Metabolic Syndrome in HIV-Infected Patients
Metabolic Syndrome in HIV-Infected Patients
Abstract & Commentary
By Dean L. Winslow, MD, FACP, Chief, Division of AIDS Medicine, Santa Clara Valley Medical Center; Clinical Professor of Medicine, Stanford University School of Medicine, is Associate Editor for Infectious Disease Alert.
Dr. Winslow serves as a consultant to Siemens Diagnostics and is on the Speakers Bureaus of Boehringer-Ingelheim and GSK.
Source: Mondy K, et al. Metabolic syndrome in HIV-infected patients from an urban, midwestern U.S. outpatient population. Clin Infect Dis. 2007;44:726-734
Synopsis: 471 HIV-infected outpatients were assessed for the presence of metabolic syndrome using standard clinical and laboratory parameters. Compared to HIV-negative subjects selected from the National Health and Nutrition Examination Survey (NHANES) cohort the prevalence of metabolic syndrome was similar.
This important study compared an outpatient cohort of 471 HIV-infected outpatients living in the Midwest to data files from the NHANES cohort of HIV-negative subjects matched by age, sex, race, and tobacco use. Using standard criteria including waist circumference, blood pressure (or use of antihypertensive agents), fasting blood glucose and lipid levels (or use of lipid-lowering agents), the prevalence of metabolic syndrome was 25.5% in HIV infected patients and 26.5% in the NHANES cohort.
Looking in greater detail at the cohorts studied, the major risk factors for metabolic syndrome reaching statistical significance, were age, white ethnicity, duration of HIV infection, family history of diabetes and coronary artery disease, elevated BMI and waist circumference. Interestingly the use of highly active antiretroviral therapy (including ritonavir-boosted PIs) did not increase the likelihood of metabolic syndrome.
Commentary
Since the mid-1990s the use of highly active antiretroviral therapy (HAART) has resulted in a dramatic reduction in mortality due to HIV. However, shortly after the introduction of HIV protease inhibitors (PIs), the association between particular PI-based HAART and metabolic complications has been appreciated. Following institution of HAART many patients experience elevations of triglycerides and LDL cholesterol, hyperglycemia (or subclinical insulin resistance), and visceral fat accumulation. These characteristic components of the metabolic syndrome are risk factors for cardiovascular disease.
While this cohort study does not give HAART a clean bill of health, the results are intriguing and suggest that traditional risk factors for metabolic syndrome are of greater importance than HAART in HIV-infected patients. Anecdotally, over the last 12 years I have often noted the phenomenon of some patients who have fairly advanced disease and experience an excellent virologic and immunologic response to HAART develop significant weight gain probably related to improved appetite and overall improved sense of well-being. This occurs on both PI and nnRTI-based HAART. Subconsciously I think many clinicians blame the resultant dyslipidemias or glucose intolerance on the HAART regimen if it contains a PI and on the weight gain if the same abnormalities appear on an nnRTI-containing HAART regimen. The reality, it seems, is that probably the biggest factors for development of metabolic syndrome in HIV-infected patients are the same ones at play in HIV-negative patients.
For those of us who began taking care of HIV patients in the early 1980s and seeing so many of our patients dying of AIDS, having to worry about risk factors for cardiovascular disease in our patients, as we do now, is indeed a blessing.
This important study compared an outpatient cohort of 471 HIV-infected outpatients living in the Midwest to data files from the NHANES cohort of HIV-negative subjects matched by age, sex, race, and tobacco use.Subscribe Now for Access
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