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REPLY

Lactic Acidosis and AIDS

right arrow Geetinder Chattha and Allen I. Arieff

15 August 1993 | Volume 119 Issue 4 | Pages 343-345


IN RESPONSE:

Four patients received intravenous thiamine before or during their lactic acidosis without response; autopsies in three patients showed no evidence for thiamine deficiency [1]. Four patients were receiving zidovudine at the time of admission, and all had received zidovudine at some time. None had specific evaluation of mitochondrial function, but two patients were discharged and continued on zidovudine therapy without recurrence of lactic acidosis. However, a recent report [2] as well as some of the patients reported in the letters suggests a possible but unproven causal association. In addition, two female patients in our study were obese (mean weight, 141 kg), with extensive fatty liver at autopsy.

Drs. Haupt, Kruse, and Carlson suggest that sepsis was not adequately ruled out. Their definition of sepsis is based on the presence of more than two of the following: identified site(s) of infection; positive blood or fluid culture; fever; and leukocytosis [3]. Using their criteria, none of the patients in our study had sepsis [3]. At the time of diagnosis and for several days thereafter, multiple cultures of blood, urine, and sputum (four to nine per patient) were sterile, and no patient had hypotension or an obvious site of infection [1]. Fever, of course, is not uncommon in patients with AIDS in the absence of sepsis.

The lactic acidosis may reflect the fact that patients with AIDS may have increased resting energy expenditure and hypermetabolism [4], possibly associated with tumor necrosis factor [5]. There may be some combination of a shift to anaerobic metabolism (resulting in less energy production per calorie) with hypermetabolism, the net result of which could be cachexia and increased lactate production with normal oxygen use.


References
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1. Chattha G, Arieff AI, Cummings C, Tierney LM Jr. Lactic acidosis complicating the acquired immunodeficiency syndrome. Ann Intern Med. 1993; 118:37-9.

2. Gopinath R, Hutcheon M, Cheema-Dhadli S, Halperin M. Chronic lactic acidosis in a patient with acquired immunodeficiency syndrome and mitochondrial myopathy: biochemical studies. J Am Soc Nephrol. 1992; 3:1212-9.

3. Gilbert EM, Haupt MT, Mandanas RY, Huaringa AJ, Carlson RW. The effect of fluid loading, blood transfusion, and catecholamine infusion on oxygen delivery and consumption in patients with sepsis. Am Rev Respir Dis. 1986; 134:873-8.

4. Grunfeld C, Feingold KR. Metabolic disturbances and wasting in the acquired immunodeficiency syndrome. N Engl J Med. 1992; 327:329-37.

5. Odeh M. The role of tumour necrosis factor-{alpha} in acquired immunodeficiency syndrome. J Intern Med. 1990; 228:549-56.

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