Journal
AIDS
Volume 26, Issue 14, Pages 1801-1805Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0b013e328357063c
Keywords
atherogenic phenotype; HIV-1; low-density lipoprotein subfractions; pravastatin; protease inhibitor; rosuvastatin
Categories
Funding
- Gilead Sciences
- Solvay
- Pfizer
- AstraZeneca
- Merck
- Sanofi Aventis
- Bristol-Myers-Squibb
- Roche
- Tibotec (Johnson and Johnson)
- GlaxoSmithKline
- Bristol-Meyers Squibb
- MSD
- Boehringer Ingelheim
- Abbott
- Boehringer-Ingelheim
- Glaxo-Smith-Kline
- Janssen
- ViiV Healthcare
- French National Agency for AIDS and Viral Hepatitis Research (ANRS)
- Astra Zeneca
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Objective: HIV infection is associated with an atherogenic lipoprotein profile, and ritonavir-boosted protease inhibitors exacerbate this phenotype. We evaluated the effect of 45 clays of rosuvastatin versus pravastatin on the low-density lipoprotein (LDL) size and the distribution of LDL subfractions in HIV-1 patients receiving boosted protease inhibitors with elevated LDL levels. Design: Substucly of the randomized double-blind multicentre ANRS 126 VIHstatine trial. Setting: Twenty clinical centres in France. Patients: HIV-infected patients receiving boosted protease inhibitors with dyslipidaemia (LDL cholesterol >4.1 mmol/l and triglycerides <8.8 mmol/l). Intervention: Rosuvastatin 10 mg/day (n = 39) or pravastatin 40 mg/day (n = 37) for 45 clays. Main outcome measure(s): LDL size and distribution of LDL subfractions blindly assessed by gradient gel electrophoresis at baseline and at day 45. Results: Rosuvastatin was more effective than pravastatin in increasing the diameter of the LDL peak. The LDL diameter change was 0.33 +/- 0.59 nm in the rosuvastatin group versus -0.01 +/- 0.52 nm in the pravastatin group (P=0.021). Rosuvastatin was also more effective in increasing significantly the percentage of large LDL (LDL1, P=0.038; LDL2, P=0.031) and in decreasing the percentage of small LDL (LDL3, P=0.009). Conclusion: Rosuvastatin was more effective than pravastatin in normalizing LDL size and LDL subfraction distributions, leading to a less atherogenic phenotype. (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
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