The basis and management of metabolic abnormalities associated with cardiovascular risk in human immunodeficiency virus infection and its treatment.

The high global prevalence of human immunodeficiency virus (HIV) infection has been associated with high morbidity and mortality. The advent of highly active antiretroviral therapy (HAART) has, however, dramatically increased survival of patients infected with HIV. These patients now survive to develop metabolic complications of HIV infection and its treatment, including increased predisposition to atherosclerotic disease. HIV infection is normally associated with hypocholesterolaemia, hypertriglyceridaemia, low plasma HDL-cholesterol as well as alterations in other cardiovascular risk factors including inflammatory markers, clotting factors, homocysteine, apolipoproteins, lipoprotein (a), oxidative stress and non-esterified fatty acids. The use of HAART is, in particular, associated with dyslipidaemia and lipodystrophy with underlying insulin resistance and associated glucose intolerance. This article explores the metabolic abnormalities associated with increased cardiovascular risk that occur in HIV infection before and after antiretroviral therapy. The laboratory investigation and clinical management of HIV-associated dyslipidaemia and lipodystrophy will be discussed.