Higher levels of small low-density lipoprotein (LDL) and lower levels of high-density lipoprotein (HDL) subclasses have been associated with increased risk of cardiovascular disease. The extent to which HIV infection and HIV/hepatitis C virus (HCV) coinfection are associated with abnormalities of lipoprotein subclasses is unknown.
Lipoprotein subclasses were measured by nuclear magnetic resonance (NMR) spectroscopy in plasma samples from 569 HIV-infected and 5948 control participants in the Fat Redistribution and Metabolic Change in HIV Infection (FRAM), Coronary Artery Risk Development in Young Adults (CARDIA), and Multi-Ethnic Study of Atherosclerosis (MESA) studies. Multivariable regression was used to estimate the association of HIV and HIV/HCV coinfection with lipoprotein measures with adjustment for demographics, lifestyle factors, and waist-to-hip ratio.
Relative to controls, small LDL levels were higher in HIV-monoinfected persons (+381 nmol/l, P <0.0001), with no increase seen in HIV/HCV coinfection (−16.6 nmol/l). Levels of large LDL levels were lower (−196 nmol/l, P <0.0001) and small HDL were higher (+8.2 μmol/l, P < 0.0001) in HIV monoinfection with intermediate values seen in HIV/HCV coinfection. Large HDL levels were higher in HIV/HCV-coinfected persons relative to controls (+1.70 μmol/l, P <0.0001), whereas little difference was seen in HIV-monoinfected persons (+0.33, P = 0.075). Within HIV-infected participants, HCV was associated independently with lower levels of small LDL (−329 nmol/l, P <0.0001) and small HDL (−4.6 μmol/l, P <0.0001), even after adjusting for demographic and traditional cardiovascular risk factors.
HIV-monoinfected participants had worse levels of atherogenic LDL lipoprotein subclasses compared with controls. HIV/HCV coinfection attenuates these changes, perhaps by altering hepatic factors affecting lipoprotein production and/or metabolism. The effect of HIV/HCV coinfection on atherosclerosis and the clinical consequences of low small subclasses remain to be determined.
aDepartment of Medicine, University of California San Francisco
bDivision of Endocrinology and Metabolism, Department of Veterans Affairs Medical Center San Francisco, San Francisco
cDepartment of Medicine, University of California, San Diego School of Medicine, San Diego, California
dDepartment of Epidemiology, University of Washington, Seattle, Washington
eDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco
fDivision of Research, Kaiser Permanente, Oakland, California, USA.
Correspondence to Phyllis Tien, MD, Infectious Disease Section, Veterans Affairs Medical Center, University of California San Francisco, 111W, 4150 Clement Street, San Francisco, CA 94121, USA. Tel: +1 415 221 4810x2577; e-mail: email@example.com
Received 8 July, 2013
Accepted 6 August, 2013
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