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In HIV-infected men, both untreated and on antiretroviral therapy, and in HIV-uninfected men, greater interleukin-6 (IL-6), D-dimer, and intercellular adhesion molecule-1 (ICAM-1) levels are associated with lower small HDL particle number (HDL-P), and greater IL-6 and ICAM-1 levels are associated with lower total HDL-P., Objective Low HDL cholesterol (HDL-C) is common in people living with HIV infection, which is associated with inflammation, and correlates with greater cardiovascular disease (CVD) risk. Particles of HDL are HDL subfractions, and in some general population studies, higher small HDL particle number (HDL-P) has been associated with lower CVD risk. The objective of this study was to determine whether HIV serostatus and systemic inflammation were associated with small HDL-P in the Multicenter AIDS Cohort Study (MACS). Method The MACS is composed of HIV-infected and HIV-uninfected men. Separate linear regression analyses were conducted to evaluate the associations between outcomes (small HDL-P, large HDL-P, total HDL-P, and HDL size) and variables of interest (interleukin-6 [IL-6], D-dimer, and intercellular adhesion molecule-1 [ICAM-1] levels), with adjustment for other CVD risk factors. Results The study population included 553 HIV-infected (88.1% on current ART) and 319 HIV-uninfected men. The mean age was 52.7 years for HIV-infected men and 55.3 years for HIV-uninfected men. In separate models of the study population, higher log IL-6 was associated with lower total and small HDL-P (P < .01 for both), independent of HIV serostatus and CVD risk factors. Similar results were seen with ICAM-1. Positive HIV serostatus was associated with lower small and total HDL-P, adjusted for inflammatory markers. Conclusions Greater systemic inflammation and HIV infection both were associated with lower atheroprotective small HDL-P. This may be a potential mechanism contributing to increased cardiovascular risk among HIV-infected people.

Methods. In a cross-sectional substudy of the Multicenter AIDS Cohort Study, noncontrast cardiac computed tomography (CT) scanning for coronary artery calcium (CAC) scoring was performed on all men, and, for men with normal renal function, coronary CT angiography (CTA) was performed. Associations between fat depots (visceral adipose tissue [VAT], abdominal subcutaneous adipose tissue [aSAT], and thigh subcutaneous adipose tissue [tSAT]) with coronary plaque presence and extent were assessed with logistic and linear regression adjusted for age, race, cardiovascular disease (CVD) risk factors, body mass index (BMI), and human immunodeficiency virus (HIV) parameters. Results. Among HIV-infected men (n = 597) but not HIV-uninfected men (n = 343), having greater VAT was positively associated with noncalcified plaque presence (odds ratio [OR] = 1.04, P < .05), with a significant interaction (P < .05) by HIV serostatus. Human immunodeficiency virus-infected men had lower median aSAT and tSAT and greater median VAT among men with BMI Conclusions. The presence of greater amounts of VAT and lower SAT may contribute to increased risk for coronary artery disease among HIV-infected persons.

Background. Although liver disease commonly causes morbidity and mortality among human immunodeficiency virus (HIV)‐infected individuals, data are limited on its prevalence in HIV monoinfection. We used the aspartate aminotransferase-to-platelet ratio index (APRI) as a surrogate marker of hepatic fibrosis to characterize liver disease in the Multicenter AIDS Cohort Study. Methods. Men were categorized based on their HIV and viral hepatitis status: uninfected (n 5 1170), HIV monoinfected (n 5 509), viral hepatitis monoinfected (n 5 74), and HIV‐viral hepatitis coinfected (n 5 66). Results. The median APRI in the HIV-monoinfected group was similar to that in the hepatitis-monoinfected group (0.42 vs 0.43; P . .05), higher than in the uninfected group (0.42 vs 0.27; P , .001) but lower than in the coinfected group (0.42 vs 1.0; P , .001). On multivariable analysis, HIV infection (1.39-fold increase [FI]; P , .001), viral hepatitis infection (1.52-FI; P , .001), and the interaction between HIV and viral hepatitis infections were independently associated with a higher APRI (1.57-FI; P , .001). Among the HIV-infected men, viral hepatitis coinfection (2.34-FI; P , .001), HIV RNA $100 000 copies/mL (1.26-FI; P 5 .007), and CD4 count #200 cells/mL (1.23-FI; P 5 .022) were independently associated with a higher APRI. Conclusions. HIV and viral hepatitis are independently associated with an increased APRI. Further studies are needed to understand the biological basis for the association between HIV and liver disease.