Effect of pravastatin on body composition and markers of cardiovascular disease in HIV-infected men--a randomized, placebo-controlled study

• Published in: AIDS (London) Vol. 20; no. 7; pp. 1003 - 1010
• Main Authors: Mallon, Patrick W G, Miller, John, Kovacic, Jason C, Kent-Hughes, Julia, Norris, Richard, Samaras, Katherine, Feneley, Michael P, Cooper, David A, Carr, Andrew
• Format: Journal Article
• Language: English
• Published: England 24.04.2006
• Subjects: Adipose Tissue - chemistry; AIDS/HIV; Antiretroviral Therapy, Highly Active - methods; Biomarkers - blood; Blood Glucose - analysis; Body Composition - drug effects; Cardiovascular Diseases - blood; Cardiovascular Diseases - diagnosis; Cholesterol - blood; Diet; Double-Blind Method; HIV Infections - complications; HIV Infections - drug therapy; HIV Infections - physiopathology; HIV Protease Inhibitors - therapeutic use; HIV-Associated Lipodystrophy Syndrome - drug therapy; HIV-Associated Lipodystrophy Syndrome - physiopathology; Human immunodeficiency virus; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Hypercholesterolemia - complications; Hypercholesterolemia - drug therapy; Hypercholesterolemia - physiopathology; Insulin - blood; Male; Middle Aged; Pilot Projects; Pravastatin - therapeutic use; Triglycerides - blood
• ISSN: 0269-9370
• DOI: 10.1097/01.aids.0000222072.37749.5a

To determine the effect of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, pravastatin, on markers of cardiovascular risk and lipodystrophy in HIV-infected, protease inhibitor (PI)-treated men with hypercholesterolaemia. A randomized, placebo-controlled, 16-week study was carried out on 33 HIV-infected, hypercholesterolaemic men (fasting total cholesterol > 6.5 mmol/L) on PI-containing therapy. Patients commenced dietary assessment and advice at week 0 and were randomized to 12 weeks pravastatin (40 mg each night) or placebo from week 4. The primary endpoint was the time-weighted change (TWAUC) in total cholesterol from week 0. Secondary endpoints included TWAUC cholesterol from week 4 (start of pravastatin), total and regional body fat, fasting lipids, glucose, insulin, and markers of cardiovascular risk. Of 33 men randomized (pravastatin n = 16, mean age 48 years), 31 completed the study. Groups were matched for baseline cholesterol and body composition. Although there was no significant between-group difference in TWAUC cholesterol from week 0 (pravastatin -0.6 +/- 1.0 versus placebo -0.4 +/- 1.0 mmol/L/week; P = 0.8), TWAUC cholesterol from week 4 decreased more in the pravastatin group (-0.8 +/- 1.0 versus -0.3 +/- 0.9 mmol/L/week; P = 0.04). Neither triglycerides nor dietary intake changed. Subcutaneous fat increased significantly with pravastatin (+0.72 +/- 1.55 versus +0.19 +/- 0.48 kg change in limb fat, P < 0.04; +5.2 +/- 8.7 versus -1.3 +/- 13.7 cm change in abdominal subcutaneous fat, P = 0.02). Apart from homocystine, which decreased in the pravastatin group, there were no significant differences in other cardiovascular, lipid or glucose parameters. Despite limited effects on cholesterol, 12 weeks use of pravastatin 40 mg each night in HIV-infected men with hypercholesterolaemia resulted in significant increases in subcutaneous fat.