Abstract
Background. Untreated human immunodeficiency virus (HIV) infection is associated with changes in blood lipids, inflammation, thrombotic activity, and increased risk for cardiovascular disease. Methods. We studied high-density lipoprotein particle (HDL p) concentrations and inflammatory (high-sensitivity C-reactive protein [hsCRP] and interleukin [IL] 6), endothelial activation (E-selectin and soluble intercellular adhesion molecule-1 [sICAM-1]), and thrombotic (fibrinogen and D-dimer) biomarkers in a group of 32 untreated HIV-infected and 29 uninfected persons. Differences in the levels of blood lipids and biomarkers by HIV status were examined before and after adjustment for age, sex, race/ethnicity, smoking status, body mass index, and the presence of hepatitis C. Results. HIV-infected participants, compared with uninfected participants, had lower HDL cholesterol (HDLc) levels (-26%) and HDLp numbers (-21%), with reductions in large (-50%) and small (-20%) HDLp, specifically (P≤.01 for all). A trend was present for higher total cholesterol (P = .15) and triglyceride levels (P = .11) among individuals with HIV infection. Levels of IL-6, sICAM-1, and D-dimer were 65%-70% higher in HIV-infected participants (P≤ .02 for all). Covariate adjustment did not diminish these associations. For HIV-infected participants, total and small HDLp (respectively) tended to correlate inversely with levels of IL-6 (P = .08 and P = .02), sICAM-1 (P<.01 for both) and D-dimer (P = .03 and P<.01). Conclusions. Persons with untreated HIV infection have lower HDLp (primarily large and small HDLp) and higher IL-6, sICAM-1, and D-dimer levels, and the relationship of these markers to HIV-mediated atherosclerotic risk requires further study.
Original language | English (US) |
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Pages (from-to) | 285-292 |
Number of pages | 8 |
Journal | Journal of Infectious Diseases |
Volume | 201 |
Issue number | 2 |
DOIs | |
State | Published - Jan 15 2010 |
Bibliographical note
Funding Information:Received 27 March 2009; accepted 25 August 2009; electronically published 1 December 2009. Potential conflicts of interest: K.H. has received research support from Bristol-Meyers Squibb, Tibotec, Glaxo-Smith-Kline, Serono, Thera, and Pfizer. All other authors: no conflicts. Financial support: National Institutes of Health (grant 5 T32 GM12453-03). Reprints or correspondence: Dr Jason Baker, 701 Park Ave, HCMC, MC G5, Minneapolis, MN 55415