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.

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.

Effects of nevirapine, compared with lamivudine, on lipids and lipoproteins in HIV-1-uninfected newborns: the stopping infection from mother-to-child via breast-feeding in Africa lipid substudy.

Background: The objective of the present study was to assess whether the high-density lipoprotein cholesterol (HDL-c)-increasing effect of nevirapine (NVP), as observed in human immunodeficiency virus type 1 (HIV-1)-infected subjects, at least in part may relate to intrinsic properties of NVP.

Methods: At 2, 6, and 12 weeks after birth, complete lipid profiles as well as plasma apolipoproteins levels were assessed in 80 HIV-uninfected newborns, half of whom received NVP and half lamivudine (3TC), respectively. Newborns were randomly selected from a randomized trial in which NVP or 3TC had been administered to HIV-uninfected infants born to HIV-infected mothers to try and prevent HIV-1 transmission from occurring during breast-feeding.

Hepatic and cardiovascular consequences of familial hypobetalipoproteinemia.

Objective: Individuals with familial hypobetalipoproteinemia (FHBL) have been reported to be prone to fatty liver disease (FLD). Conversely, the profound reduction of low-density lipoprotein (LDL) cholesterol in this disorder might decrease cardiovascular risk. In the present study, we assessed hepatic steatosis as well as noninvasive surrogate markers for cardiovascular disease (CVD) in subjects with FHBL and in matched controls.

Surrogate markers for atherosclerotic disease.

Purpose Of Review: Novel treatment modalities for cardiovascular prevention are emerging rapidly. Since it is virtually impossible to evaluate all these new compounds in long-term trials using clinical end points, there is an urgent need for validated surrogate markers of atherosclerosis to save both time and costs. Over the last decade, the use of imaging markers has been widely introduced into drug-development strategies.