RSS Feeds
Lactic Acidosis and AIDS
- Daniel Baram; and
- Joseph Cooke
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TO THE EDITOR:
In 1991, we had a patient with a clinical course similar to that in the patients described in the recent report by Chattha and coworkers [1], in which a cause of lactic acidosis was found at autopsy. Our patient was a 45-year-old, HIV-positive woman given zidovudine and trimethoprim-sulfamethoxazole. After oral fluconazole therapy for severe oral thrush failed, she was admitted to the hospital for fluids, intravenous fluconazole, and esophageal biopsy after a bout of progressive odynophagia and dehydration. The admission examination was remarkable only for oral thrush and evidence of dehydration. Laboratory values showed a HCO3 level of 22 mEq/L, with an anion gap of 13 mEq/L and a pH of 7.43.
After 8 days, her HCO3 level decreased to no measurable amount; her pH was 7.05 and her lactate level was 21.3 mEq/L. She was relatively hypotensive with increasing confusion and was transferred to the intensive care unit. Despite aggressive hemodynamic support and broad-spectrum antibiotics, she died 72 hours later. Several cultures and extensive imaging studies were done, but no source of sepsis or other cause of acidosis was found.
Autopsy showed healing esophagitis, cytomegalovirus adrenalitis, mild pancreatitis, and cerebral atrophy. Of importance, focal necrosis of the claustrum and fornix and petechiae in the mamillary bodies were also noted. On the basis of these findings, a diagnosis of thiamine deficiency leading to Wernicke encephalopathy was made. Thiamine deficiency is a known cause of lactic acidosis [2]. A therapeutic response to thiamine would have been needed to prove that thiamine deficiency caused this patient's acidosis; however, no other pathologic finding or premortem study was sufficient to explain the acidosis or her death.
Thiamine deficiency is an underdiagnosed entity; it is common in alcoholic persons and in those with malignancy, malabsorptive states, and AIDS. Several of the patients reported by Chattha and colleagues had gastrointestinal complaints, which predisposed them to malnutrition and vitamin deficiencies. It would be interesting to know if their autopsies showed evidence of Wernicke encephalopathy or if, on retrospective analysis, thiamine administration separated survivors from nonsurvivors.
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
Include no more than 300 words of text, three authors, and five references
Type with double-spacing
Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright 2004 by the American College of Physicians
