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Impact of genetic polymorphisms on the risk of lipid disorders in patients on anti-HIV therapy
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Eric Bonnet
Published/Copyright:
July 8, 2007
Abstract
Active anti-HIV therapy can induce hypertriglyceridemia, low high-density lipoprotein (HDL) and insulin resistance, eventually accompanied by clinical lipodystrophy, associated loss of subcutaneous adipose tissue and an increase in abdominal adiposity. The frequency of these metabolic disorders is approximately 50% and host genetic factors might confer particular susceptibility. Variants of apolipoproteins (apo) A5 and C3, interacting with APOE genotypes, have been associated with the severity of antiretroviral therapy-induced dyslipidemia and with occurrence of lipodystrophy, and for APOC3, with objective criteria of fat redistribution. Genetic polymorphisms of the nuclear transcription-factor sterol response element-binding proteins (SREBP1c) and of tumor necrosis factor-α (TNFα) have yielded contrasting results. Other candidate genes will be explored to define a pharmacogenomic strategy to identify patients at high risk of metabolic disorders upon antiretroviral therapy.
Clin Chem Lab Med 2007;45:815–21.
Keywords: antiretroviral therapy; apolipoprotein A-V; apolipoprotein C-III; apolipoprotein E; dyslipidemia; HIV; lipodystrophy; pharmacogenomics; protease inhibitors; tumor necrosis factor-α (TNFα)
Received: 2006-12-4
Accepted: 2007-1-15
Published Online: 2007-07-08
Published in Print: 2007-07-01
©2007 by Walter de Gruyter Berlin New York
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Keywords for this article
antiretroviral therapy;
apolipoprotein A-V;
apolipoprotein C-III;
apolipoprotein E;
dyslipidemia;
HIV;
lipodystrophy;
pharmacogenomics;
protease inhibitors;
tumor necrosis factor-α (TNFα)
Articles in the same Issue
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