OBJECTIVE: This study measured the prevalence of lipodystrophy and the metabolic effects of highly active antiretroviral therapy (HAART) in HIV-infected African subjects. METHODS: Prevalence was measured in 571 Rwandans receiving HAART for > or = 6 months. Metabolic variables were measured in 100 HIV-positive adults with lipodystrophy, 50 HIV-positive nonlipodystrophic adults, and 50 HIV-negative controls. RESULTS: A HAART regimen of stavudine, lamivudine, and nevirapine was used by 81.6% of subjects; none received protease inhibitors. Lipodystrophy was observed in 34% (48.5% in urban groups and 17.3% in rural groups) of subjects, with a prevalence of 69.6% in those receiving HAART for >72 weeks. Peripheral lipoatrophy combined with abdominal lipohypertrophy was observed in 72% of lipodystrophic subjects. HIV-positive adults with lipodystrophy had a significantly higher waist-to-hip ratio (WHR; 0.99 +/- 0.05 vs. 0.84 +/- 0.03: P < 0.0005) than HIV-positive nonlipodystrophic adults. Total cholesterol concentrations (median [interquartile range], mmol/L) were significantly higher in the HIV-positive adults with lipodystrophy (3.60 [1.38]) than in HIV-positive nonlipodystrophic adults (3.19 [0.65]; P < 0.005) and control (3.13 [0.70]; P < 0.0005) groups. Impaired fasting glucose was observed in 18% of HIV-positive adults with lipodystrophy, 16% of HIV-positive nonlipodystrophic adults, and 2% of controls, but insulin levels did not differ. CONCLUSIONS: African subjects with lipodystrophy have increased WHR, glucose, and cholesterol levels. Glucose concentrations are also elevated in nonlipodystrophic HIV-positive subjects. Therefore, factors other than body fat redistribution contribute to the glucose intolerance.
OBJECTIVE: This study measured the prevalence of lipodystrophy and the metabolic effects of highly active antiretroviral therapy (HAART) in HIV-infected African subjects. METHODS: Prevalence was measured in 571 Rwandans receiving HAART for > or = 6 months. Metabolic variables were measured in 100 HIV-positive adults with lipodystrophy, 50 HIV-positive nonlipodystrophic adults, and 50 HIV-negative controls. RESULTS: A HAART regimen of stavudine, lamivudine, and nevirapine was used by 81.6% of subjects; none received protease inhibitors. Lipodystrophy was observed in 34% (48.5% in urban groups and 17.3% in rural groups) of subjects, with a prevalence of 69.6% in those receiving HAART for >72 weeks. Peripheral lipoatrophy combined with abdominal lipohypertrophy was observed in 72% of lipodystrophic subjects. HIV-positive adults with lipodystrophy had a significantly higher waist-to-hip ratio (WHR; 0.99 +/- 0.05 vs. 0.84 +/- 0.03: P < 0.0005) than HIV-positive nonlipodystrophic adults. Total cholesterol concentrations (median [interquartile range], mmol/L) were significantly higher in the HIV-positive adults with lipodystrophy (3.60 [1.38]) than in HIV-positive nonlipodystrophic adults (3.19 [0.65]; P < 0.005) and control (3.13 [0.70]; P < 0.0005) groups. Impaired fasting glucose was observed in 18% of HIV-positive adults with lipodystrophy, 16% of HIV-positive nonlipodystrophic adults, and 2% of controls, but insulin levels did not differ. CONCLUSIONS: African subjects with lipodystrophy have increased WHR, glucose, and cholesterol levels. Glucose concentrations are also elevated in nonlipodystrophic HIV-positive subjects. Therefore, factors other than body fat redistribution contribute to the glucose intolerance.
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