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 |
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Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Amsterdam
Elsevier Ireland Ltd
2006
Elsevier |
Subjects: | |
Online Access: | Get full text |
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9150 1879-1484 |
DOI: | 10.1016/j.atherosclerosis.2005.04.013 |