OBJECTIVE: To report 6 cases of osteonecrosis in HIV-infected patients treated with highly active antiretroviral therapy (HAART) and compare the observed risk factors with those of published cases. CASE SUMMARIES: Osteonecrosis was diagnosed between 1999 and 2002 in 6 of 417 HIV-infected patients in our department of infectious diseases. At the time of diagnosis, mean patient age was 42 years, and 5 patients had developed AIDS. Mean CD4+ lymphocyte count was 563.5 cells/mm(3) and viral load was undetectable (<50 copies/mL) in 5 patients. The patients' mean body mass index was 22.5 kg/m(2). Four had lipodystrophy. All were receiving HAART, including a protease inhibitor in 4 patients; the remaining 2 patients had a history of protease inhibitor treatment. Median time from the first antiretroviral therapy to osteonecrosis diagnosis was 46.5 months. Established risk factors were the use of corticosteroids in 2 patients and dyslipidemia in all patients. All of the patients developed pain and functional impotence of the hip or ankle joints. Osteonecrosis of the hip was bilateral in 4 cases. Three patients required surgical intervention, all of whom had favorable outcomes. DISCUSSION: HIV-infected patients are at a higher risk for the development of osteonecrosis and are more likely to be exposed to predisposing factors to its development. The HAART implication as a predisposing factor remains controversial. CONCLUSIONS: The pathogenesis of osteonecrosis in HIV-infected individuals may be multifactorial; the reasonable approach for clinicians consists of treating concomitant predisposing conditions that might further cause osteonecrosis.
OBJECTIVE: To report 6 cases of osteonecrosis in HIV-infectedpatients treated with highly active antiretroviral therapy (HAART) and compare the observed risk factors with those of published cases. CASE SUMMARIES: Osteonecrosis was diagnosed between 1999 and 2002 in 6 of 417 HIV-infectedpatients in our department of infectious diseases. At the time of diagnosis, mean patient age was 42 years, and 5 patients had developed AIDS. Mean CD4+ lymphocyte count was 563.5 cells/mm(3) and viral load was undetectable (<50 copies/mL) in 5 patients. The patients' mean body mass index was 22.5 kg/m(2). Four had lipodystrophy. All were receiving HAART, including a protease inhibitor in 4 patients; the remaining 2 patients had a history of protease inhibitor treatment. Median time from the first antiretroviral therapy to osteonecrosis diagnosis was 46.5 months. Established risk factors were the use of corticosteroids in 2 patients and dyslipidemia in all patients. All of the patients developed pain and functional impotence of the hip or ankle joints. Osteonecrosis of the hip was bilateral in 4 cases. Three patients required surgical intervention, all of whom had favorable outcomes. DISCUSSION: HIV-infectedpatients are at a higher risk for the development of osteonecrosis and are more likely to be exposed to predisposing factors to its development. The HAART implication as a predisposing factor remains controversial. CONCLUSIONS: The pathogenesis of osteonecrosis in HIV-infected individuals may be multifactorial; the reasonable approach for clinicians consists of treating concomitant predisposing conditions that might further cause osteonecrosis.