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At least 505 records · Page 28Linked to original sources
PubMed1998

Lactic acidosis rates in type 2 diabetes.

OBJECTIVE: To provide a context for the interpretation of lactic acidosis risk among patients using metformin, we measured rates of lactic acidosis in patients with type 2 diabetes before metformin was approved for use in the U.S. RESEARCH DESIGN AND METHODS: Using electronic databases of hospital discharge diagnoses and laboratory results maintained by a large, nonprofit health maintenance organization (HMO). we identified possible lactic acidosis events in three geographically and racially diverse populations with type 2 diabetes. We then reviewed hard-copy clinical records to confirm and describe each event and determine its likely cause(s). RESULTS: From >41.000 person-years of experience, we found four confirmed, three possible, and three borderline cases of lactic acidosis. In each case, we identified at least one severe medical condition that could have caused the acidosis. The annual confirmed event rate is similar to published rates of metformin-associated lactic acidosis. CONCLUSIONS: Lactic acidosis occurs regularly, although infrequently, among persons with type 2 diabetes, at rates similar to its occurrence among metformin users. The medical conditions with which both metformin-associated and naturally occurring lactic acidosis co-occur are also its potential causes. The observed association between metformin and lactic acidosis may be coincidental rather than causal. This possibility merits further study

Acidosis, Lactic↗
PubMed1992

[Acid-base balance disorder in various diseases--diabetes mellitus].

Metabolic acidosis is the serious acid-base balance disorder complicated in diabetes mellitus. The pathogenesis and treatment of various type of metabolic acidosis (Keto-acidosis, lactic acidosis, hyperchloremic acidosis and type IV renal tubular acidosis) are discussed. Metabolic acidosis in the diabetic patient is associated with an increased anion-gap caused by the presence of organic anion (beta-hydroxybutyrate, acetoacetate, and lactate). The rise in anion-gap usually equals the fall in plasma bicarbonate. With appropriate therapy, progressive decline in the anion-gap is one of the best indications of successful treatment. If hyperchloremic acidosis is established, appropriate infusion of hypochloremic rehydration fluid may be useful.

Acidosis, Lactic↗
PubMed1982

Treatment of lactic acidosis with dichloroacetate in dogs.

Lactic acidosis is a clinical condition due to accumulation of H(+) ions from lactic acid, characterized by blood lactate levels >5 mM and arterial pH <7.25. In addition to supportive care, treatment usually consists of intravenous NaHCO(3), with a resultant mortality >60%. Dichloroacetate (DCA) is a compound that lowers blood lactate levels under various conditions in both man and laboratory animals. It acts to increase pyruvate oxidation by activation of pyruvate dehydrogenase. We evaluated the effects of DCA in the treatment of two different models of type B experimental lactic acidosis in diabetic dogs: hepatectomy-lactic acidosis and phenformin-lactic acidosis. The metabolic and systemic effects examined included arterial blood pH and levels of bicarbonate and lactate; the intracellular pH (pHi) in liver and skeletal muscle; cardiac index, arterial blood pressure and liver blood flow; liver lactate uptake and extrahepatic splanchnic (gut) lactate production; and mortality. Effects of DCA were compared with those of either NaCl or NaHCO(3). The infusion of DCA and NaHCO(3), delivered equal amounts of volume and sodium, although the quantity of NaHCO(3) infused (2.5 meq/kg per h) was insufficient to normalize arterial pH. In phenformin-lactic acidosis, DCA-treated animals had a mortality of 22%, vs. 89% in those treated with NaHCO(3). DCA therapy increased arterial pH and bicarbonate, liver pHi and cardiac index, with increased liver lactate uptake and a fall in blood lactate. With NaHCO(3) therapy, there were decrements of cardiac index and liver pHi, with an increase in venous pCO(2) and gut production of lactate. Dogs with hepatectomy-lactic acidosis were either treated or pretreated with DCA. Treatment with DCA resulted in stabilization of cardiac index, a fall in blood lactate, and 17% mortality. NaHCO(3) was associated with a continuous decline of cardiac index, rise in blood lactate, and 67% mortality. In dogs pretreated with NaCl, mortality was 33%, but all dogs pretreated with DCA survived. Dogs pretreated with DCA also had lower blood lactate and higher arterial pH and bicarbonate than did those pretreated with NaCl.Thus, in either of two models of type B experimental lactic acidosis, treatment with DCA improves cardiac index, arterial pH, bicarbonate and lactate, and liver pHi. The mortality in dogs with type B lactic acidosis was significantly less in DCA-treated animals than in those treated with other modalities.

Acetates↗
PubMed1996

Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy.

Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidification defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

C-peptide blood levels in keto-acidosis and in hyperosmolar non-ketotic diabetic coma.

For further evaluation of B-cell secretion in diabetic keto-acidosis (KA) and in non-ketotic hyperosmolar coma (NKHC), basal and post-i.v. tolbutamide blood CPR and IRI values were measured in 34 patients (22 KA and 12 NKHC). FFA, cortisol and HGH measurements were also performed. IRI was low in both KA and NKHC (0.07 +/- 0.01 and 0.082 +/- 0.01 nmol/l) as opposed to CPR which was significantly higher in NKHC (1.14 +/- 0.1 nmol/l) than in KA (0.21 +/- 0.03 nmol/l). After tolbutamide injection, CPR and IRI levels did not change in any of the KA cases, whereas they significantly increased in half of the NKHC cases. Cortisol and FFA values were similarly increased in both situations, as opposed to HGH which was significantly higher (6.1 +/- 1.2 ng/ml) in KA than in NKHC (1.9 +/- 0.2 ng/ml). These results suggest that B-cell function is less deficient in NKHC than in KA. Residual insulin amounts reaching the liver via the portal vein could partly account for the absence of ketosis in NKHC.

Adult↗
PubMed2005

Fulminant lactic acidosis in two patients with Type 2 diabetes treated with metformin.

Lactic acidosis is a known adverse risk of metformin treatment. We report two cases in whom fulminant lactic acidosis developed during treatment. There were no contraindications to metformin treatment and both were admitted with abdominal discomfort for some days, causing dehydration. Both patients had renal failure on admission, developed multiple organ failure and both suffered a massive stroke. One patient died and the other survived but is severely disabled. We suggest, in both cases, that acute renal failure developed as a result of dehydration, causing metformin accumulation and lactic acidosis. We recommend that all patients on metformin should consider discontinuation of metformin treatment in the event of a severe medical condition causing dehydration.

Acidosis, Lactic↗