High-density lipoprotein particles and markers of inflammation and thrombotic activity in patients with untreated HIV infection

Jason Baker, Woubeshet Ayenew, Harrison Quick, Katherine Huppier Hullsiek, Russell Tracy, Keith Henry, Daniel Duprez, James D. Neaton

Research output: Contribution to journalArticlepeer-review

62 Scopus citations

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 languageEnglish (US)
Pages (from-to)285-292
Number of pages8
JournalJournal of Infectious Diseases
Volume201
Issue number2
DOIs
StatePublished - 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

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