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Original Articles

Treatment of Severe Lactic Acidosis with Dichloroacetate

  1. Perry J Blackshear,
  2. Leslie S-T Fang and
  3. Lloyd Axelrod
  1. Howard Hughes Medical Institute Laboratory, Harvard Medical School; the Diabetes Unit and Renal Unit, Medical Services, Massachusetts General Hospital; and the Department of Medicine, Harvard Medical School Boston, Massachusetts
  1. Address reprint requests to Perry J. Blackshear, Diabetes Unit, Massachusetts General Hospital, Boston, Massachusetts 02114.
Diabetes Care 1982 Jul; 5(4): 391-394. https://doi.org/10.2337/diacare.5.4.391
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Abstract

Four patients with severe lactic acidosis associated with septic shock were treated with sodium dichloroacetate (DCA) (50 mg/kg body wt), an activator of pyruvate dehydrogenase. All patients were in a group with an expected mortality rate of 90–100%, based on previous studies. In one patient, treatment with DCA was associated with a decrease in blood lactate levels from 11.2 mM before treatment to 0.8 mM 16 h later. Markedly elevated blood pyruvate and alanine levels also decreased to normal. After treatment, the arterial blood pH rose to 7.53, and vasopressor agents were no longer needed to support blood pressure. Some degree of biochemical improvement was also noted in the other cases in whom the blood lactate levels before treatment were 15, 17, and 31 mM. However, all three patients eventually died of refractory acidosis.

  • Copyright © 1982 by the American Diabetes Association

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July 1982, 5(4)
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Treatment of Severe Lactic Acidosis with Dichloroacetate
Perry J Blackshear, Leslie S-T Fang, Lloyd Axelrod
Diabetes Care Jul 1982, 5 (4) 391-394; DOI: 10.2337/diacare.5.4.391

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Treatment of Severe Lactic Acidosis with Dichloroacetate
Perry J Blackshear, Leslie S-T Fang, Lloyd Axelrod
Diabetes Care Jul 1982, 5 (4) 391-394; DOI: 10.2337/diacare.5.4.391
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© 2021 by the American Diabetes Association. Diabetes Care Print ISSN: 0149-5992, Online ISSN: 1935-5548.