Treatment with pravastatin and fenofibrate improves atherogenic lipid profiles but not inflammatory markers in ACTG 5087

ObjectivesStatins and fibrates alter lipids, apolipoproteins, and inflammatory markers in persons without HIV. The objective of this study was to evaluate changes in lipoproteins, apolipoproteins, and other markers of inflammation with the use of pravastatin and fenofibrate.DesignEvaluation of participants in ACTG A5087, a randomized trial of pravastatin 40 mg/day or fenofibrate 200 mg/day for the treatment of dyslipidemia. Participants that failed single-agent therapy at week 12 were given the combination.MethodsParticipants with available specimens were tested for apolipoproteins A1 and B, adiponectin, plasminogen-activator inhibitor type 1 (PAI-1), P-selectin, and high-sensitivity C-reactive protein (hs-CRP).ResultsA total of 74 participants (37 per randomized arm) received either pravastatin or fenofibrate for 12 weeks with 60 receiving combination treatment from weeks 12 to 48. There were no significant changes in hs-CRP, PAI-1, and P-selectin. From baseline to week 12, the median Apo B levels (−8 mg/dL, P = .01 for fenofibrate and −27 mg/dL, P < .01 for pravastatin) and ApoB/A1 ratios (−0.16, P < .01 for both arms) significantly decreased. From baseline to week 48, median adiponectin (−1 ng/dL, P < .01), Apo B (−22 mg/dL, P < .01) and Apo B/A1 ratios (−0.2, P < .01) all decreased in those who went on combination therapy, whereas Apo A1 (9.5 mg/dL, P = .01) levels increased.ConclusionTreatment with pravastatin or fenofibrate improves the atherogenic lipid profile within the first 12 weeks and is sustained through 48 weeks with combination therapy. Adiponectin levels decrease with lipid-lowering therapy. However, markers of inflammation and platelet activation were not appreciably changed suggesting that the biologic properties of these agents differ in persons with HIV infection.