Protease inhibitor-based HAART, HDL, and CHD-risk in HIV-infected patients

To study the effects of HIV-infection and protease inhibitor (PI)-based highly active anti-retroviral therapy (HAART) on the lipid and high-density lipoprotein (HDL) subpopulation profile and to relate the changes to coronary heart disease (CHD)-risk. The lipid and HDL subpopulation profiles of HIV-...

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Published in:Atherosclerosis Vol. 184; no. 1; pp. 72 - 77
Main Authors: Asztalos, Bela F., Schaefer, Ernst J., Horvath, Katalin V., Cox, Caitlin E., Skinner, Sally, Gerrior, Jul, Gorbach, Sherwood L., Wanke, Christine
Format: Journal Article
Language:English
Published: Amsterdam Elsevier Ireland Ltd 2006
Elsevier
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Summary:To study the effects of HIV-infection and protease inhibitor (PI)-based highly active anti-retroviral therapy (HAART) on the lipid and high-density lipoprotein (HDL) subpopulation profile and to relate the changes to coronary heart disease (CHD)-risk. The lipid and HDL subpopulation profiles of HIV-positive subjects ( n = 48) were studied prospectively by comparing pre- and post-PI-HAART data as well as cross-section by comparing the profiles to HIV-negative subjects with ( n = 96) and without CHD ( n = 96). HIV-infected HAART-naïve subjects had lower concentrations of low-density lipoprotein cholesterol (LDL-C) and HDL-C and higher concentration of triglycerides (TG) than healthy controls. After receiving PI-based HAART, LDL-C and TG concentrations increased, while HDL-C concentrations remained unchanged. The HDL subpopulation profiles of HAART-naïve HIV-positive patients were significantly different from those of healthy controls and were similar to those with CHD. Moreover, the HDL subpopulation profile changed unfavorably after PI-based HAART, marked with increased concentrations of the small, lipid-poor pre-β-1 HDL (32% or 3.9 mg/dl; p < 0.001), and decreased concentration of the large, cholesterol-rich α-1 HDL(9% or 1 mg/dl ns). An already unfavorable lipid and HDL subpopulation profile of HIV-positive HAART-naïve subjects further deteriorated after receiving PI-based treatment, which may cause increased CHD-risk in these subjects.
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ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2005.04.013