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], 12+/-5.3 kg). Median venous plasma lactate levels were > or =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.

A 73-year-old man treated with long-term hemodialysis, erythropoietin, and intravenous iron sucrose infusions developed Vibrio vulnificus infection after eating raw oysters harvested from the Alabama coast. Five of the 31 persons with cases of V. vulnificus infection reported to the Alabama Department of Public Health (Montgomery) during 1996-2002 (including the patient described here) also had renal disease. Persons with renal disease, especially those treated with long-term hemodialysis and intravenous iron infusions, may have an increased risk of infection with V. vulnificus.