Until recently, the prognosis for people with AIDS was so poor that concerns about other long-term health problems seemed irrelevant. The introduction of antiretroviral treatment with protease inhibitors has had a profound impact on mortality from AIDS. 1 After two young AIDS patients on protease inhibitors under our care developed coronary artery disease, we examined lipid abnormalities among HIV-1-infected people receiving protease inhibitors and designed an intervention based on the National Cholesterol Education Program (NCEP) guidelines. 2 A 26-year-old HIV-1-infected man (CD4 T cell count< 10 cells/μL) was admitted with angina. He had a history of cigarette smoking and occasional cocaine use (none recently). The plasma HIV-1-RNA level was more than 1000000 copies/mL, so 4 weeks before admission he was started on directly-observed ritonavir, saquinavir, lamivudine, and stavudine. Coronary angiography showed a large occlusive thrombus within the right coronary artery. A 37-year old HIV-1-infected man presented with angina after shovelling snow. His lowest CD4 T-cell count was 14 cells/μL with a peak plasma HIV-1 RNA level of 685 000 copies/mL. He had developed cytomegalovirus retinitis and diabetes mellitus before starting protease inhibitors at age 35. He had a family history of heart disease but no history of cigarette smoking. His cholesterol concentration increased from 4· 28 mmol/L before starting indinavir to 8· 46 mmol/L 5 months later. 7 months before presentation his fasting cholesterol was 12· 3 mmol/L, high-density cholesterol (HDL) 0· 46 mmol/L, and triglycerides 22· 14 mmol/L, while his plasma HIV RNA level was< 500 copies/μL. He developed a right cervical region fat pad. He was taking gemibrozil 600 mg orally twice daily, aspirin, indinavir, zidovudine, and lamivudine. Coronary arteriography revealed occlusion of the left anterior descending artery and severe atherosclerosis involving the right coronary artery.

A review of 124 patients on protease inhibitors in our HIV clinic identified 41 (33%) with raised lipid concentrations who were referred for NCEP intervention. For 15 patients (mean fasting lipids-cholesterol 6· 35 mmol/L; triglycerides 3· 6 mmol/L), a diet exercise programme was instituted. 26 patients (mean fasting lipids-cholesterol 8· 98 mmol/L; mean triglycerides 19· 2 mmol/L) were referred for drug treatment (gemfibrozil for 3 months then atorvastatin). Peripheral lipodystrophy has been reported in patients receiving protease inhibitors. 3, 4 In one study, metabolic abnormalities (higher triglyceride, cholesterol, insulin, and C-peptide levels, and insulin resistance scores) were described in 72 (64%) of 116 patients after a mean 10 months on treatment. 5 Clinicians need to be aware of the potential for accelerated atherosclerosis in patients treated with protease inhibitors. For now, we obtain a fasting lipid profile before and then 3–6 months after the start of protease inhibitor therapy and then use NCEP guidelines to treat abnormalities identified.