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  14th European AiDS Conference
Oct 16-19 2013
Brussels, Belgium
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Low HDL Cholesterol Is Main Lipid Abnormality in HIV+/HIV- Comparison in HIV UPBEAT Study


14th European AIDS Conference. October 16-19, 2013. Brussels
Mark Mascolini
Low "good" high-density lipoprotein (HDL) cholesterol rather than high "bad" low-density lipoprotein (LDL) cholesterol proved the principal lipid abnormality in a prospective cohort of HIV-positive and negative people in Ireland [1]. HIV infection independently predicted a higher (worse) total-to-HDL cholesterol ratio, an established cardiovascular risk factor.
Despite ongoing study since the dawn of combination antiretroviral therapy (cART), lipid abnormalities in cART-treated people remain incompletely characterized, especially in relation to lipids in a similar cohort of HIV-negative people. To address this issue, researchers in Ireland and the United Kingdom analyzed lipid levels in 210 HIV-positive and 264 HIV-negative members of the prospective HIV UPBEAT cohort in Ireland. They compared fasting lipids between the two groups, including total cholesterol, HDL cholesterol, LDL cholesterol, total-to-HDL cholesterol ratio, and triglycerides.
Recruited between February 2011 and July 2012, HIV-positive and negative cohort members differed significantly in median age (39 with HIV versus 42 without HIV, P = 0.03), proportion of men (58.6% versus 43.6%, P = 0.001), proportion of Caucasians (60.5% versus 75.4%, P = 0.001), median body mass index (26 versus 27 kg/m(2), P = 0.05), median systolic blood pressure (127 versus 123 mm Hg, P = 0.05), proportion of current smokers (16.2% versus 36.3%, P = 0.0001), and proportion of statin users (3.1% versus 12.6%, P = 0.0002).
Compared with HIV-negative people, those with HIV had significantly lower HDL cholesterol (1.1 versus 1.4 mmol/L, P = 0.0001) and total cholesterol (4.7 versus 4.9 mmol/L, P = 0.01) and significantly higher total-to-HDL ratio (4.0 versus 3.4, P = 0.0001). While proportions with total cholesterol above 5.18 mmol/L did not differ significantly between groups (33.2% versus 39.4%, P = 0.21), a significantly higher proportion with HIV had a total-to-HDL ratio above 6.0 (13.2% versus 5.0%, P = 0.004). LDL cholesterol was marginally lower in the HIV group (2.9 versus 3.0 mmol/L, P = 0.09), while triglycerides were significantly higher in HIV-positive people (1.1 versus 0.9 mmol/L, P = 0.0001; proportion above 1.7 mmol/L, 21.6% versus 11.2%, P = 0.004).
A linear regression model adjusted for age, gender, ethnicity, smoking, and body mass index found no association between HIV and total cholesterol (parameter estimate [PE] -0.15, P = 0.11) or LDL cholesterol (PE -0.05, P = 0.57). But the same analysis linked HIV infection to significantly lower HDL cholesterol (PE -0.20, P = 0.0001), higher total-to-HDL ratio (PE 0.06, P = 0.0001), and higher triglycerides (PE 0.11, P = 0.0001).
Defining abnormal lipid values according to National Cholesterol Education Program cutoffs, the researchers found similar results in a regression model adjusted for the same variables. Odds of abnormal total cholesterol and LDL cholesterol did not differ significantly between the HIV-positive and negative groups. But the HIV group had significantly higher odds of abnormal HDL cholesterol (odds ratio [OR] 3.61, P = 0.0001), total-to-HDL ratio (OR 2.67, P = 0.01), and triglycerides (OR 2.37, P = 0.005). Repeating this analysis after excluding people taking statins or those with a drug-injecting history did not alter the results.
The HIV UPBEAT team concluded that in this contemporary prospective cohort, the principal lipid abnormalities involve HDL cholesterol and triglycerides, not LDL cholesterol. The independent association between HIV infection and a worse total-to-HDL ratio, the researchers noted, is driven by low HDL cholesterol.
1. Cotter AG, Sabin CA, Simelane S, et al. Reduced high density lipoprotein cholesterol rather than elevated low density lipoprotein is the principal dyslipidaemia in HIV-positive subjects on contemporary antiretroviral therapy. 14th European AIDS Conference. October 16-19, 2013. Brussels. Abstract PE 11/28.
Reported by Jules Levin