Unprecedented advances in the treatment of HIV-1 infection can be attributed in a large part to the use of protease inhibitors. 1 Protease inhibitors are metabolised by the hepatic cytochrome P450 system of enzymes, and interactions at this site of metabolism are a cause of the side effects associated with these medications. Protease inhibitors can affect lipid metabolism, 2 and glucose tolerance. 3 We report a patient who developed unusual fatty deposits (benign symmetric lipomatosis) while on indinavir, lamivudine, and zidovudine. A 34-year-old man has been seen for HIV-1 infection as an outpatient at our clinic since May, 1995. In October 1993 he and his wife both tested positive for HIV-1. At that time he was without symptoms and his CD4 count was 285106/L. Zidovudine was begun in November, 1993, and trimethoprim/sulfamethoxasole prophylaxis in August, 1994. Other than an episode of herpes zoster he remained well. In

April and June, 1996, lamivudine and indinavir were added to his medications. In August, 1996, myalgia and weakness prompted a measurement of his creatine kinase (CK), which was elevated. Without any change in treatment, his myalgia and weakness resolved within 3 weeks, although his CK has remained elevated. At a follow up in December 1996 a “buffalo hump”—accumulation of fat in the cervical fat pad area and across the shoulders—was noted (figure). He also had fatty changes in the supraclavicular area, but no other features suggestive of Cushing’s syndrome at that time. Blood tests revealed only a minimally elevated blood glucose. Electrolytes and cholesterol were normal. A low-dose dexamethasone suppression test was normal, ruling out Cushing’s syndrome. His HIV-1 RNA viral load was undetectable, and he has continued on what has otherwise been a successful regimen for his HIV-1 infection without any worsening of fat deposition. Benign symmetric lipomatosis is an uncommon condition seen predominantly in male alcoholics. Apart from alcohol, associations have included glucose intolerance, hyperlipidemia, hyperuricemia, and polyneuropathy. 4 Studies have implicated abnormal lipolytic responses of adipocytes to catecholamine and elevated levels of lipoprotein lipase and lipoprotein 1. 5 Our patient has never drunk alcohol. The temporal association between starting his medications and developing his “buffalo hump”, the effect of protease inhibitors on P450 enzymes, and the recent associations between indinavir use and glucose and lipid metabolism lead us to believe indinavir may be implicated in the development of benign symmetric lipomatosis.