Chattha and colleagues [1] recently reported seven patients with AIDS who had type B lactic acidosis without other obvious causes. We report an additional case of unexplained lactic acidosis in a 25-year-old, HIV-infected patient with hemophilia. He had been receiving zidovudine for 10 months, had a CD4 count ranging from 230/µL to 160/µL, and had been symptomatic with ophthalmic herpes zoster 2 years before. He had a hepatitis C infection and mild chronic elevations of his transaminase levels. His symptoms in June 1990 were anorexia, hyperventilation, and weight loss, and he was found to have lactic acidosis with a serum lactate level of 10.4 mmol/L. There was an associated elevation of his aspartate aminotransferase level to 128 U/L (normal range, 8 to 39 U/L), lactate dehydrogenase level to 581 U/L (normal range, 94 to 200 U/L), total bilirubin count to 1.7 mg/dL, and uric acid level to 15 mg/dL without azotemia. An extensive evaluation showed no evidence of hypoxia, hypotension, ischemia, or malignancy. A computed tomographic scan of the abdomen showed diffuse hypodensity of the liver consistent with fatty infiltration. Zidovudine was discontinued, and the acidosis, worsening of liver function tests, and hyperuricemia resolved within 3 months.

The zidovudine therapy was reinstituted in September 1990. He had transient proximal muscle weakness during the months after the acidosis but did not have an increased creatine kinase level. The patient remained well until January 1992 when lactic acidosis recurred, with a peak lactic acid level of 3.6 mmol/L, again associated with worsening of his liver function tests. Zidovudine was discontinued, and dideoxyinosine was begun. The acidosis again resolved spontaneously by March 1992, and he is currently asymptomatic. We are uncertain as to the cause of the acidosis but suspect that it is related to his liver disease in conjunction with his HIV infection. Unfortunately, the patient declined biopsy of the liver or muscle during the episodes of acidosis. We do not believe the zidovudine was the cause of the acidosis because he continued taking zidovudine from September 1990 to January 1992 without acidosis.

We believe that the patient had the same syndrome as described by Chattha and colleagues. His longer survival than the patients in Chattha and coworkers' series may be related to the less advanced stage of his HIV infection. We are curious if Chattha and colleagues noted abnormal liver function tests, hyperuricemia, or a history of hepatitis in the patients in their study.