Serum adiponectin and metabolic parameters in HIV-1-infected patients after substitution of nevirapine for protease inhibitors

• Published in: European journal of clinical investigation 2004-08, Vol.34 (8), p.569-575
• Main Authors: Petit, J. M., Duong, M., Masson, D., Buisson, M., Duvillard, L., Bour, J. B., Brindisi, M. C., Galland, F., Guiguet, M., Gambert, P., Portier, H., Vergès, B.
• Format: Article
• Language: English
• Subjects: Adiponectin; Adult; Anti-HIV Agents - therapeutic use; CETP; Female; HIV Infections - drug therapy; HIV Infections - metabolism; HIV protease inhibitors; HIV Protease Inhibitors - therapeutic use; HIV-1; Human immunodeficiency virus 1; Humans; Insulin Resistance; insulin sensitivity; Intercellular Signaling Peptides and Proteins; Lipids - blood; Male; metabolism abnormalities; Middle Aged; nevirapine; Nevirapine - therapeutic use; Proteins - metabolism; Serum
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/j.1365-2362.2004.01379.x

Background  In the context of HIV infection and antiretroviral therapy, adiponectin concentrations have been shown to be related to lipodystrophy, metabolic alterations and HIV‐protease inhibitor (PI) use. The replacement of PI by nevirapine has improved the lipid profile of patients under antiretroviral therapy. The aim of the present study was to examine whether adiponectin concentration or insulin sensitivity level correlate with the modifications of lipid parameters after the switch of PI by nevirapine. Material and methods  The evolution of metabolic parameters before and after 6 months of substitution of nevirapine for protease inhibitors was evaluated in a cohort of 55 HIV‐1 infected patients. Adiponectin concentration, insulin sensitivity, lipid profile, cholesterol ester transfer protein (CETP) mass concentration and triglyceride enrichment of HDL were determined before and after the replacement of PI by nevirapine. Insulin sensitivity was evaluated by the HOMA model assessment. Results  Twenty‐four weeks of treatment with nevirapine improved significantly the lipid profile with a significant reduction of apoB (from 0·98 to 0·92 g L−1; P = 0·005) and triglyceride (from 2·02 to 1·66 mmol L−1; P = 0·02). HDL cholesterol and apoA1 increased significantly (from 0·99 to 1·19 mmol L−1; P = 0·001 and from 1·40 to 1·57 g L−1; P