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1 December 2001

Volume 33, Number 11
Clinical Infectious Diseases 2001;33:1914–1921
© 2001 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2001/3311-0018$03.00
DOI: 10.1086/323783
HIV/AIDS MAJOR ARTICLE

Symptomatic Lactic Acidosis in Hospitalized Antiretroviral‐Treated Patients with Human Immunodeficiency Virus Infection: A Report of 12 Cases

Michael E. Coghlan,1

Jean‐Pierre Sommadossi,2

Nirag C. Jhala,3

Wickliffe J. Many,1

Michael S. Saag,1 and

Victoria A. Johnson1,4

Departments of 1Medicine, 2Pharmacology and Toxicology, and 3Anatomic Pathology, University of Alabama at Birmingham School of Medicine, and the 4Birmingham Veterans Affairs Medical Center, Birmingham, Alabama

We retrospectively investigated the clinical and histopathologic features of hospitalized patients infected with human immunodeficiency virus who had symptomatic lactic acidosis syndrome at a university teaching hospital during 1995–2000. Twelve patients were identified, 11 during 1998–2000; of these, 5 died with rapid progression to otherwise unexplained multiple‐organ failure. All had extensive prior exposure to nucleoside analog reverse‐transcriptase inhibitors (NRTIs). At presentation, the most commonly identified NRTI component of antiretroviral regimens was stavudine plus didanosine. Eleven patients presented with abdominal pain, nausea, and/or emesis. Eight patients had prior acute weight loss (mean [±SD], kg). Median venous plasma lactate levels were 2‐fold greater than the upper limit of normal (2.1 mmol/L). Serum transaminase levels were near normal limits at presentation. Histopathologic studies confirmed hepatic macrovesicular and microvesicular steatosis in 6 patients. Concurrent chemical pancreatitis was identified in 6 patients. The increasing number of cases identified during the study period suggests that physicians better recognize symptomatic lactic acidosis and/or that cumulative NRTI exposure may increase the risk for this syndrome.

Received 27 October 2000; revised 29 May 2001; electronically published 24 October 2001.

Reprints or correspondence: Dr. Victoria A. Johnson, Division of Infectious Diseases, University of Alabama at Birmingham School of Medicine, THT 229, 1530 3rd Ave. South, Birmingham, AL 35294‐0006 ().

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  • Presented in part: 38th Annual Meeting of the Infectious Diseases Society of America, New Orleans, LA, 7–10 September 2000 (abstract 377).

    The institutional review board for the rights of human patients at the University of Alabama at Birmingham (UAB) School of Medicine granted approval for this project.

    Financial support: V.A.J. and J.‐P.S acknowledge the support of the National Institutes of Health/National Institute of Allergy and Infectious Diseases (grants 1‐RO1‐AI33239 and 1‐RO1‐AI40876) and the Uuniversity of Alabama Health Services Foundation support of the UAB Liver Center. V.A.J. acknowledges the support of the Core Laboratory Research Facilities of the UAB School of Medicine, UAB Center for AIDS Research, the Birmingham Veterans Affairs Medical Center, the UAB Liver Center, and the UAB Center for AIDS Research Biostatistics Core Grant (5P30 AI27767‐14). M.E.C. acknowledges training support from the UAB General Clinical Research Center Clinical Research Training Program (grant SK30 HL04146‐03).

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