Does HIV Infection Predispose to the Metabolic Syndrome?
Does HIV Infection Predispose to the Metabolic Syndrome?
A large cohort study suggests that neither HIV infection nor antiretroviral treatment confers additional risk.
Several large studies have suggested an increased cardiovascular risk from long-term use of antiretroviral therapy, but few researchers have attempted to establish the independence of this association from the burgeoning epidemic of obesity-related cardiovascular illness in the U.S. To address this question, investigators compared the prevalence of the metabolic syndrome in HIV-infected and -uninfected populations.
The metabolic syndrome was diagnosed in 120 (25%) of 471 HIV-infected patients who attended a single Midwestern urban clinic in 2005 and had complete clinical and laboratory information available. Independent predictors of metabolic syndrome in multivariate analysis were older age, higher CD4-cell count, white race, and higher BMI. Use of potent combination antiretroviral therapy and the type of drugs used were not significant predictors.
The prevalence of the metabolic syndrome was virtually the same in this cohort as in a control group selected from the large national NHANES database and matched for age, sex, race, and tobacco use. However, among both those with the syndrome and those without it, individual metabolic parameters differed significantly between groups: The HIV-infected group had a smaller mean waist circumference, lower mean BMI, and a lower mean glucose level than did the NHANES group. They also had a lower mean HDL-cholesterol level and higher fasting triglyceride level, and nearly twice as many were receiving lipid-lowering therapy. Mean Framingham scores of coronary disease risk were similar in the groups.
These findings suggest that the metabolic syndrome is no more common among HIV-infected people than among their uninfected peers; thus, traditional risks for coronary disease could be more important in an aging HIV-infected population than are the specific risks imposed by either HIV infection or its treatment. However, the lipid abnormalities in this HIV-infected group were quite prominent, raising the possibility that we might eventually need to reconfigure our calculation of cardiac risk for people with HIV infection to account for the severity of the dyslipidemia. As always, clinical endpoints, rather than a tangle of surrogate markers, are sorely needed.
A large cohort study suggests that neither HIV infection nor antiretroviral treatment confers additional risk.
Several large studies have suggested an increased cardiovascular risk from long-term use of antiretroviral therapy, but few researchers have attempted to establish the independence of this association from the burgeoning epidemic of obesity-related cardiovascular illness in the U.S. To address this question, investigators compared the prevalence of the metabolic syndrome in HIV-infected and -uninfected populations.
The metabolic syndrome was diagnosed in 120 (25%) of 471 HIV-infected patients who attended a single Midwestern urban clinic in 2005 and had complete clinical and laboratory information available. Independent predictors of metabolic syndrome in multivariate analysis were older age, higher CD4-cell count, white race, and higher BMI. Use of potent combination antiretroviral therapy and the type of drugs used were not significant predictors.
The prevalence of the metabolic syndrome was virtually the same in this cohort as in a control group selected from the large national NHANES database and matched for age, sex, race, and tobacco use. However, among both those with the syndrome and those without it, individual metabolic parameters differed significantly between groups: The HIV-infected group had a smaller mean waist circumference, lower mean BMI, and a lower mean glucose level than did the NHANES group. They also had a lower mean HDL-cholesterol level and higher fasting triglyceride level, and nearly twice as many were receiving lipid-lowering therapy. Mean Framingham scores of coronary disease risk were similar in the groups.
These findings suggest that the metabolic syndrome is no more common among HIV-infected people than among their uninfected peers; thus, traditional risks for coronary disease could be more important in an aging HIV-infected population than are the specific risks imposed by either HIV infection or its treatment. However, the lipid abnormalities in this HIV-infected group were quite prominent, raising the possibility that we might eventually need to reconfigure our calculation of cardiac risk for people with HIV infection to account for the severity of the dyslipidemia. As always, clinical endpoints, rather than a tangle of surrogate markers, are sorely needed.
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