Nevirapine increases high-density lipoprotein cholesterol concentration by stimulation of apolipoprotein A-I production.

Objective: The purpose of this study was to investigate the mechanism by which the nonnucleoside reverse transcriptase inhibitor (NNRTI) nevirapine (NVP) increases high-density lipoprotein cholesterol (HDLc) in treatment-experienced human immunodeficiency virus-1 (HIV-1)-infected patients.

Methods And Results: Twelve HIV-1 infected patients, with stably suppressed HIV-1 viral load using AZT/3TC/abacavir for > or =6 months, added NVP to their current antiretroviral regimen. Patients received a primed bolus infusion of the stable isotope L-[1-(13)C]-valine for 12 hours before, as well as 6 and 24 weeks after, the addition of NVP to study apolipoprotein A-I (apoA-I) kinetics.

Increased carotid intima-media thickness in HIV patients treated with protease inhibitors as compared to non-nucleoside reverse transcriptase inhibitors.

Background: Prolonged exposure to protease inhibitor (PI)-, but not non-nucleoside reverse transcriptase inhibitor (NNRTI)-containing combination antiretroviral therapy (CART) has been associated with an increased cardiovascular risk, partly explained by the different effects of these drugs on plasma lipids. Most markedly, NNRTIs have been associated with increases in high density lipoprotein cholesterol (HDL-C), which may be atheroprotective.

Methods: In a cross-sectional study we investigated the impact of PI- vs.

Pharmacokinetics and pharmacodynamics of combined use of lopinavir/ritonavir and rosuvastatin in HIV-infected patients.

Background: Lopinavir/ritonavir-containing antiretroviral therapy can cause hyperlipidaemia. However, most statins are contraindicated due to drug-drug interactions. Rosuvastatin undergoes minimal metabolism by CYP450, so no CYP450-based interaction with lopinavir/ritonavir is expected.

Atherosclerotic vascular disease in HIV: it is not just antiretroviral therapy that hurts the heart!

Purpose Of Review: Although potent combination antiretroviral therapy has heralded an unparalleled improvement in the treatment of HIV-1-infected patients, the now well known metabolic complications of treatment, which include dyslipidemia, insulin resistance and changes in body fat distribution, are thought to contribute to an increased risk of atherosclerotic (cardio)vascular disease. Atherogenic changes in plasma lipids as well as some evidence of increased atherogenesis, however, had already been described in HIV-1-infected patients prior to the availability of combination antiretroviral therapy and even prior to that of suboptimal antiretroviral therapy. In this review, we will summarize the various possible factors and mechanisms involved in atherogenesis in HIV-1-infected individuals, with a focus on those mechanisms related to the infection itself and its immunological consequences.