Up-to-date therapy has in recent years substantially modified the clinical course of HIV infections and AIDS. The progress of the disorder has changed-today it is a chronic disease of many years. Already in 1997 and 1998 it transpired that long-term HAART, highly active antiretroviral therapy, produced adverse metabolic changes, which significantly affect the subsequent progress of the disease. The mechanism responsible for these metabolic changes has not, as yet, been fully clarified-in all probability its etiology is multifactorial. Even prior to the introduction of HAART, some metabolic changes were observed in HIV-infected subjects. These changes are, however, not specific for the pathogen concerned, they are generally seen in acute inflammatory reactions. Since the introduction of HAART in 1996 the range of metabolic changes has expanded. Gradually we detect more and more anthropometric, metabolic and coagulation changes, closely resembling changes seen in the metabolic syndrome (SIR, syndrome of insulin resistance), well known from cardiology and internal medicine-dyslipoproteinaemia, insulin resistance, abdominal obesity. A combination of these disorders is clinically significant due to their role in the development of atherosclerosis and their by no means negligible involvement in the onset of ischaemic heart disease. In view of the much lower mean age of HIV-positive subjects the earlier mentioned complications should be expected in much lower age categories than with HIV-negative individuals. The paper discusses the possible pathogenesis and potential mechanisms of metabolic complications related to HAART, its impact on the cardiovascular risk and the possibilities of hypolipidaemic therapy in HIV-positive patients.