NDLI: HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : Role of protease inhibitor exposure

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HAART drugs induce oxidative stress in human endothelial cells and increase endothelial recruitment of mononuclear cells : Exacerbation by inflammatory cytokines and amelioration by antioxidants

HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : Role of protease inhibitor exposure

Cardiovascular Toxicology : Volume 4, Issue 2, June 2004

Cardiovascular Toxicology : Volume 4, Issue 1, March 2004

Cardiovascular Toxicology : Volume 3

Cardiovascular Toxicology : Volume 2

Cardiovascular Toxicology : Volume 1

HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : Role of protease inhibitor exposure

Content Provider	Springer Nature Link
Author	Hurwitz, Barry E. Klimas, Nancy G. Llabre, Maria M. Maher, Kevin J. Skyler, Jay S. Bilsker, Martin S. McPherson Baker, Shvawn Lawrence, Peter J. LaPerriere, Arthur R. Greeson, Jeffrey M. Klaus, Johanna R. Lawrence, Rasha Schneiderman, Neil
Copyright Year	2004
Abstract	Differences on measures of metabolic syndrome X and coronary heart disease (CHD) risk, as well as potential pathophysiological mediators, inflammation, and oxidative stress, were examined as a function of HIV serostatus and highly active antiretroviral therapy (HAART) regimen with and without protease inhibitors (PIs). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HIV$^{+}$ subjects who were free of hepatitis C virus and were on a stable HAART regimen for ≥6 mo, with 82 seronegative subjects matched on age, sex, body mass index, and ethnicity. For the HIV$^{+}$ subjects, after controlling for diabetes status and HIV disease progression, PI exposure was associated with greater oxidative stress, triglyceridemia, and lipidemia than it was for non-PI-exposed HIV$^{+}$ subjects, and the risk of a future myocardial infarction was up to 56% greater in PI-exposed than in non-PI-exposed subjects and 129% greater than in controls. Although it is likely that the greatest proportion of CHD risk in the HIV$^{+}$ subjects may be accounted for by pathological conditions linked to HIV infection in interaction with mediating processes such as inflammation, central obesity, and dyslipidemia, which was greater than in controls, it appears that PI medications may exacerbate oxidative stress and hypertriglyceridemia to enhance this risk.
Starting Page	303
Ending Page	315
Page Count	13
File Format	PDF
ISSN	15307905
Journal	Cardiovascular Toxicology
Volume Number	4
Issue Number	3
e-ISSN	15590259
Language	English
Publisher	Humana Press
Publisher Date	2004-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	HIV/AIDS HAART coronary heart disease risk metabolic syndrome X inflammation oxidative stress Pharmacology/Toxicology Cardiology
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Toxicology Cardiology and Cardiovascular Medicine

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