HIV infection and its treatment have been associated with adipose tissue changes and disorders of glucose and lipid metabolism. not accurately predict risk in the HIV setting due to HIV-related factors such as inflammation that are not accounted for. The relationship between HIV and diabetes mellitus (DM) risk has also been debated. We summarize the recent literature on metabolic syndrome DM and cardiovascular risk in HIV-infected adults. Keywords: HIV Metabolic Syndrome Diabetes Cardiovascular Risk Framingham Risk Score Lipodystrophy Syndrome Introduction Metabolic perturbations including insulin resistance diabetes and dyslipidemia have been of significant concern in HIV-infected adults since the introduction of effective antiretroviral therapy. This has been followed by studies showing that HIV-infected adults may be at risk of accelerated atherosclerosis and cardiovascular disease (CVD).1-4 While HIV infection and its therapies have been associated with adipose tissue changes and disorders of glucose and lipid metabolism that may prematurely U0126-EtOH increase CVD risk 5 more recent data suggest that immune activation and inflammation from chronic U0126-EtOH HIV infection may also play an important role.6 7 An understanding of the factors associated with metabolic perturbations and cardiovascular risk and their impact on vascular disease in the HIV-infected population is critical especially with the growing proportion of U.S. HIV-infected adults over the age of 50 years.8 The combination of HIV and aging related comorbidities on cardiovascular risk poses an important health challenge in these patients. We summarize the recent literature on the association of HIV with the metabolic syndrome diabetes mellitus (DM) and cardiovascular risk. U0126-EtOH Metabolic Syndrome The concept of a cluster of fat and metabolic factors associated with elevated risk for CVD in the general population was first described in 1977. Reaven et al9 refined this concept and described the cluster of factors as “syndrome X ” which is now commonly described as the metabolic syndrome and has been associated with CVD and death in several general population studies.10 11 While the specific criteria for metabolic U0126-EtOH syndrome has varied in national guidelines the most widely used definition clinically and in recent studies was developed in a 2004 collaboration Rabbit Polyclonal to CDKL1. between the American Heart Association and the NIH’s Heart Lung and Blood Institute to update the National Cholesterol Education Program Adult Treatment Panel III from 2001.12 The panel defined metabolic syndrome by three of the following five criteria: abdominal obesity (having a waist circumference >102 cm and >88 cm for men and women respectively); triglycerides ≥150 mg/dL; HDL cholesterol <40 mg/dL and <50 mg/dL for men and women respectively; blood pressure ≥130/≥85 mm Hg or on medication for hypertension; and fasting glucose ≥100 mg/dL or on medication for hyperglycemia. The predominance of HIV studies examining the metabolic syndrome has used this definition. Prior to studies of the metabolic syndrome in HIV-infected adults an "HIV-associated lipodystrophy syndrome" was described that included central lipohypertrophy or fat gain in central sites (abdominal obesity buffalo hump and breast enlargement in women) and lipoatrophy or fat loss in the periphery including the face arms legs and buttocks accompanied by insulin resistance and dyslipidemia.13 These fat and metabolic changes were observed soon after the introduction of highly active antiretroviral therapy (HAART) in the mid-1990s and thought to be attributed to HIV protease inhibitors.13 However subsequent studies found that in fact different factors were associated with each of the components of the lipodystrophy syndrome. Both the Study of Fat Redistribution and Metabolic Change in HIV infection (FRAM)14 15 and the Women's Interagency HIV Study (WIHS)16 found that when compared to HIV-uninfected adults HIV infection was neither associated with increased visceral adipose tissue measured by U0126-EtOH MRI nor central lipohypertrophy determined by self-report of fat gain in regional body sites and confirmed by regional anthropometry respectively. In the WIHS the rate of fat gain was similar in both.