Hyperlipidemia and glucose intolerance in patients with HIV infection receiving antiretroviral therapy]

Objective. To determine the prevalence of secondary effects on lipid metabolism as a result of highly active antiretroviral therapy (HAART), as well as the impact of different types of antiretroviral regimens on lipids and glucose in a group of patients in Yucatan, Mexico. Material and Methods. A cross-sectional study was conducted. A questionnaire created for this study was administered to each patient and total cholesterol, triglycerides and fasting glucose values were determined. The presence of hyperlipidemia and alterations in glucose were determined as well as their relation to the epidemiological variables obtained from the questionnaire. Results. A total of 211 subjects were studied [36 (17%) of which were women and 175 (83%) men]. Ninety-two patients (44%) were found to have hyperlipidemia. Of these, 43 (20%) had hypercholesterolemia (HC) and 82 (39%) hypertriglyceridaemia (HT). The presence of combined HC and HT was observed in 30 (14%) patients. Nineteen (9%) patients had alterations in glucose, six (3%) diabetes mellitus and 13 (6%) impaired glucose tolerance. The variables associated with the presence of hyperlipidemia were: levels of lymphocytes CD49 > 350 cells/mu l (OR= 2.79 1.08-7.27, p= 0.03), male gender (OR= 3.6 1.4-9.12, p= 0.006) and the use of nucleoside-reverse transcriptase inhibitors (NRTI) (OR= 3.1 1.2-8.1, p=0.01). Conclusions. Patients with HIV infection who receive HAART have an increased risk of presenting hyperlipidemia. In this group of patients the presence of hyperlipidemia and impaired glucose tolerance was significant. Unlike what has been indicated in most published reports, the alterations of lipids were associated more frequently with INTR use, for which it is concluded that the pathogeny of these alterations is not unique, that it is probable that concurrent effects exist between different antiretroviral drug families and that other host factors are involved in the pathogenic mechanism of these alterations.