HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk

Role of protease inhibitor exposure

Barry Hurwitz, Nancy G. Klimas, Maria Llabre, Kevin J. Maher, Jay S Skyler, Martin S Bilsker, Shvawn McPherson-Baker, Peter J. Lawrence, Arthur R. LaPerriere, Jeffrey M. Greeson, Johanna R. Klaus, Rasha Lawrence, Neil Schneiderman

Research output: Contribution to journalArticle

28 Citations (Scopus)

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 (Pls). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HlV+ 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 HlV+ 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.

Original languageEnglish
Pages (from-to)303-315
Number of pages13
JournalCardiovascular Toxicology
Volume4
Issue number3
DOIs
StatePublished - Oct 29 2004

Fingerprint

Metabolic Syndrome X
Oxidative stress
Protease Inhibitors
Coronary Disease
Oxidative Stress
HIV
Inflammation
Highly Active Antiretroviral Therapy
Inflammation Mediators
Abdominal Obesity
Hypertriglyceridemia
Medical problems
Dyslipidemias
Hyperlipidemias
Viruses
Hepacivirus
HIV Infections
Disease Progression
Body Mass Index
Myocardial Infarction

Keywords

  • Coronary heart disease risk
  • HAART
  • HIV/AIDS
  • Inflammation
  • Metabolic syndrome X
  • Oxidative stress

ASJC Scopus subject areas

  • Toxicology
  • Cardiology and Cardiovascular Medicine

Cite this

HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : Role of protease inhibitor exposure. / Hurwitz, Barry; Klimas, Nancy G.; Llabre, Maria; 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.

In: Cardiovascular Toxicology, Vol. 4, No. 3, 29.10.2004, p. 303-315.

Research output: Contribution to journalArticle

Hurwitz, Barry ; Klimas, Nancy G. ; Llabre, Maria ; 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. / HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : Role of protease inhibitor exposure. In: Cardiovascular Toxicology. 2004 ; Vol. 4, No. 3. pp. 303-315.
@article{18e907a8474648029bb34beb63575de0,
title = "HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk: Role of protease inhibitor exposure",
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 (Pls). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HlV+ 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 HlV+ 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.",
keywords = "Coronary heart disease risk, HAART, HIV/AIDS, Inflammation, Metabolic syndrome X, Oxidative stress",
author = "Barry Hurwitz and Klimas, {Nancy G.} and Maria Llabre and Maher, {Kevin J.} and Skyler, {Jay S} and Bilsker, {Martin S} and Shvawn McPherson-Baker and Lawrence, {Peter J.} and LaPerriere, {Arthur R.} and Greeson, {Jeffrey M.} and Klaus, {Johanna R.} and Rasha Lawrence and Neil Schneiderman",
year = "2004",
month = "10",
day = "29",
doi = "10.1385/CT:4:3:303",
language = "English",
volume = "4",
pages = "303--315",
journal = "Cardiovascular Toxicology",
issn = "1530-7905",
publisher = "Humana Press",
number = "3",

}

TY - JOUR

T1 - HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk

T2 - Role of protease inhibitor exposure

AU - Hurwitz, Barry

AU - Klimas, Nancy G.

AU - Llabre, Maria

AU - Maher, Kevin J.

AU - Skyler, Jay S

AU - Bilsker, Martin S

AU - McPherson-Baker, Shvawn

AU - Lawrence, Peter J.

AU - LaPerriere, Arthur R.

AU - Greeson, Jeffrey M.

AU - Klaus, Johanna R.

AU - Lawrence, Rasha

AU - Schneiderman, Neil

PY - 2004/10/29

Y1 - 2004/10/29

N2 - 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 (Pls). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HlV+ 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 HlV+ 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.

AB - 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 (Pls). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HlV+ 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 HlV+ 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.

KW - Coronary heart disease risk

KW - HAART

KW - HIV/AIDS

KW - Inflammation

KW - Metabolic syndrome X

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=20844453563&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=20844453563&partnerID=8YFLogxK

U2 - 10.1385/CT:4:3:303

DO - 10.1385/CT:4:3:303

M3 - Article

VL - 4

SP - 303

EP - 315

JO - Cardiovascular Toxicology

JF - Cardiovascular Toxicology

SN - 1530-7905

IS - 3

ER -