular passive shunts, with maintenance of arterial hepatic flow, were evaluated for pH, carbon dioxide tension (PCO2, base deficit (BD and oxygen tension (PO2 in portal, caval and systemic arterial blood, as well as for increments of BD (DBD in portal and caval blood. With a confidence level of 95%, the results showed that: 1. There were not changes of pH anDBD in portal and systemic arterial blood in the majority of studied times; 2. There was metabolic acidosis in caval blood; 3. The negative increments of BD (DBD were higher in caval blood than in splancnic venous blood at T10, T30 and T105; and, 4. Deoxigenation of portal and caval blood were detected. Acid-base metabolism and oxigenation monitoring of subdiaphramatic venous blood can constitute an effective way to evaluate experimental passive portal-jugular and caval-jugular bypass in dogs.A descompressão venosa subdiafragmática durante a fase anhepática do transplante ortotópico de fígado em cães atenua a estase de sangue nas veias Porta e Cava Inferior e minimiza a hipoperfusão tissular e a acidose metabólica observadas na oclusão dessas veias. Durante duashoras, seis cães submetidos a desvios porta-jugular e cava-jugular passivos, com permanência do fluxo arterial hepático, foram avaliados através de pH, PCO2, DB e PO2 no sangue portal, da Veia Cava Inferior e arterial sistêmico, bem como por incrementos de DB (DDB no sangue portal e da Veia Cava Inferior. Os resultados obtidos permitem concluir com uma confiança de 95% que: 1. Não foram constatadas alterações de pH e DB no sangue portal e arterial sistêmico na maioria dos tempos estudados; 2. Houve acidose

  11. 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

    Institute of Scientific and Technical Information of China (English)

    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

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

    OpenAIRE

    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...

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

    DEFF Research Database (Denmark)

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

    2011-01-01

    acids. In humans, inflammation has been linked to metabolic diseases. In cattle, studies into the possible links between acid-base changes, inflammation/innate immunity and metabolic disease are warranted as this might improve our understanding of the production disease complexes occurring in particular...

  14. Recurrent lactic acidosis secondary to hand sanitizer ingestion.

    Science.gov (United States)

    Wilson, M E; Guru, P K; Park, J G

    2015-01-01

    Due to their ability to decrease the spread of infection, hand sanitizers are now ubiquitous in health care settings. We present the case of a 50-year-old woman who was admitted with acute alcohol intoxication and had near complete recovery in 12 hrs. Subsequently, she was found unresponsive on the floor of her hospital room on two separate occasions. Evaluations revealed repeatedly elevated levels of ethanol, acetone, and lactate as well as increased anion gap and hypotension, requiring intensive care unit evaluation and intubation for airway protection. During the second episode, she was found next to an empty bottle of ethanol-based hospital hand sanitizer. She confirmed ingesting hand sanitizer in order to become intoxicated. PMID:25684875

  15. Recurrent lactic acidosis secondary to hand sanitizer ingestion

    OpenAIRE

    Wilson, M E; Guru, P. K.; Park, J. G.

    2015-01-01

    Due to their ability to decrease the spread of infection, hand sanitizers are now ubiquitous in health care settings. We present the case of a 50-year-old woman who was admitted with acute alcohol intoxication and had near complete recovery in 12 hrs. Subsequently, she was found unresponsive on the floor of her hospital room on two separate occasions. Evaluations revealed repeatedly elevated levels of ethanol, acetone, and lactate as well as increased anion gap and hypotension, requiring inte...

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

    DEFF Research Database (Denmark)

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

    1985-01-01

    showed impaired capacity for acidification of urine. The lowest urinary pH was 5.53 +/- 0.10 in 10 bypass patients and 4.76 +/- 0.06 in 6 controls. The corresponding values for standard bicarbonate in plasma were 15.0 +/- 0.3 mM and 15.8 +/- 0.3 mM. Glomerular filtration rate was identical in the two...

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

    Science.gov (United States)

    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...

  18. Genetics Home Reference: renal tubular acidosis with deafness

    Science.gov (United States)

    ... 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 ...

  19. Dynamic evolution of brain magnetic resonance imaging findings in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes syndrome%线粒体脑肌病伴高乳酸血症和卒中样发作综合征患者的脑磁共振成像改变动态演变规律

    Institute of Scientific and Technical Information of China (English)

    赵丹华; 王朝霞; 于磊; 肖江喜; 谢晟; 袁云; 黄一宁

    2014-01-01

    Objective To analyze the dynamic evolution of brain MRI in patients with mitochondrial myopathy,encephalopathy,lactic acidosis,and stroke-like episodes (MELAS) syndrome.Methods A retrospective study was performed on 58 MELAS cases with pathologically and (or) molecularly confirmed diagnosis.MRI were repeated within 60 days after the onset of stroke-like episodes (SLE) and the evolution changes of cerebral lesions were accessed.Brain atrophy index (BAI) was calculated in the remission stage from 31 patients with MELAS,and the correlation between BAI,age and disease duration was analyzed.Results The proportion of lesions expansion,migration and shrink within 30 days after the onset of SLE was 64.1% (25/39),10.2% (4/39),17.9% (7/39),respectively,and 13% (3/23),21.7% (5/23),56.5% (13/23),between 30-60 days after the onset of SLE respectively.In the recovery stage of SLE,the BAI in 31 patients with MELAS was 15.2% ±2.8%.The correlation coefficient between BAI and the age,total disease course and duration of encephalopathy was 0.329 (P =0.043),0.405 (P =0.012) and 0.649 (P =0.000).Conclusions Brain atrophy in the studied MELAS patients gradually develops and strokelike lesions shrink with progression of the disease.However,the migration of lesions is persistent.%目的 分析线粒体脑肌病伴高乳酸血症和卒中样发作(MELAS)综合征患者的脑MRI改变动态演变规律.方法 收集经肌肉病理检查和(或)基因检测确诊的58例MELAS患者的资料,于卒中样发作(SLE)后60 d内进行重复脑MRI检查,分析其病灶的演变规律;计算31例患者缓解期头MRI的脑萎缩指数以及与其年龄及病程之间的相关性.结果 SLE后30 d内64.1% (25/39)的病灶扩大,10.2% (4/39)的病灶转移,17.9%(7/39)的病灶缩小.在30 ~60 d内13%(3/23)的病灶扩大,21.7%(5/23)的病灶转移和56.5%(13/23)的病灶缩小.31例患者SLE缓解期脑萎缩指数为15.2%±2.8%,与年龄、总病程、脑内症

  20. 线粒体DNA G13513A突变所致线粒体脑肌病伴高乳酸血症和脑卒中样发作/Leigh重叠综合征%Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes/Leigh overlap syndrome caused by mutation of mitochondrial DNA G13513A

    Institute of Scientific and Technical Information of China (English)

    韩漫夫; 白润涛; 冯宏业; 陶唯宜; 王朝霞; 袁云

    2009-01-01

    Objective To describe the chnical, neuroimagine, pathological and genetic features in a case with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS)/Leigh overlap syndrome.Methods The ease was a 22-year-old woman with recurrent headache, loss of visual acuity and general seizures over 11 years.MRI demonstrated symmetrical high T2-weighted signals in occipital and parietal lobes, in the late stage of the disease, the above imagine changes on MRJ were also shown in the bilateral basal ganglion and brainstem.She died of status epilepticus at age of 22.Brain autopsy and mitochondrial DNA (mtDNA) analysis were performed in the patient.Results The main neuropathological findings were muhifocal and lamilar spongiform in the cortex of the whole brain, the basal ganglion and middle brain.Gliosis, macrophagie reaction and capillary endothelial proliferation were observed in these areas.All 6 layers of the cortex and subcortical white matter in occipital and parietal lobes were severely affected.GI3513A mutation was found in the gene of mitochondria encoded NADH dehydrogenase subunit 5 (MTNDS).Conclusions MELAS/Leigh overlap syndrome presents the symptoms predominantly affecting the cerebral cortex.Neuroimagines suggested that the lesion initially involves the cerebral cortex and in the late stage implicates the basal ganglion and the brainstem, possibly caused by pathological changes of spongiform with capillary proliferation in these areas.%目的 报道1例线粒体DNA G13513A点突变所致线粒体脑肌病伴高乳酸血症和脑卒中样发作(MELAS)/Leigh重叠综合征的临床、影像学、神经病理学改变特点.方法 患者为22岁女性,反复出现头痛、视力下降和肢体抽动11年,因癫疴持续状态而死亡.之前多次MRI检查发现大脑皮质大片长T1长T2异常信号,病灶从枕叶开始,逐渐波及顶叶,疾病后期累及双侧基底节区及脑干灰质核团.对患者进行脑局部尸体解

  1. A Case Misdiagnosed as Cerebral Infarct:Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis and Stroke-Like Episodes%线粒体脑肌病伴高乳酸血症和卒中样发作误诊为脑梗死

    Institute of Scientific and Technical Information of China (English)

    肖展翅; 吕衍文; 王洪敏; 王佳君; 周刚; 姜华

    2014-01-01

    Objective To explore the diagnostic criteria, misdiagnosis causes and preventive measures of mitochon-drial myopathy, encephalopathy, lactic acidosis and stroke-like episodes ( MELAS) . Methods Clinical data of the MELAS patient misdiagnosed as cerebral infarct was retrospectively analyzed. Results The patient with double eyes vision loss for a day was hospitalized, and diagnosed as cerebral infarction after the body and head MRI examinations, vision of double eyes were mildly better after treatment. By DSA, MRS examinations and genetic testing, the patient was eventually confirmed as MELAS syndrome in stead of cerebral infarction. After 3-month treatment such as improving the metabolism and blood supply of the brain, the patient got better obviously, and MRI showed that the focus of head disappeared. Conclusion Clinical mani-festations being similar to acute cerebral infarction, head MRI showing cerebral infarction and knowledge of doctors being nar-row were the main causes of misdiagnosis. Strengthening learning to understand and mastering relevant knowledge of mitochon-dria encephalo-myopathy can prevent or reduce the misdiagnosis.%目的:探讨线粒体脑肌病伴高乳酸血症和卒中样发作的诊断要点、误诊原因及防范措施。方法对我院近期收治的误诊为脑梗死的线粒体脑肌病伴高乳酸血症和卒中样发作1例的临床资料进行回顾性分析。结果患者因双眼突发视力减退1 d入院,经查体及头颅MRI等相关检查考虑脑梗死,予相应治疗,视力稍好转。后患者行头颅数字减影血管造影及磁共振波谱检查排除脑梗死,最终经基因检查确诊线粒体脑肌病( MELAS综合征)。予改善代谢及脑供血等治疗3个月,患者病情明显好转,头颅MRI检查示病灶消失。结论临床表现与急性脑梗死相似、头颅MRI检查提示脑梗死及接诊医生知识面狭窄是导致本例误诊的主要原因。加强学习、拓宽知识面、了解

  2. 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

    Directory of Open Access Journals (Sweden)

    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

  3. 成人线粒体脑肌病伴高乳酸血症和卒中样发作(MELAS)综合征浅析%Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome in adult:a case report with literature review

    Institute of Scientific and Technical Information of China (English)

    冯全志; 韩彤; 雷静

    2015-01-01

    Objective To investigate the clinical and imaging characteristics of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome in adult, and to enhance the knowledge of this disease and decrease misdiagnose. Methods Relevant literatures were reviewed, and two cases of MELAS syndrome proved by muscle pathology were retrospectively analyzed. Results The two patients presented with the onset of stroke and seizures. Imaging examination: “cerebral infarction”-like lesions asymmetrically involving temporal parietal occipital lobe. CT scan showed patchy low density shadow. On MRI, lesions showed slightly long T1 and T2 signals, hyperintensity on FLAIR and DWI, slightly low signal on ADC map. The lesions involved the territories of middle cerebral artery and the posterior cerebral artery. Brain MRA scan showed supply artery stenosis or occlusion. The perfusion weighted imaging showed abnormal hyperperfusion in the lesion area. Magnetic resonance spectroscopy (TE=135 ms) scan showed obvious inverted lactate peak at lesions. Laboratory tests showed the lactate level of blood and cerebrospinal fluid increased significantly. For biceps brachii biopsy, the scattered and ragged red fibers can be seenon modified Gomori-trichrome. The two cases of last diagnosis is MELAS syndrome. For the mt DNA A3243G of detection, the first case was negative, but the second case was positive. The first patient returned one year later due to second onset, the new lesion involved temporal pole, brain atrophy was seen at the primary lesion area. Conclusion MELAS syndrome is rare in clinic, and clinical and imaging manifestations have certain characteristics. Multi-modality MRI has important value in the diagnosis of the disease. Final diagnosis relies on muscle histological examination.%目的:探讨成人MELAS综合征的临床表现和影像特点,提高对该病的认识,减少误诊。方法复习线粒体脑肌病

  4. Effects of Subacute Ruminal Acidosis on Plasma Cytokine and Hormone Contents in Dairy Goats%亚急性瘤胃酸中毒对奶山羊血浆细胞因子和激素含量的影响

    Institute of Scientific and Technical Information of China (English)

    胡红莲; 谢天宇; 杨淑青; 高民; 姚焰础

    2015-01-01

    本试验旨在研究以递增饲粮非纤维性碳水化合物与中性洗涤纤维比( NFC/NDF)方式诱导奶山羊发生亚急性瘤胃酸中毒( SARA)后,血浆细胞因子和激素含量的变化。选取9只体况良好,体重接近的泌乳期莎能奶山羊,随机分为3组(对照组、SARA组、恢复组, n=3),对照组饲喂基础饲粮,SARA组和恢复组先后饲喂NFC/NDF为1.40、1.79、2.31、3.23的4种试验饲粮诱导SARA发生,每种饲喂15 d,恢复组奶山羊诱导SARA后自由采食青干草30 d。对照组3只羊分别在饲养30、60(与SARA组同时)和90 d(与恢复组同时)屠宰。结果表明:1) SARA长期提高了血浆LPS浓度,恢复组与SARA组差异不显著( P>0.05)。2)与对照组相比,SARA组奶山羊血浆中促炎性细胞因子肿瘤坏死因子-α( TNF-α)、白细胞介素( IL)-1β和IL-6含量呈升高趋势(P>0.05),IL-2含量显著升高(P0.05),γ-干扰素(IFN-γ)含量显著降低(P0.05);SARA组奶山羊血浆中生长激素、胰岛素样生长因子-Ⅰ、胰岛素含量变化不显著(P>0.05),催乳素(PRL)和皮质醇(COR)含量均显著升高(P0.05),而COR含量则回归到对照组水平( P>0.05)。本研究结果显示,SARA可引起奶山羊血浆中长时间含有一定量的LPS,引发机体免疫和炎症反应,并引起内分泌激素的变化,这一系列变化导致奶山羊长期处于应激状态。%This experiment was conducted to investigate the effects of subacute ruminal acidosis ( SARA) in-duced by gradually increasing dietary non-fiber carbohydrate/neutral detergent fiber ratios ( NFC/NDF ) on plasma hormone and cytokine contents in dairy goats. Nine healthy lactating Saanen dairy goats with similar body weight were randomly allocated to three groups ( control group, SARA group and recovery group, n=3 ) . Dairy goats in control group were fed a basal diet;those in SARA group and recovery group were fed diets with different NFC/NDF (1.40, 1.79, 2.31 and 3.23, respectively, each for 15 days

  5. 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

    Institute of Scientific and Technical Information of China (English)

    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

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

    NARCIS (Netherlands)

    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

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

    NARCIS (Netherlands)

    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

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

    NARCIS (Netherlands)

    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

  9. Intraoperative acidosis is a new predictor for postoperative pancreatic ifstula after pancreati-coduodenectomy

    Institute of Scientific and Technical Information of China (English)

    Erdem Kinaci; Mert Mahsuni Sevinc; Abdulkerim Ozakay; Savas Bayrak; Ekrem Cakar; Serkan Sari

    2015-01-01

    BACKGROUND: Early diagnosis of postoperative pancreatic ifstula (POPF) is important for proper interventions. The pre-operative, intraoperative and early postoperative biochemical markers have predictive value of POPF. The present study was to evaluate several simple biochemical parameters in the pre-diction of POPF. METHODS: Patients who underwent pancreaticoduodenec-tomy in our center between 2006 and 2015 were reviewed ret-rospectively. Preoperative and early postoperative biochemi-cal parameters were evaluated. Additionally, the relationship between POPF and pH and lactate level at the end of surgery were analyzed, and neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and red cell distribution width-to-platelet ratio (RPR) were calculated for postoperative days (PODs) 1 and 3. Diagnosis and grading of POPF were per-formed according to the standards of the International Study Group on Pancreatic Fistula. The patients were divided into two groups: Group 1 with no ifstula or grade-A ifstula; group 2 with grade-B or -C ifstula. These simple biochemical markers were then compared between the two groups. RESULTS: Serum amylase level was signiifcantly higher at POD3, and pH level was signiifcantly lower at the end of op-eration in group 2 compared with those in group 1. However, the serum amylase was below the upper limit of normal serum level and therefore, the difference was not signiifcant in clini-cal practice. Receiver operating charecteristic curve analysis showed that pH level was a reliable predictor of POPF (area under the curve: 0.713; 95% CI: 0.573-0.853). CONCLUSIONS: A low pH level at the end of pancreaticoduo-denectomy was a risk factor of POPF. NLR, PLR, and RPR had no predictive value of POPF after pancreaticoduodenectomy.

  10. Effect of haemodilution, acidosis, and hypothermia on the activity of recombinant factor VIIa (NovoSeven)

    DEFF Research Database (Denmark)

    Viuff, D.; Lauritzen, B.; Pusateri, A.E.;

    2008-01-01

    BACKGROUND: A range of plasma volume expanders is used clinically, often in settings where haemostasis may already be impaired. The haemostatic agent, recombinant activated factor VII (rFVIIa, NovoSeven), may be used to improve haemostasis but potential interactions with different volume expanders......%, or hydroxyethyl starch (HES) solutions [MW (molecular weight) 130-670 kDa]; by adjusting pH to 6.8 with 1 M HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulphonic acid) buffer; or by reducing temperature to 32 degrees C. We also studied the effect of low vs high MW HES (MW 200 vs 600 kDa) and rFVIIa on in vivo...

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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.

  13. Cold intermittent cardioplegia reduces the acidosis during prolonged cardiac surgery with cardiopulmonary bypass.

    Science.gov (United States)

    Nollo, Giandomenico; Ferrari, Paolo; Graffigna, Angelo C

    2011-01-01

    The effect on acid-base balance efficacy of intermittent warm and cold blood cardioplegia (IWBC, ICBC) was assessed in 44 patients who underwent cardiac surgery with prolonged aortic cross clamping. With this purpose a customized multi sensor probe was inserted in the coronary sinus, and pH, PO(2), PCO(2) and temperature were continuously measured at 1 Hz sampling rate. The mean cross-clamping time was of 76 ± 26 min on 19 IWBC cases and of 80 ± 24 min on 14 ICBC cases. With IWBC perfusion, at the end of every ischemic period, the lowest pH and PO(2) progressively decreased and the maximal PCO(2) increased. During ICBC the minimum of pH and PO(2) and maximum of PCO2 at the end of different ischemic period during time were constant, also during long cross-clamping time. With IWBC, myocardial ischemia seemed not completely reversed by standardized reperfusions, as reflected by steady deterioration of PCO(2) and pH after each reperfusion.

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

    DEFF Research Database (Denmark)

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

    2014-01-01

    at the 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....

  15. Intraoperative acidosis is a new predictor for postoperative pancreatic ifstula after pancreati-coduodenectomy

    Institute of Scientific and Technical Information of China (English)

    Erdem Kinaci; Mert Mahsuni Sevinc; Abdulkerim Ozakay; Savas Bayrak; Ekrem Cakar; Serkan Sari

    2016-01-01

    BACKGROUND: Early diagnosis of postoperative pancreatic ifstula (POPF) is important for proper interventions. The pre-operative, intraoperative and early postoperative biochemical markers have predictive value of POPF. The present study was to evaluate several simple biochemical parameters in the pre-diction of POPF. METHODS: Patients who underwent pancreaticoduodenec-tomy in our center between 2006 and 2015 were reviewed ret-rospectively. Preoperative and early postoperative biochemi-cal parameters were evaluated. Additionally, the relationship between POPF and pH and lactate level at the end of surgery were analyzed, and neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and red cell distribution width-to-platelet ratio (RPR) were calculated for postoperative days (PODs) 1 and 3. Diagnosis and grading of POPF were per-formed according to the standards of the International Study Group on Pancreatic Fistula. The patients were divided into two groups: Group 1 with no ifstula or grade-A ifstula; group 2 with grade-B or -C ifstula. These simple biochemical markers were then compared between the two groups. RESULTS: Serum amylase level was signiifcantly higher at POD3, and pH level was signiifcantly lower at the end of op-eration in group 2 compared with those in group 1. However, the serum amylase was below the upper limit of normal serum level and therefore, the difference was not signiifcant in clini-cal practice. Receiver operating charecteristic curve analysis showed that pH level was a reliable predictor of POPF (area under the curve: 0.713; 95% CI: 0.573-0.853). CONCLUSIONS: A low pH level at the end of pancreaticoduo-denectomy was a risk factor of POPF. NLR, PLR, and RPR had no predictive value of POPF after pancreaticoduodenectomy.

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

    Science.gov (United States)

    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

  17. Placental endoplasmic reticulum stress and acidosis: relevant aspects in gestational diabetes.

    Science.gov (United States)

    Jawerbaum, Alicia

    2016-10-01

    In this issue, Yung and colleagues (doi: 10.1007/s00125-016-4040-2 ) report endoplasmic reticulum stress in the placenta of patients with gestational diabetes mellitus. With the use of a trophoblast-like cell line, these authors identify putative mechanisms involved in, and treatments to prevent the induction of endoplasmic reticulum stress. Here, the relevance and possible implications of these findings and areas for further research are discussed.

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

    DEFF Research Database (Denmark)

    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......+ concentration and K+ accumulation during exercise. Seven healthy subjects performed one-legged knee-extensor exercise on two separate days with and without sodium citrate ingestion. Interstitial H+ and K+ concentrations were measured with the microdialysis technique. Citrate ingestion reduced the plasma H......+ concentration and increased the plasma HCO3- concentration. Citrate had no effect on interstitial H+ at rest. The increase in interstitial H+ concentration during intense exercise was significantly lower (P citrate ingestion compared to control (peak interstitial H+ concentration 79 versus 131 n...

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

    DEFF Research Database (Denmark)

    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....

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

    DEFF Research Database (Denmark)

    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...

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

    DEFF Research Database (Denmark)

    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...

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

    Energy Technology Data Exchange (ETDEWEB)

    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.

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

    NARCIS (Netherlands)

    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

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

    Directory of Open Access Journals (Sweden)

    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.

  5. D(—–Lactic Acid Producing Probiotics, D(—–Lactic Acidosis and Infants

    Directory of Open Access Journals (Sweden)

    David R Mack

    2004-01-01

    Full Text Available There is mounting evidence that ingestion of selected probiotics can modify disease morbidity for specific conditions affecting humans, and there is growing interest in the amelioration or prevention of disease with probiotics. Modulation in gene expression of the cellular elements of the intestinal mucosa and interbacterial interactions are leading theories as to the mechanism whereby probiotics can effect benefit for the host. Furthermore, gene-environmental interactions are considered to be important in the development of disease in those at genetic risk. With the intestinal tract harbouring large numbers of bacteria, alteration of the microbial environment with probiotic microbes is being considered as a controllable factor that may limit disease expression for those at genetic risk. This reasoning has led to interest in the administration of probiotics to infants. However, there are significant developmental changes occurring in many organ systems from the time of parturition and during the first months of life. Because there is little in the published scientific medical literature regarding the effects of long-term administration of probiotics to infants, potential problems must be considered; one such issue is that of administration of D(--lactate-producing probiotics. An appraisal of the current knowledge of this potential adverse effect is the subject of this communication.

  6. Elucidation of how cancer cells avoid acidosis through comparative transcriptomic data analysis.

    Directory of Open Access Journals (Sweden)

    Kun Xu

    Full Text Available The rapid growth of cancer cells fueled by glycolysis produces large amounts of protons in cancer cells, which tri mechanisms to transport them out, hence leading to increased acidity in their extracellular environments. It has been well established that the increased acidity will induce cell death of normal cells but not cancer cells. The main question we address here is: how cancer cells deal with the increased acidity to avoid the activation of apoptosis. We have carried out a comparative analysis of transcriptomic data of six solid cancer types, breast, colon, liver, two lung (adenocarcinoma, squamous cell carcinoma and prostate cancers, and proposed a model of how cancer cells utilize a few mechanisms to keep the protons outside of the cells. The model consists of a number of previously, well or partially, studied mechanisms for transporting out the excess protons, such as through the monocarboxylate transporters, V-ATPases, NHEs and the one facilitated by carbonic anhydrases. In addition we propose a new mechanism that neutralizes protons through the conversion of glutamate to γ-aminobutyrate, which consumes one proton per reaction. We hypothesize that these processes are regulated by cancer related conditions such as hypoxia and growth factors and by the pH levels, making these encoded processes not available to normal cells under acidic conditions.

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

    OpenAIRE

    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...

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

    Science.gov (United States)

    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

  9. Genetics Home Reference: pseudohypoaldosteronism type 2

    Science.gov (United States)

    ... 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 ...

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

    OpenAIRE

    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...

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

    OpenAIRE

    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...

  12. Use of an electronic medical record to detect patients at high risk of metformin-induced lactic acidosis.

    Science.gov (United States)

    Dunham, Daniel P; Baker, David

    2006-04-01

    The Notes section welcomes the following types of contributions: (1) practical innovations or solutions to everyday practice problems, (2) substantial updates or elaborations on work previously published by the same authors, (3) important confirmations of research findings previously published by others, and (4) short research reports, including practice surveys, of modest scope or interest. Notes should be submitted with AJHP's manuscript checklist. The text should be concise, and the number of references, tables, and figures should be limited. PMID:16554290

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

    OpenAIRE

    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...

  14. Effects of acidosis, alkalosis, hyperthermia and hypothermia on haemostasis : results of point of care testing with the thromboelastography analyser

    NARCIS (Netherlands)

    Ramaker, Albert J. D. W. R.; Meyer, Peter; van der Meer, Jan; Struys, Michel M. R. F.; Lisman, Ton; van Oeveren, Wim; Hendriks, Herman G. D.

    2009-01-01

    In this study we assessed the effects of changes in pH, temperature, and their combination in whole blood on thromboelastographic variables. Blood was collected from six healthy volunteers. Thromboelastograph (TEG series 5000; Haemoscope Corporation, Illinois, USA) channels were set at temperatures

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

    DEFF Research Database (Denmark)

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

    2014-01-01

    mesenteric (MA), middle cerebral (MCA), and left coronary arteries (LCA) of lean vs. obese rats and minipigs. Male Sprague Dawley rats were fed a high-fat (FAT; N=5), high-fructose (FRUC; N=7), high-fat/high-fructose (FAT/FRUC; N=7) or standard diet (STD; N=7-11) for 28 Weeks. FAT and FAT/FRUC became obese...... no transcriptional changes in FRUC. Castrated male Göttingen minipigs with or without diabetes were fed a diet rich in fat, cholesterol and fructose (OB+DIAB; N=3 vs. OB; N=2, respectively) or a standard diet (STD; N=3) for 22-45 weeks. Body weight, total body fat content and plasma triglyceride levels were...... increased in OB and OB+DIAB. BKca, IKca, SKca and/or LTCC mRNA was up-regulated in LCA from OB and OB+DIAB (n.s.). Expression of BKca mRNA was increased, whereas IKca mRNA decreased in MCA from OB (n.s.). SKca mRNA was decreased in MA from OB (n.s.). Diet-induced obesity in rats and minipigs lead to complex...

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

    Institute of Scientific and Technical Information of China (English)

    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.

  17. Genetics Home Reference: mitochondrial complex III deficiency

    Science.gov (United States)

    ... 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 ...

  18. A patient with acute liver failure and extreme hypoglycaemia with lactic acidosis who was not in coma : causes and consequences of lactate-protected hypoglycaemia

    NARCIS (Netherlands)

    Oldenbeuving, G.; McDonald, J. R.; Goodwin, M. L.; Sayilir, R.; Reijngoud, D. J.; Gladden, L. B.; Nijsten, M. W. N.

    2014-01-01

    Lactate can substitute for glucose as a metabolic substrate. We report a patient with acute liver failure who was awake despite a glucose level of 0.7 mmol/l with very high lactate level of 25 mmol/l. The hypoglycaemia+hyperlactataemia combination may be considered paradoxical since glucose is the m

  19. Fanconi Bickel Syndrome: Novel Mutations in GLUT 2 Gene Causing a Distinguished Form of Renal Tubular Acidosis in Two Unrelated Egyptian Families

    Directory of Open Access Journals (Sweden)

    Mohammad Al-Haggar

    2011-01-01

    Full Text Available Background. Fanconi-Bickel syndrome (FBS is an autosomal recessive disorder caused by defects in facilitative glucose transporter 2 (GLUT2 or SLC2A2 gene mapped on chromosome 3q26.1-26.3, that codes for the glucose transporter protein 2. Methods. Two unrelated Egyptian families having suspected cases of FBS were enrolled after taking a written informed consent; both had positive consanguinity, and index cases had evidences of proximal renal tubular defects with hepatomegaly; they were subjected to history taking, signs of rickets as well as anthropometric measurements. Laboratory workup included urinalysis, renal and liver function tests including fasting and postprandial blood sugar; serum calcium, phosphorus, alkaline phosphatase, sodium and potassium, lipid profile, and detailed blood gas. Imaging including bone survey and abdominal ultrasound, and liver biopsy were done to confirm diagnosis. Molecular analysis of the GLUT2 gene was done for DNA samples extracted from peripheral blood leukocyte. All coding sequences, including flanking introns in GLUT2 gene, were amplified using PCR followed by direct sequencing. Results. Two new mutations had been detected, one in each family, in exon 3 two bases (GA were deleted (c.253 254delGA and in exon 6 in the second family, G-to-C substitution at position-1 of the splicing acceptor site (c.776-1G>C or IVS5-1G>A. Conclusion. FBS is a rare disease due to mutation in GLUT2 gene; many mutations were reported, about half were novel mutations; yet none of these mutations is more frequent. A more extensive survey for the most frequent mutations among FBS has to be contemplated to allow for use of molecular screening tests like ARMS.

  20. Mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS) in a Donegal kindred--clinical features and molecular genetic analysis.

    Science.gov (United States)

    McEntagart, M; Droogan, O; Burke, M; Brett, F; Murphy, S; Farrell, M

    1997-01-01

    A 19 year old female with a background history of migraine, sensorineural deafness and recent personality change developed a parieto-occipital cerebral infarct. Investigations revealed altered lactate to pyruvate ratios, ragged red fibres in muscle and an A-G point mutation at position 3243 in mitochondrial DNA. Subsequent clinical and molecular genetic analysis of 14 family members in three generations identified 12 affected individuals, two of whom were asymptomatic. Maternal inheritance was confirmed. MEALS is an important but under recognised cause of stroke and seizures in the young. There is insufficient data available to determine if the treatment of asymptomatic individuals retards the onset or reduces the severity of stroke.

  1. Infantile diabetics presenting dehydration and acidosis%以脱水及酸中毒为首发表现的婴儿糖尿病

    Institute of Scientific and Technical Information of China (English)

    郭毅; 陈沫; 熊嗣玉

    2004-01-01

    婴幼儿胰岛素依赖型糖尿病临床并不少见,但我们收治的1例情况特殊.患儿父母同患甲状腺功能亢进症(甲亢),经放射免疫治疗后均发生甲状腺功能减退症(甲减),均以左甲状腺素维持治疗.并在治疗期间生育,患儿于1岁时发病。现报告如下:

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

    OpenAIRE

    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...

  3. MELAS 综合征的 MRI 诊断%The MRI findings of mitochondrial encephalomyopathy,lactic acidosis and stroke-like episodes

    Institute of Scientific and Technical Information of China (English)

    王柳仙; 席一斌; 田萍; 李陈; 印弘

    2016-01-01

    目的:回顾性分析线粒体脑肌病伴高乳酸血症和卒中样发作(MELAS)综合征的 MR 表现特点,提高对 MELAS 综合征早期诊断的能力。方法收集经临床诊断的 MELAS 综合征共16例,均由肌肉病理活检证实。所有患者均行 MR 平扫,其中3例行 ASL 扫描,15例行 MRA 检查,14例行 DWI 扫描,3例行 MRS 扫描,并回顾性综合分析其影像学资料。结果MRI 检查发现,本组 MELAS 综合征多表现为大脑半球各叶大小不等片状病灶,病变多位于大脑半球后部脑皮质区,向皮层下的白质蔓延,病灶的分布与脑血供分布不一致;自旋回波 T1 WI 呈低信号、T2 WI 呈高信号,FLAIR 呈高信号;DWI 呈高信号;3例行 MRS 分析提示病灶区典型乳酸峰;其中1例 MRA 检查提示病灶区分支血管增多,1例分支血管减少;3例行 ASL 检查提示病灶区高灌注。16例中4例随访病灶具有游走性、多变性、此起彼伏等表现,旧病灶有脑萎缩、脑软化等表现。16例行肌组织活检见破碎样红纤维(RRF);电镜见线粒体体积增大、数量增多,肌纤维粗细不等,少数萎缩变细。3例行线粒体基因测序发现线粒体 DNA(mtDNA)A3243G 点突变。结论DWI、MRS 及 ASL 在 MELAS 综合征诊断中具有良好的价值。%Objective To analyze retrospectively the MR features of MELAS patients,in order to improve the early diagnosis of MELAS.Methods MR data of 1 6 MELAS patients confirmed by clinical diagnose and muscle biopsy were retrospectively analyzed. MR features of plain scan(n=1 6),ASL(n=3),MRA(n=1 5),DWI(n=14)and MRS(n=3)were analyzed.Results MRI data demonstrated brain lesions mainly distributed in posterior cerebral hemisphere extending to subcortical area,which was not consistent with the vascular supply territories.The lesions were observed as low signal on Spin-echo sequence of T1 WI,while high signal on T2 WI, FLAIR and DWI.The focal lesions showed increasing Lac peak on MRS.Fifteen of 16 patients underwent MRA and one showed increased arterial branches in lesion zones.Three patients had ASL scanning demonstrating high irrigation in lesion zones which would wander once relapsed.Meanwhile,old lesions showed encephalatrophy and cerebromalacia.All patients’muscle biopsy pathology showed ragged red muscle fibers.Under electron-microscopic,bioblasts were bigger and more than average level and muscle fibers atrophied.Mitochondrial DNA sequence of 3 patients showed mtDNA A3243G transgenation.Conclusion The DWI,MRS and ASL sequences show good ability in MELAS diagnosis and differential diagnosis.

  4. Osteomalacia

    Science.gov (United States)

    ... 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 ...

  5. Lactic acid test

    Science.gov (United States)

    ... 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 ...

  6. Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia.

    NARCIS (Netherlands)

    Nizet, T.; Heijdra, Y.F.; Elshout, F.J.J. van den; Ven, M.J.T. van de; Bosch, F.H.; Mulder, P.H.M. de; Folgering, H.T.M.

    2009-01-01

    Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilator

  7. Disease: H00429 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available 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

  8. Genetics Home Reference: glutaric acidemia type II

    Science.gov (United States)

    ... 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 ...

  9. Short bowel syndrome

    Science.gov (United States)

    ... 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 ...

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

    Science.gov (United States)

    ... 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. ...

  11. Potassium test

    Science.gov (United States)

    ... 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 ...

  12. Genetics Home Reference: glutathione synthetase deficiency

    Science.gov (United States)

    ... 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. ...

  13. Interstitial nephritis

    Science.gov (United States)

    ... 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/ ...

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

    Science.gov (United States)

    ... 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 ...

  15. Chloride Test

    Science.gov (United States)

    ... 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 ). ...

  16. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  17. 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.

    Science.gov (United States)

    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

  18. 大鼠细动脉平滑肌细胞内酸中毒对ATP敏感钾通道的影响%Effect of intracellular acidosis on ATP-sensitive K+ channels in arteriolar smooth muscle cells

    Institute of Scientific and Technical Information of China (English)

    刘杰; 赵克森; 金春华

    1999-01-01

    目的:研究细胞内酸中毒对细动脉平滑肌细胞膜KATP通道的影响.方法:应用膜片钳技术的内面向外式记录酶性分离的细动脉平滑肌上KATP通道.结果:当细胞内无ATP时,细胞内酸中毒降低通道电导,通道平均开放时间(Tom)和开放时间长成分有所增大,对通道开放概率无明显影响;当细胞内有ATP时,细胞内酸中毒使通道电导增大,通道开放概率增加.结论:平滑肌细胞内酸中毒减弱ATP对KATP通道的抑制作用,并能在ATP存在条件下激活KATP通道,是酸中毒降低血管平滑肌反应性的重要机制之一.

  19. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  20. 肺心病呼吸性酸中毒合并代谢性碱中毒52例临床分析%The lung worry breath acidosis combines clinical supersession nature alkalosis 52 examples analysis

    Institute of Scientific and Technical Information of China (English)

    孟晓皓

    2009-01-01

    目的:对肺心病急性发作期呼吸性酸中毒合并代谢性碱中毒患者的诊断及治疗进行探讨.方法:对52例肺心病急性发作期呼吸性酸中毒合并代谢性碱中毒患者的血气分析及电解质进行调查,并查找诱发因素.结果:因为不适当应用利尿剂24例,糖皮质激素18例,应用碱性药物1例,呼吸兴奋剂3例,呼吸机治疗1例,呕吐4例,呕血3例,有两种以上诱因8例,死亡3例.结论:呼吸性酸中毒合并代谢性碱中毒对肺心病患者极为不利,临床要重视该酸碱平衡紊乱.

  1. 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

    Institute of Scientific and Technical Information of China (English)

    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].

  2. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  3. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  4. 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

    OpenAIRE

    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...

  5. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  6. Acid-Base and the Skeleton

    Science.gov (United States)

    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.

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

    Science.gov (United States)

    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

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

    OpenAIRE

    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...

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

    Directory of Open Access Journals (Sweden)

    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

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

    Science.gov (United States)

    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

  11. Optic nerve pH and PO2

    DEFF Research Database (Denmark)

    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...

  12. Hyperchloremische metabole acidose bij een patiënt met een brickerlis

    NARCIS (Netherlands)

    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

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

    DEFF Research Database (Denmark)

    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....

  14. Svaer metabolisk acidose hos en kronisk alkoholiker

    DEFF Research Database (Denmark)

    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....

  15. 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

    DEFF Research Database (Denmark)

    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)...

  16. Disease: H01347 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available H01347 MELAS Syndrome; Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, Stroke-like episo...des MELAS Syndrome (Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes) i...oga Y, Povalko N, Nishioka J, Katayama K, Kakimoto N, Matsuishi T MELAS and L-arginine therapy: pathophysiology of stroke-like episo

  17. Behandling af metforminassocieret laktatacidose med hæmodialyse

    DEFF Research Database (Denmark)

    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...

  18. 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

    OpenAIRE

    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...

  19. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  20. 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

    Institute of Scientific and Technical Information of China (English)

    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.

  1. 线粒体脑肌病伴高乳酸血症和卒中样发作综合征的临床诊断治疗再认识%Rethinking of clinical diagnosis and management in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes syndrome

    Institute of Scientific and Technical Information of China (English)

    沈定国

    2011-01-01

    @@ 线粒体脑肌病伴高乳酸血症和卒中样发作(MELAS)综合征为最常见的一类以综合征表现的线粒体疾病,是因mtDNA及核DNA基因突变,导致蛋白合成障碍引起的多器官、多组织的进行性变性疾病,临床表现为卒中样发作(stmke-like episodes,SLEs)、脑病、肌病、乳酸性酸中毒及耳、眼、心、肾、胃肠道、内分泌等多系统损害[1-4].

  2. Clinical, imaging and pathology features of mitochondrial encephalopathy with 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的临床、影像学及病理学特点

    Institute of Scientific and Technical Information of China (English)

    谢成娟; 汪凯

    2014-01-01

    目的 探讨线粒体脑肌病伴高乳酸血症和脑卒中样发作(MELAS)综合征的临床、影像及病理学特点.方法 回顾性分析7例MELAS综合征患者的临床资料.结果 本组患者中,男1例,女6例,平均年龄21.3岁;均为卒中样起病伴癫痫发作,其中视力减退6例,运动后乏力5例,认知功能障碍2例,精神异常1例.头颅MRI检查示顶、枕叶和(或)颞叶T1WI/T2 WI长或稍长信号及Flair高信号病灶,呈脑回样改变,均未见强化.4例患者肌肉活检发现有肌纤维变性,横纹消失或断裂,肌膜下出现不规则的不整红边纤维(RRF).2例行基因检测发现有mtDNA A3243G位点突变.结论 MELAS综合征好发于青少年,以卒中样起病伴癫痫发作,可有视听力减退以及认知功能障碍等;影像学特征为病变主要累及双侧大脑半球后部皮质,呈脑回样改变;肌肉活检发现RRF.

  3. Clinical Characteristics of children with syndrome of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode%儿童线粒体脑肌病伴乳酸酸中毒和卒中样发作的临床特征

    Institute of Scientific and Technical Information of China (English)

    马秀伟; 侯豫; 王三梅; 辜蕊洁; 刘京京; 王永霞; 封志纯

    2015-01-01

    目的 总结儿童线粒体脑肌病伴乳酸酸中毒和卒中样发作(MELAS)的临床、影像学及分子遗传学特征,以提高诊疗水平.方法 对7例经基因突变或线粒体呼吸链酶学确诊的MELAS患儿的临床表现及实验室检查、影像学资料、基因突变、酶学特点进行回顾性分析,并对临床转归进行随访.结果 所有患儿均有卒中样发作、头痛、呕吐、惊厥.7例患儿均有乳酸升高.头颅MRI均显示T1WI低信号及T2WI高信号,常多个脑叶同时受累,容易受累部位主要为顶叶、颞叶和枕叶,额叶、基底节区、小脑及丘脑亦可受累.陈旧病灶均呈脑萎缩.4例白细胞线粒体DNA有A3243G突变,突变率为29.7%~60%,其中l例母亲存在同样突变.3例行线粒体呼吸链酶学检测,2例显示复合物Ⅰ缺陷,1例显示复合物Ⅰ、Ⅳ缺陷.随访7例,均有不同程度智力损害,并仍需继续服用抗癫痫药物.结论 充分认识儿童MELAS的临床、实验室检查、头颅影像、基因突变、呼吸链酶学特点,有助于早期诊断、治疗和遗传咨询.

  4. Warburg′s effect on solid tumors

    Directory of Open Access Journals (Sweden)

    Talal El Imad

    2014-01-01

    Full Text Available Lactic acidosis is the result of imbalance between the systemic formation of lactate and its hepatic metabolism. In cancer patients, lactic acidosis is mainly associated with hematologic malignancies (leukemia and lymphomas and the mechanism is known as Warburg′s effect. We report a 76-year-old male known to have hypertension and coronary artery disease, who presented with abdominal distension and lactic acidosis. His initial evaluation showed multiple liver masses that were biopsied and the patient was diagnosed with undifferentiated carcinoma of unknown primary, involving the liver. The patient had progression of lactic acidosis leading to his death on day-15. As the lactic acidosis was not in the setting of hypoxia or hemodynamic instability, we made the diagnosis of malignancy-associated type B lactic acidosis, also known as the Warburg′s effect. Warburg′s effect can occur in solid cancer if the tumor involves the liver. It has bad prognostic implications. The use of intravenous bicarbonate as a temporary measure is of controversial benefit, as it can potentially worsen the metabolic acidosis and its use should be limited to patients with very low pH. In cancer patients, the use of lactatebased intravenous fluids can be potentially harmful and can increase the risk of tumor metastasis, at least in animal malignancy models.

  5. Atypical MR lenticular signal change in infantile isovaleric acidemia.

    Science.gov (United States)

    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

  6. Hipoglicemia neonatal: Un caso de galactosemia

    OpenAIRE

    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

  7. Mucormycosis

    Science.gov (United States)

    ... 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 ...

  8. Ribosome profiling reveals features of normal and disease-associated mitochondrial translation

    NARCIS (Netherlands)

    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

  9. 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

    OpenAIRE

    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

  10. Ethylene glycol poisoning

    Science.gov (United States)

    ... products, including: Antifreeze De-icing products Detergents Paints Cosmetics Note: This list may not be all-inclusive ... vein (IV) to reverse severe acidosis Antidotes that slow the formation of the poisonous by-products in ...

  11. Citric acid urine test

    Science.gov (United States)

    ... 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

  12. The intracellular to extracellular proton gradient following maximal whole body exercise and its implication for anaerobic energy production

    DEFF Research Database (Denmark)

    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....

  13. Macular pattern dystrophy and homonymous hemianopia in MELAS syndrome.

    Science.gov (United States)

    Kamal-Salah, Radua; Baquero-Aranda, Isabel; Grana-Pérez, María Del Mar; García-Campos, Jose Manuel

    2015-03-12

    We report an unusual association of a pattern dystrophy of the retinal pigment epithelium and homonymous hemianopia in a woman diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes syndrome.

  14. Disease: H00473 [KEGG MEDICUS

    Lifescience Database Archive (English)

    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

  15. A60

    Directory of Open Access Journals (Sweden)

    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.

  16. Hashimoto Thyroiditis and Nephrocalcinosis in a Child with Down Syndrome

    OpenAIRE

    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 ...

  17. Hyperkalaemic quadriparesis secondary to chronic diclofenac treatment

    OpenAIRE

    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 ...

  18. Ocular and skin manifestations in systemic pseudohypoaldosteronism

    OpenAIRE

    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...

  19. Hyperkalaemia induced by carbonic anhydrase inhibitor.

    OpenAIRE

    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...

  20. Hjertestopbehandling. Nyere aspekter af kardiopulmonal genoplivning

    DEFF Research Database (Denmark)

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

    1989-01-01

    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...... effects from calcium-entry blockers. Ischaemia and, in particular, reperfusion release cell and vessel damaging free oxygen redicals. Intensive investigations are being conducted at present about the value of anti-oxidants for cerebral and myocardial protection....

  1. The Effect of CO2-Pneumoperitoneum on Ventilation Perfusion Distribution of the Lung

    OpenAIRE

    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...

  2. Predictive Value of Capnography for Suspected Diabetic Ketoacidosis in the Emergency Department

    OpenAIRE

    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) ...

  3. Acute barium intoxication following ingestion of soap water solution

    Directory of Open Access Journals (Sweden)

    Nandita Joshi

    2012-01-01

    Full Text Available We present a rare case in which a young girl ingested a solution of a hair-removing soap. The ingestion resulted in profound hypokalemia and severe acidosis leading to flaccid paralysis, respiratory arrest and ventricular arrhythmias. Ultimately the patient made complete recovery. The soapwas found to contain barium sulfide. The degree of paralysis and acidosis appeared to be directly related to serum potassium levels.

  4. Renal ammonia excretion in response to hypokalemia: effect of collecting duct-specific Rh C glycoprotein deletion

    OpenAIRE

    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...

  5. Disease: H00428 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available ne, env_factor, marker) Rodriguez Soriano J Renal tubular acidosis: the clinical ...) PMID:11045400 (gene) Rodriguez-Soriano J New insights into the pathogenesis of ...a DM, Oliveira EA, Silva AC Molecular pathophysiology of renal tubular acidosis. Curr Genomics 10:51-9 (2009...1 (gene) Fry AC, Karet FE Inherited renal acidoses. Physiology (Bethesda) 22:202-11 (2007) PMID:12138150 (ge

  6. 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

    OpenAIRE

    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...

  7. Identification of peripartum near-miss for perinatal audit

    OpenAIRE

    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...

  8. Bone Disease in Medullary Sponge Kidney and Effect of Potassium Citrate Treatment

    OpenAIRE

    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...

  9. Simple Diagnostic Tests to Detect Toxic Alcohol Intoxications

    OpenAIRE

    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...

  10. Extracellular proton depression of peak and late Na+ current in the canine left ventricle

    OpenAIRE

    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...

  11. A Rare Side Effect of Metformin: Metformin-Induced Hepatotoxicity

    OpenAIRE

    AKSAY, Ersin

    2007-01-01

    Metformin is an oral hypoglycemic agent that is commonly used in the treatment of type 2 diabetes mellitus. While metformin-associated metabolic acidosis is a widely recognized side effect of this drug, metformin-induced hepatotoxicity has been rarely reported in the literature. We present herein the case of a 52-year-old male in whom metformin-associated lactic acidosis and metformin-induced hepatotoxicity developed.

  12. Brinzolamide-induced retinopathy in neonatal rats: an alternative animal model of retinal neovascularization

    OpenAIRE

    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...

  13. Acute cyanide Intoxication: A rare case of survival

    OpenAIRE

    Durga Jethava; Priyamvada Gupta; Sandeep Kothari; Puneet Rijhwani; Ankit Kumar

    2014-01-01

    A 30-year-old male jewellery factory worker accidentally ingested silver potassium cyanide and was brought to the emergency department in a state of shock and profound metabolic acidosis. This patient was managed hypothetically with use of injection thiopentone sodium intravenously until the antidote was received. Cyanide is a highly cytotoxic poison and it rapidly reacts with the trivalent iron of cytochrome oxidase thus paralysing the aerobic respiration. The result is severe lactic acidosi...

  14. Interpreting the Consequences of Metformin Accumulation in an Emergency Context: Impact of the Time Frame on the Blood Metformin Levels

    Directory of Open Access Journals (Sweden)

    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.

  15. Acidic environment leads to ROS-induced MAPK signaling in cancer cells.

    Directory of Open Access Journals (Sweden)

    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.

  16. Con: Higher serum bicarbonate in dialysis patients is protective.

    Science.gov (United States)

    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

  17. A Case Report of Inflammatory Myopathy and Sideroblastic Anemia

    Directory of Open Access Journals (Sweden)

    F Binesh

    2007-01-01

    Full Text Available Mitochondrial myopathy, lactic acidosis, and siderobastic anemia (MLA SA syndrome is one of the newly reported mitochondrial diseases, seven cases of which have been reported. We report a child with inflammatory myopathy, sideroblastic anemia and lactic acidosis .The patient is a 8.5 year old boy with normal cognitive function suffering from chronic progressive weakness in lower extremities, inability to walk since four months and pallor. In paraclinical evaluation, sideroblastic anemia, mild lactic acidosis and elevated muscle enzymes were seen. Inflammatory myopathy (myositis in muscle biopsy was detected as well .The patient was administered oral prednisolone, folic acid, B6 and underwent regular physiotherapy. He ambulated after four months and resumed education and schooling.

  18. Carbon dioxide in the critically ill: too much or too little of a good thing?

    Science.gov (United States)

    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

  19. Propylene Glycol Poisoning From Excess Whiskey Ingestion

    Science.gov (United States)

    Ku, Kevin; Sue, Gloria R.

    2015-01-01

    In this report, we describe a case of high anion gap metabolic acidosis with a significant osmolal gap attributed to the ingestion of liquor containing propylene glycol. Recently, several reports have characterized severe lactic acidosis occurring in the setting of iatrogenic unintentional overdosing of medications that use propylene glycol as a diluent, including lorazepam and diazepam. To date, no studies have explored potential effects of excess propylene glycol in the setting of alcohol intoxication. Our patient endorsed drinking large volumes of cinnamon flavored whiskey, which was likely Fireball Cinnamon Whisky. To our knowledge, this is the first case of propylene glycol toxicity from an intentional ingestion of liquor containing propylene glycol. PMID:26904700

  20. Optic nerve pH and PO2

    DEFF Research Database (Denmark)

    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. Rickets-vitamin D deficiency and dependency

    Directory of Open Access Journals (Sweden)

    Manisha Sahay

    2012-01-01

    Full Text Available Rickets is an important problem even in countries with adequate sun exposure. The causes of rickets/osteomalacia are varied and include nutritional deficiency, especially poor dietary intake of vitamin D and calcium. Non-nutritional causes include hypophosphatemic rickets primarily due to renal phosphate losses and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism. Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

  2. Renal acidification defects in medullary sponge kidney

    DEFF Research Database (Denmark)

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

    1988-01-01

    Thirteen patients with medullary sponge kidney underwent a short ammonium chloride loading test to investigate their renal acidification capacity. All but 1 presented with a history of recurrent renal calculi and showed bilateral widespread renal medullary calcification on X-ray examination. Nine...... patients had some form of renal acidification defect; 8 had the distal type of renal tubular acidosis, 2 the complete and 6 the incomplete form. One patient had proximal renal tubular acidosis. These findings, which suggest that renal acidification defects play an important role in the pathogenesis...... of renal calculi in medullary sponge kidney, have considerable therapeutic implications....

  3. Cetoacidosis alcohólica y complicaciones neurológicas reversibles de la hipofosfatemia Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia

    Directory of Open Access Journals (Sweden)

    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

  4. Metabolic studies of transient tyrosinemia in premature infants

    Science.gov (United States)

    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.

  5. quadriparesis in sjogren syndrome.

    Directory of Open Access Journals (Sweden)

    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

  6. Nutritional Strategies to Modulate Intracellular and Extracellular Buffering Capacity During High-Intensity Exercise

    OpenAIRE

    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...

  7. Differential uptake of Tc-99m DMSA and Tc-99m EC in renal tubular disorders: Report of two cases and review of the literature

    International Nuclear Information System (INIS)

    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

  8. MLASA SYNDROME: A CASE REPORT

    Directory of Open Access Journals (Sweden)

    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.

  9. MELAS syndrome presenting as an acute surgical abdomen.

    Science.gov (United States)

    Dindyal, S; Mistry, K; Angamuthu, N; Smith, G; Hilton, D; Arumugam, P; Mathew, J

    2014-01-01

    MELAS (mitochondrial cytopathy, encephalomyopathy, lactic acidosis and stroke-like episodes) is a syndrome in which signs and symptoms of gastrointestinal disease are uncommon if not rare. We describe the case of a young woman who presented as an acute surgical emergency, diagnosed as toxic megacolon necessitating an emergency total colectomy. MELAS syndrome was suspected postoperatively owing to persistent lactic acidosis and neurological symptoms. The diagnosis was later confirmed with histological and genetic studies. This case highlights the difficulties in diagnosing MELAS because of its unpredictable presentation and clinical course. We therefore recommend a high index of suspicion in cases of an acute surgical abdomen with additional neurological features or raised lactate.

  10. Metformin poisoning: which therapy?

    Directory of Open Access Journals (Sweden)

    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.

  11. Succinyl-CoA Ligase Deficiency: A Mitochondrial Hepatoencephalomyopathy

    NARCIS (Netherlands)

    J.L.K. van Hove; M.S. Saenz; J.A. Thomas; R.C. Gallagher; M.A. Lovell; L.Z. Fenton; S. Shanske; S.M. Myers; R.J.A. Wanders; J. Ruiter; M. Turkenburg; H.R. Waterham

    2010-01-01

    This patient presented on the first day of life with pronounced lactic acidosis with an elevated lactate/pyruvate ratio. Urine organic acids showed Krebs cycle metabolites and mildly elevated methylmalonate and methylcitrate. The acylcarnitine profile showed elevated propionylcarnitine and succinylc

  12. Clinical Manifestation and a New "ISCU" Mutation in Iron-Sulphur Cluster Deficiency Myopathy

    Science.gov (United States)

    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…

  13. Resuscitation og abdominalkirurgiske aspekter ved damage control-kirurgi

    DEFF Research Database (Denmark)

    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 "bloo...

  14. Dietary acid load and risk of hypertension : the Rotterdam Study

    NARCIS (Netherlands)

    Engberink, Marielle F.; Bakker, Stephan J. L.; Brink, Elizabeth J.; van Baak, Marleen A.; van Rooij, Frank J. A.; Hofman, Albert; Witteman, Jacqueline C. M.; Geleijnse, Johanna 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

  15. Dietary acid load and risk of hypertension: The Rotterdam study

    NARCIS (Netherlands)

    M.F. Engberink (Marielle); S.J.L. Bakker (Stephan); E.J. Brink (Elizabeth); M.A. van Baak (Marleen); F.J.A. van Rooij (Frank); A. Hofman (Albert); J.C.M. Witteman (Jacqueline); J.M. Geleijnse (Marianne)

    2012-01-01

    textabstractBackground: 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: Th

  16. Dietary acid load and risk of hypertension: The Rotterdam study

    NARCIS (Netherlands)

    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

  17. Dietary acid load and risk of hypertension: The Rotterdam Study

    NARCIS (Netherlands)

    Engberink, M.F.; Bakker, S.J.L.; Brink, E.J.; Baak, van M.A.; Rooij, van F.J.A.; 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). Design: The analyses included 2241 participants aged =55 y who were free of hypertension at baseline (1990–1993) and who had complete dietary and BP data. Dietary data were obtained from a 1

  18. "Herbal remedy is natural and safe"--truth or myth?

    Science.gov (United States)

    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

  19. A dynamic mechanistic model of lactic acid metabolism in the rumen

    NARCIS (Netherlands)

    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

  20. Refractory rickets in the tropics.

    Science.gov (United States)

    Sahay, M; Sahay, R K

    2010-06-01

    Rickets is an important problem in children. The majority of rickets in children is due to deficiency of calcium, phosphorus or vitamin D. However, rickets may also be a feature of renal diseases, e.g. renal tubular acidosis, hypophosphatemic rickets or rickets associated with renal insufficiency. The treatment varies with etiology and hence complete workup is essential before initiating therapy.

  1. Renal failure

    Institute of Scientific and Technical Information of China (English)

    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.

  2. Hemlock water dropwort poisoning.

    OpenAIRE

    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.

  3. Evaluation of electrolyte imbalance among tuberculosis patients receiving treatments in Southwestern Nigeria

    Directory of Open Access Journals (Sweden)

    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.

  4. Malignant Hyperthermia in Dental and Facial Plastic surgeries

    OpenAIRE

    Ramin Maheri; Samad EJ Golzari; Reza Rikhtegar

    2015-01-01

    Preoperative evaluation of the patients scheduled for ambulatory surgery is of great importance in regards of both surgery and anesthesia considerations. Malignant Hyperthermia (MH) is a pharmacogenetic clinical syndrome which mostly arises from volatile anesthesia with halothane and the depolarizing muscle relaxant succinylcholine. Clinical manifestations of MH are acidosis and rhabdomyolysis which occur following uncontrolled increases in skeletal muscle metabolism and rapidly increasing bo...

  5. Experiment list: SRX100917 [Chip-atlas[Archive

    Lifescience Database Archive (English)

    Full Text Available karyotype=cancer || cell lineage=ectoderm || cell sex=F || treatment=Hypoxia_LacAcid || treatment description=Hypoxia and Lactic aci...dosis: 1% p02 and 10 mM Lactate, pH of 6.7 for 24 hours (Crawford) || labversion=al

  6. Hipoglicemia neonatal: Un caso de galactosemia

    Directory of Open Access Journals (Sweden)

    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

  7. Association between serum bicarbonate and pH with depression, cognition and sleep quality in hemodialysis patients.

    Science.gov (United States)

    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.

  8. Association between serum bicarbonate and pH with depression, cognition and sleep quality in hemodialysis patients.

    Science.gov (United States)

    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

  9. Association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers

    DEFF Research Database (Denmark)

    Arngrim, Nanna; Schytz, Henrik Winther; Asghar, Mohammad Sohail;

    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...

  10. NUTRITION AND HEALTH OF HIGH-PRODUCTIVE COWS Питание и здоровье высокопродуктивных коров

    Directory of Open Access Journals (Sweden)

    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

  11. 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

    Directory of Open Access Journals (Sweden)

    Ryadchikov V. G.

    2012-05-01

    Full Text Available 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

  12. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI

    International Nuclear Information System (INIS)

    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.)

  13. Succinyl-CoA:acetoacetate transferase deficiency : identification of a new patient with a neonatal onset and review of the literature

    NARCIS (Netherlands)

    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,

  14. Succinyl-CoA : acetoacetate transferase deficiency: identification of a new patient with a neonatal onset and review of the literature

    NARCIS (Netherlands)

    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

  15. Bicarbonate correction of ketoacidosis alters host-pathogen interactions and alleviates mucormycosis.

    Science.gov (United States)

    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

  16. Effects of rapid versus slow infusion of sodium bicarbonate on cerebral hemodynamics and oxygenation in preterm infants.

    NARCIS (Netherlands)

    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

  17. A Fatal, Systemic Mitochondrial Disease with Decreased Mitochondrial Enzyme Activities, Abnormal Ultrastructure of the Mitochondria and Deficiency of Heat Shock Protein 60

    NARCIS (Netherlands)

    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

  18. Acute esophageal necrosis caused by alcohol abuse

    Institute of Scientific and Technical Information of China (English)

    Tetsu Endo; Juichi Sakamoto; Ken Sato; Miyako Takimoto; Koji Shimaya; Tatsuya Mikami; Akihiro Munakata; Tadashi Shimoyama; Shinsaku Fukuda

    2005-01-01

    Acute esophageal necrosis (AEN) is extremely rare and the pathogenesis of this is still unknown. We report a case of AEN caused by alcohol abuse. In our case, the main pathogenesis could be accounted for low systemic perfusion caused by severe alcoholic lactic acidosis. After the healing of AEN, balloon dilatation was effective to manage the stricture.

  19. Milk production is unaffected by replacing barley or sodium hydroxide wheat with maize cob silage in rations for dairy cows

    DEFF Research Database (Denmark)

    Hymøller, Lone; Hellwing, Anne Louise Frydendahl; Lund, Peter;

    2014-01-01

    in the energy metabolism of dairy cows but are also the main cause of ruminal acidosis and depressed feed intake. The aim of the present study was to compare maize cob silage (MCS) as an energy supplement in rations for dairy cows with highly rumen-digestible rolled barley and with sodium hydroxide wheat (SHW...

  20. Diabetic Ketoacidosis in a Patient with Type 2 Diabetes After Initiation of Sodium-Glucose Cotransporter 2 Inhibitor Treatment

    DEFF Research Database (Denmark)

    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...

  1. Sammenligning af profylaktisk ephedrin- og profylaktisk phenylephrininfusion ved spinal anaestesi til kejsersnit

    DEFF Research Database (Denmark)

    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...

  2. Disease: H00241 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available nherited renal acidoses. Physiology (Bethesda) 22:202-11 (2007) PMID:12138150 (gene, env_factor, marker) Rodriguez...0 PMID:11045400 (gene) Rodriguez-Soriano J New insights into the pathogenesis of renal tubular acidosis--fro...um supplement Sodium bicarbonate [D01203] ICD-10: N25.8 MeSH: D000141 OMIM: 25973

  3. Disease: H00243 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available iology of renal tubular acidosis. Curr Genomics 10:51-9 (2009) PMID:11045400 (gene) Rodriguez-Soriano J New ...rol 14:1121-36 (2000) PMID:12138150 (gene, env_factor, marker, drug) Rodriguez Soriano J Renal tubular acido

  4. Macromolecule absorption and cortisol secretion in newborn calves derived from in vitro produced embryos

    DEFF Research Database (Denmark)

    Jacobsen, H; Sangild, P T; Schmidt, M;

    2002-01-01

    an altered macromolecule absorption (immunoglobulin G (IgG) and porcine serum albumin (PSA)) compared with AI calves and whether the macromolecule absorption could be related to the degree of acidosis or to the cortisol secretion around birth. Hence, IgG and PSA absorption in control AI calves (n=7...

  5. Effect of urinary pH on the progression of urinary bladder tumours

    NARCIS (Netherlands)

    Lina, B.A.R.; Garderen-Hoetmer, A. van

    1999-01-01

    Systemic alkalosis has been postulated to enhance tumorigenesis, whereas systemic acidosis has been implicated to exert a favourable influence on tumour control and regression. In the present study the urinary pH was influenced by feeding acid-forming or base-forming diets, and the effect of alkalin

  6. A cow-level association of ruminal pH on body condition score, serum beta-hydroxybutyrate and postpartum disorders in Thai dairy cattle

    NARCIS (Netherlands)

    Inchaisri, C.; Chanpongsang, S.; Noordhuizen, J.; Hogeveen, H.

    2014-01-01

    Subacute ruminal acidosis in dairy cows occurs when ruminal pH is below about 5.5. However, the exact threshold level of ruminal pH affecting cow health is still in debate. This investigation was carried out in 505 cows within 31 farms. The postpartum disorders, including dystocia, retained placenta

  7. No effect of bicarbonate treatment on insulin sensitivity and glucose control in non-diabetic older adults

    Science.gov (United States)

    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...

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

    NARCIS (Netherlands)

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

    2001-01-01

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

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

    NARCIS (Netherlands)

    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

  10. Enfermedad de Von Gierke: Reporte de tres casos

    Directory of Open Access Journals (Sweden)

    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.

  11. Two cases of infectious purpura fulminans and septic shock caused by Capnocytophaga canimorsus transmitted from dogs

    DEFF Research Database (Denmark)

    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...

  12. Is Lactate Production Related to Muscular Fatigue? A Pedagogical Proposition Using Empirical Facts

    Science.gov (United States)

    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…

  13. Preoperative prognostic factors for mortality in peptic ulcer perforation: a systematic review

    DEFF Research Database (Denmark)

    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...

  14. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI

    Energy Technology Data Exchange (ETDEWEB)

    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.

  15. Metformin treatment is associated with a low risk of mortality in diabetic patients with heart failure: a retrospective nationwide cohort study

    DEFF Research Database (Denmark)

    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...

  16. Short-term starvation with a near-fatal asthma attack induced ketoacidosis in a nondiabetic pregnant woman: A case report.

    Science.gov (United States)

    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

  17. Incidence and Risk Factors for Delirium among Mechanically Ventilated Patients in an African Intensive Care Setting: An Observational Multicenter Study

    Directory of Open Access Journals (Sweden)

    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.

  18. Metformin in chronic kidney disease

    DEFF Research Database (Denmark)

    Heaf, James

    2014-01-01

    Metformin has traditionally been regarded as contraindicated in chronic kidney disease (CKD), though guidelines in recent years have been relaxed to permit therapy if the glomerular filtration rate (GFR) is > 30 mL/min. The main problem is the perceived risk of lactic acidosis (LA). Epidemiological...

  19. Infants with FPIES to solid food proteins--chicken, rice and oats.

    Science.gov (United States)

    Cunningham, K; Scanlan, B; Coghlan, D; Quinn, S

    2014-05-01

    We present two cases of Food Protein Induced Enterocolitis Syndrome (FPIES), a non-IgE mediated food hypersensitivity. FPIES induces severe vomiting 1.5-to-3 hours post ingestion of the offending food, and may be associated with diarrhoea, hypovolemic shock and acidosis. Avoidance of that food will lead to resolution of symptoms and prevents further episodes.

  20. 75 FR 32184 - Government-Owned Inventions; Availability for Licensing

    Science.gov (United States)

    2010-06-07

    ... acidosis and stroke-like episodes), NARP (Neuropathy ataxia, retinitis pigmentosa), and LHON (Leber hereditary optic neuropathy) by increasing PINK1 or Parkin expression or activity, as well as methods of... inventions listed below are owned by an agency of the U.S. Government and are available for licensing in...

  1. Cyclic vomiting syndrome masking a fatal metabolic disease.

    LENUS (Irish Health Repository)

    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.

  2. Heliox reduces respiratory system resistance in respiratory syncytial virus induced respiratory failure

    NARCIS (Netherlands)

    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

  3. A Rare Case of β-Ketothiolase Deficiency

    Directory of Open Access Journals (Sweden)

    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.

  4. Mitochondrial DNA m.3242G > A mutation, an under diagnosed cause of hypertrophic cardiomyopathy and renal tubular dysfunction?

    NARCIS (Netherlands)

    Wortmann, S.B.; Champion, M.P.; Heuvel, L.P. van den; Barth, H.; Trutnau, B.; Craig, K.; Lammens, M.M.; Schreuder, M.F.; Taylor, R.W.; Smeitink, J.A.M.; Wevers, R.A.; Rodenburg, R.J.T.; Morava, E.

    2012-01-01

    We present two new patients with the recently described mitochondrial m.3242G > A mutation. Although the mutation is situated next to the well known m.3243A > G mutation, the most common alteration associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode

  5. Early cardiac involvement in children carrying the A3243G mtDNA mutation.

    NARCIS (Netherlands)

    Wortmann, S.B.; Rodenburg, R.J.T.; Backx, A.P.C.M.; Schmitt, E.; Smeitink, J.A.M.; Morava, E.

    2007-01-01

    The phenotypic spectrum of the mitochondrial A3243G DKA mutation is highly variable, particularly when occuring in childhood. In contrast to the classical presentation in adulthood (MELAS syndrome; mitochondria! myopathy, encephalopathy, lactic acidosis and stroke-like episodes) children show a diff

  6. 1 case report of MELAS syndrome%MELAS综合征1例

    Institute of Scientific and Technical Information of China (English)

    裘五四

    2004-01-01

    MELAS(Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes)综合征,即线粒体脑肌病伴乳酸血症和卒中样发作,临床比较少见,本文l例,经肌活检及电镜证实,现报道如下。

  7. The mitochondrial 13513G > A mutation is most frequent in Leigh syndrome combined with reduced complex I activity, optic atrophy and/or Wolff-Parkinson-White.

    NARCIS (Netherlands)

    Ruiter, E.M.; Siers, M.H.; Elzen, C. van der; Engelen, B.G.M. van; Smeitink, J.A.M.; Rodenburg, R.J.T.; Hol, F.A.

    2007-01-01

    The m.13513G > A transition in the mitochondrial gene encoding the ND5 subunit of respiratory chain complex I, can cause mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and has been reported to be a frequent cause of Leigh syndrome (LS). We determined the fre

  8. Metformin-associated risk of acute dialysis in patients with type 2 diabetes

    DEFF Research Database (Denmark)

    Carlson, Nicholas; Hommel, Kristine; Olesen, Jonas Bjerring;

    2016-01-01

    Recent guidelines governing anti-diabetic medications increasingly advocate metformin as first-line therapy in all patients with type 2 diabetes. However, metformin could be associated with increased risk of acute kidney injury (AKI), acute dialysis, and lactate acidosis in marginal patients. In ...

  9. Short-term starvation with a near-fatal asthma attack induced ketoacidosis in a nondiabetic pregnant woman

    Science.gov (United States)

    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

  10. Tissue pH in cold-stored human donor livers preserved in University of Wisconsin solution - A noninvasive clinical study with P-31-magnetic resonance spectroscopy

    NARCIS (Netherlands)

    Wolf, RFE; vanderHoeven, JAB; Kamman, RL; Busza, AL; Ploeg, RJ; Sluiter, WJ; Slooff, MJH

    1996-01-01

    It is not known whether the tissue acidosis that accompanies cold storage is the beginning of irreversible cell injury, ultimately leading to cell death, or whether it is a natural ''protective'' mechanism for cells to survive hypoxic periods. To answer this question, the tissue pH of 45 cold-stored

  11. Laktatacidose ved behandling af type 2-diabetes med metformin

    DEFF Research Database (Denmark)

    Holst, Helle; Eldrup, Ebbe; Guldstad, Nana Harriet;

    2012-01-01

    Metformin (MET) is the first-line agent in treatment of type 2 diabetes. However, MET has been associated with lactic acidosis (MALA), a potential but rare complication which has influenced treatment strategies in decades. Recently, guidelines have been changed in regards of age and heart failure...

  12. [Hemolytic uremic syndrome. Clinical manifestations. Treatment].

    Science.gov (United States)

    Exeni, Ramón A

    2006-01-01

    Clinical manifestation are described in children with epidemic HUS. The intestinal involvement in the prodromic period, is outlined and the most common disturbances such acute renal failure, thrombocytopenia, hemolytic anemia, leucocitosis hypertension, neurological, pancreatic and cardiac manifestations are described. We discuss the acid-base and electrolyte disturbances, metabolic acidosis, hyponatremia, hyperkalemia. The etiopathogenic treatment and the control of renal sequelae are also discussed.

  13. Effects of various starch feeding regimens on responses of dairy cows to intramammary lipopolysaccharide infusion.

    Science.gov (United States)

    Gott, P N; Hogan, J S; Weiss, W P

    2015-03-01

    Endotoxin tolerance (ET) can develop in mammals that have been challenged repeatedly with sublethal amounts of lipopolysaccharide (LPS). Previous research has shown that subclinical ruminal acidosis can increase circulating concentrations of LPS. We investigated whether ET would develop in Holstein cows that were subjected to chronic subacute ruminal acidosis (SARA) or acute SARA followed by intramammary infusion of LPS. Twenty-four cows, both primiparous and multiparous, were assigned to 8 blocks of 3 cows. Cows within blocks were randomly assigned to 1 of 3 treatments: (1) control (diet DM was 24% starch and 35% NDF), (2) high starch (formulated to induce chronic milk fat depression with 29% starch and 32% NDF), and (3) acidosis (designed to cause acute bouts of milk fat depression by short-term feeding of a diet with 32% starch, some of which came from wheat grain, and 30% NDF). Cows on the control and high-starch treatments were fed their respective diets throughout the 24-d trial. The acidosis cows were fed the control diet during most of the experiment, except during two 2-d bouts (d 10 and 11 and 17 and 18 of the experiment) in which a high-starch diet was fed. Cows on the high-starch and acidosis treatments produced milk fat with an altered fatty acid profile indicative of SARA (e.g., increased concentrations of specific trans, and odd-, and branched-chain fatty acids), but only cows on the high-starch treatment had milk fat depression. Concentrations of serum amyloid A were elevated in cows on the acidosis treatment, but did not differ between control and high-starch cows. On d 20 of the experiment, all cows were given an intramammary infusion of 10 µg of LPS into 1 mammary quarter 3h after morning milking. Milk yield and DMI decreased the day of the infusion, but the response was not affected by dietary treatment. No systemic indicators of ET were observed among treatments, but evidence of an ET response at the local level of the mammary gland was

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

    Directory of Open Access Journals (Sweden)

    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.

  15. Balancing risk and benefit with oral hypoglycemic drugs.

    Science.gov (United States)

    Hamnvik, Ole-Petter R; McMahon, Graham T

    2009-06-01

    Clinicians are faced with an expansive array of treatment choices when caring for patients with type 2 diabetes. Because patient compliance may be affected when media sensationalism about controversial findings is misunderstood, we sought to clarify the recent controversy surrounding the cardiovascular and bone-health risks of thiazolidinediones, the risk of lactic acidosis with metformin, and the risk of hypoglycemia with oral therapies. The side effect profile of thiazolidinediones includes fluid retention, heart failure; and an increased risk of fracture. A recent controversial meta-analysis suggested that rosiglitazone increases the risk of myocardial infarction, which is possibly related to thiazolidinedione-induced lipid changes, weight gain, congestive heart failure, and anemia. Metformin is restricted to patients with normal renal function because of concerns that metformin may cause lactic acidosis. However, few cases of metformin-associated lactic acidosis have been reported, and most have occurred in patients with other reasons for developing lactic acidosis, such as sepsis or renal failure. Although the use of metformin continues to increase, observational studies have not been able to demonstrate an increased incidence of lactic acidosis in metformin-treated patients, even when it is used in populations with relative contraindications. Some oral hypoglycemic medications can cause hypoglycemia. Hypoglycemia is especially common in older patients, alcoholics, and patients with liver or renal disease. Patients on sulfonylureas and meglitinides have the highest incidence of hypoglycemia because of their pharmacological action of increasing insulin secretion. Of the sulfonylureas, glyburide presents the highest risk of hypoglycemia. Combination therapies, especially those regimens containing a sulfonylurea, increase the risk of hypoglycemia. PMID:19421967

  16. Cyanide poisoning after bitter almond ingestion

    Directory of Open Access Journals (Sweden)

    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.

  17. Propylene Glycol Poisoning From Excess Whiskey Ingestion

    Directory of Open Access Journals (Sweden)

    Courtney A. Cunningham MD

    2015-09-01

    Full Text Available In this report, we describe a case of high anion gap metabolic acidosis with a significant osmolal gap attributed to the ingestion of liquor containing propylene glycol. Recently, several reports have characterized severe lactic acidosis occurring in the setting of iatrogenic unintentional overdosing of medications that use propylene glycol as a diluent, including lorazepam and diazepam. To date, no studies have explored potential effects of excess propylene glycol in the setting of alcohol intoxication. Our patient endorsed drinking large volumes of cinnamon flavored whiskey, which was likely Fireball Cinnamon Whisky. To our knowledge, this is the first case of propylene glycol toxicity from an intentional ingestion of liquor containing propylene glycol.

  18. Control of lipid oxidation during exercise: role of energy state and mitochondrial factors

    DEFF Research Database (Denmark)

    Sahlin, K; Harris, R C

    2008-01-01

    Despite considerable progress during recent years our understanding of how lipid oxidation (LOx) is controlled during exercise remains incomplete. This review focuses on the role of mitochondria and energy state in the control of LOx. LOx increases in parallel with increased energy demand up...... 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 reduction in LOx...

  19. Acid-base equilibrium during capnoretroperitoneoscopic nephrectomy in patients with end-stage renal failure: a preliminary report.

    Science.gov (United States)

    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

  20. Euglycemic Diabetic Ketoacidosis in a Patient with Cocaine Intoxication.

    Science.gov (United States)

    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.

  1. Increased requirement for minute ventilation and negative arterial to end-tidal carbon dioxide gradient may indicate malignant hyperthermia.

    Science.gov (United States)

    Lin, Ho-Tien; Wang, Shen-Chih; Zuo, Zhiyi; Tsou, Mei-Yung; Chan, Kwok-Hon; Yuan, Hui-Bih

    2014-04-01

    Characteristic signs of malignant hyperthermia (MH) include unexplained tachycardia, increased end-tidal carbon dioxide (Etco₂) concentration, metabolic and respiratory acidosis, and an increase in body temperature above 38.8°C. We present the case of a patient with highly probable MH. In addition to sinus tachycardia and metabolic and respiratory acidosis, this patient also had a negative arterial to Etco₂ gradient and an increased requirement for minute ventilation to maintain a normal Etco₂ concentration, with signs of increased CO₂ production. Despite these signs of MH, the patient's rectal temperature monitoring equipment did not show an increase in temperature, although the temperature measured in the mouth was increased. This case illustrates the unreliability of measuring rectal temperature as a means of reflecting body temperature during MH and the usefulness of increased CO₂ production signs in helping to diagnose MH. PMID:24560543

  2. A case report of recurrent hypokalaemic periodic paralysis in a young male patient

    Directory of Open Access Journals (Sweden)

    Pulin Gupta

    2015-01-01

    Full Text Available A 21-year-old normotensive male patient presented with acute-onset flaccid paralysis with the history of a similar episode a few months back. Clinical and laboratory evaluation revealed lower motor neuron type of flaccid quadriparesis with hypokalaemia, normal anion gap metabolic acidosis, bicarbonaturia and transtubular potassium concentration gradient more than 7. Subsequently, urine acidification test (by ammonium chloride challenge test was performed and diagnosis of renal tubular acidosis was established. The patient ultrasound did not show nephrocalcinosis, and history of recurrent diarrhoea preceding the attack revealed that the patient also had coeliac disease. The patient responded to conservative management (Sohl′s solution and gluten-free diet.

  3. A rapid decrease in pulmonary arterial pressure by noninvasive positive pressure ventilation in a patient with chronic obstructive pulmonary disease

    Directory of Open Access Journals (Sweden)

    Dursunoglu Nese

    2007-01-01

    Full Text Available The natural history of chronic obstructive pulmonary disease (COPD is characterized by progressive decrements in expiratory airflow, increments in end-expired pulmonary volume, hypoxaemia, hypercapnia and the progression of pulmonary arterial hypertension (PAH. Noninvasive positive pressure ventilation (NPPV treatment is increasingly used for the treatment of acute and chronic respiratory failure in patients with COPD. NPPV can increase PaO2 and decrease PaCO2 by correcting the gas exchange in such patients. The acute effect of NPPV on decreasing PAP is seen in patients with respiratory failure, probably due to the effect on cardiac output. Here, a case with COPD whose respiratory acidosis and PAH rapidly improved by NPPV was presented and therefore we suggested to perform an echocardiographic assessment to reveal an improvement of PAH as well as respiratory acidosis, hypercapnia and hypoxemia with that treatment.

  4. A young man with polyuria and lethargy

    Directory of Open Access Journals (Sweden)

    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.

  5. Practical management of diabetic ketoacidosis in childhood and adolescence.

    Science.gov (United States)

    Silink, M

    1998-10-01

    Diabetic ketoacidosis results from insulin deficiency and insulin resistance and is marked by hyperglycaemia, ketoacidosis, dehydration and electrolyte losses. Management includes correction of shock, dehydration, electrolyte deficits, hyperglycaemia, acidosis and sepsis (if present). Warning signs include severe dehydration, shock, pH 360 mmoll(-1), (iv) normal saline for rehydration unless the patient is hypernatraemic, (v) avoidance of bicarbonate unless acidosis is interfering with myocardial contractility, (vi) insulin infusion to achieve a fall in blood glucose levels of 5 mmol h(-1), (vi) potassium, (vii) use of 5% glucose when the blood glucose level falls <12mmoll(-1), (ix) treatment of any complications and (x) change to subcutaneous insulin when diabetic ketoacidosis is controlled.

  6. 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

    Directory of Open Access Journals (Sweden)

    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.

  7. A newborn with diabetic ketoacidosis and thalassemia major: A rare case

    Directory of Open Access Journals (Sweden)

    Ünal Uluca

    2012-03-01

    Full Text Available Diabetic ketoacidosis is a systemic situation caused byabsolute insulin deficiency and characterized by hyperglycemia,ketonemia, acidemia, glycosuria and ketonuria.Thalassemia Major is a very serious hereditary blooddisorder due to low levels or absence of “beta globulin”chain, characterized by requiring a blood transfusion from3-4. month of life due to the relatively short life of red cells.We, herein presented a rare case of 20 day-old newbornwith anemia, hyperglycemia, vomiting, acidosis being diagnosedas thalassemia major that required blood transfusionin the early period of life and diabetic ketoacidosiswithout ketonuria who born from 24 year old father carrierof thalassemia and 23-year-old mother with carrier of thalassemiaand gestational diabetes.The case was presented in order to emphasize that diabeticketoacidosis can occur in newborns without ketonuriaand thalassemia major may cause anemia in the earlyperiod of life due to hyperglycemia and acidosis.

  8. Metabolik Asidozda Arteriyal, Serebro-Spinal pH ilişkisi ve NaHCO3 Tedavisinde Cevabı

    OpenAIRE

    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...

  9. Acid-base equilibrium during capnoretroperitoneoscopic nephrectomy in patients with end-stage renal failure: a preliminary report.

    Science.gov (United States)

    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.

  10. Carbon dioxide: Global warning for nephrologists.

    Science.gov (United States)

    Marano, Marco; D'Amato, Anna; Cantone, Alessandra

    2016-09-01

    The large prevalence of respiratory acid-base disorders overlapping metabolic acidosis in hemodialysis population should prompt nephrologists to deal with the partial pressure of carbon dioxide (pCO2) complying with the reduced bicarbonate concentration. What the most suitable formula to compute pCO2 is reviewed. Then, the neglected issue of CO2 content in the dialysis fluid is under the spotlight. In fact, a considerable amount of CO2 comes to patients' bloodstream every hemodialysis treatment and "acidosis by dialysate" may occur if lungs do not properly clear away this burden of CO2. Moreover, vascular access recirculation may be easy diagnosed by detecting CO2 in the arterial line of extracorporeal circuit if CO2-enriched blood from the filter reenters arterial needle. PMID:27648406

  11. Development and characterization of a nonprimate animal model of methanol-induced neurotoxicity

    Energy Technology Data Exchange (ETDEWEB)

    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.

  12. Recurrent Attacks of Hypokalemic Quadriparesis: An Unusual Presentation of Primary Sjögren Syndrome.

    Science.gov (United States)

    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

  13. Glycolysis in energy metabolism during seizures

    Institute of Scientific and Technical Information of China (English)

    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.

  14. Cetrimide-chlorhexidine-induced multiorgan failure in surgery of pulmonary hydatid cyst.

    Science.gov (United States)

    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

  15. Unmeasured anions and mortality in critically ill patients in 2016.

    Science.gov (United States)

    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

  16. Effect of diet on maintenance of acid-basal balance in blood of dairy cows

    Directory of Open Access Journals (Sweden)

    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.

  17. Hashimoto Thyroiditis and Nephrocalcinosis in a Child with Down Syndrome

    Science.gov (United States)

    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

  18. Mitochondria: role of citrulline and arginine supplementation in MELAS syndrome.

    Science.gov (United States)

    El-Hattab, Ayman W; Emrick, Lisa T; Chanprasert, Sirisak; Craigen, William J; Scaglia, Fernando

    2014-03-01

    Mitochondria are found in all nucleated human cells and generate most of the cellular energy. Mitochondrial disorders result from dysfunctional mitochondria that are unable to generate sufficient ATP to meet the energy needs of various organs. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a frequent maternally inherited mitochondrial disorder. There is growing evidence that nitric oxide (NO) deficiency occurs in MELAS syndrome and results in impaired blood perfusion that contributes significantly to several complications including stroke-like episodes, myopathy, and lactic acidosis. Both arginine and citrulline act as NO precursors and their administration results in increased NO production and hence can potentially have therapeutic utility in MELAS syndrome. Citrulline raises NO production to a greater extent than arginine, therefore, citrulline may have a better therapeutic effect. Controlled studies assessing the effects of arginine or citrulline supplementation on different clinical aspects of MELAS syndrome are needed.

  19. The effect of citrulline and arginine supplementation on lactic acidemia in MELAS syndrome.

    Science.gov (United States)

    El-Hattab, Ayman W; Emrick, Lisa T; Williamson, Kaitlin C; Craigen, William J; Scaglia, Fernando

    2013-12-01

    Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a mitochondrial disorder in which nitric oxide (NO) deficiency may play a role in the pathogenesis of several complications including stroke-like episodes and lactic acidosis. Supplementing the NO precursors arginine and citrulline restores NO production in MELAS syndrome. In this study we evaluated the effect of arginine or citrulline on lactic acidemia in adults with MELAS syndrome. Plasma lactate decreased significantly after citrulline supplementation, whereas the effect of arginine supplementation did not reach statistical significance. These results support the potential therapeutic utility of arginine and citrulline in MELAS syndrome and suggest that citrulline supplementation may be more efficacious. However, therapeutic efficacy of these compounds should be further evaluated in clinical trials.

  20. Euglycemic Diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SGLT2) inhibitor Canagliflozin.

    Science.gov (United States)

    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