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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

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Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

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Impact of genetic polymorphisms on the risk of lipid disorders in patients on anti-HIV therapy

Eric Bonnet1 / Annelise Genoux2 / Jacques Bernard3 / Josette Fauvel4 / Patrice Massip5 / Bertrand Perret6

1INSERM U563, Department of Lipoproteins and Lipid Mediators, CHU, Toulouse, France and Department of Infectious Diseases, Université Paul Sabatier, CHU, Toulouse, France

2INSERM U563, Department of Lipoproteins and Lipid Mediators, CHU, Toulouse, France

3Department of Infectious Diseases, Université Paul Sabatier, CHU, Toulouse, France

4INSERM U563, Department of Lipoproteins and Lipid Mediators, CHU, Toulouse, France

5Department of Infectious Diseases, Université Paul Sabatier, CHU, Toulouse, France

6INSERM U563, Department of Lipoproteins and Lipid Mediators, CHU, Toulouse, France

Corresponding author: Bertrand Perret, INSERM U563, bâtiment C, BP 3028, Hôpital Purpan, 31024 Toulouse Cédex 3, France Phone: +33-5-61779404, Fax: +33-5-61779401

Citation Information: Clinical Chemical Laboratory Medicine. Volume 45, Issue 7, Pages 815–821, ISSN (Online) 14374331, ISSN (Print) 14346621, DOI: 10.1515/CCLM.2007.140, July 2007

Publication History

Published Online:


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)

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