Division of Infectious Diseases, Department of Internal Medicine, University of Cincinnati College of Medicine, PO Box 670405, 231 Albert Sabin Way, Cincinnati, OH 45267-0405, USA.
J Clin Lipidol. 2010 Jul-Aug;4(4):279-87. doi: 10.1016/j.jacl.2010.04.003.
Statins 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.
Evaluation 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.
Participants 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).
74 participants (37 per randomized arm) received either pravastatin or fenofibrate for 12 weeks with 60 receiving combination treatment from weeks 12-48. 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=0.01 for fenofibrate and -27 mg/dL, P<0.01 for pravastatin) and ApoB/A1 ratios (-0.16, P<0.01 for both arms) significantly decreased. From baseline to week 48, median adiponectin (-1 ng/dL, P<0.01), Apo B (-22 mg/dL, P<0.01) and Apo B/A1 ratios (-0.2, P<0.01) all decreased in those who went on combination therapy, whereas Apo A1 (9.5 mg/dL, P=0.01) levels increased.
Treatment 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.
他汀类药物和贝特类药物可改变无 HIV 感染者的脂质、载脂蛋白和炎症标志物。本研究旨在评估普伐他汀和非诺贝特的应用对脂蛋白、载脂蛋白和其他炎症标志物的影响。
评价 ACTG A5087 参与者，这是一项普伐他汀 40mg/天或非诺贝特 200mg/天治疗血脂异常的随机试验。在第 12 周未能单药治疗的参与者接受联合治疗。
有可用标本的参与者接受载脂蛋白 A1 和 B、脂联素、纤溶酶原激活物抑制剂-1（PAI-1）、P 选择素和高敏 C 反应蛋白（hs-CRP）检测。
74 名参与者（随机分组每组 37 名）接受普伐他汀或非诺贝特治疗 12 周，其中 60 名从第 12 周到第 48 周接受联合治疗。hs-CRP、PAI-1 和 P 选择素无显著变化。从基线到第 12 周，载脂蛋白 B 水平中位数下降（非诺贝特组下降 8mg/dL，P=0.01；普伐他汀组下降 27mg/dL，P<0.01），载脂蛋白 B/载脂蛋白 A1 比值中位数下降（两组均下降 0.16，P<0.01）。从基线到第 48 周，接受联合治疗者的脂联素中位数下降（-1ng/dL，P<0.01）、载脂蛋白 B 中位数下降（-22mg/dL，P<0.01）、载脂蛋白 B/载脂蛋白 A1 比值中位数下降（-0.2，P<0.01），而载脂蛋白 A1 水平升高（9.5mg/dL，P=0.01）。
普伐他汀或非诺贝特治疗可在最初 12 周内改善致动脉粥样硬化脂质谱，联合治疗可持续至 48 周。脂联素水平随降脂治疗而下降。然而，炎症和血小板活化标志物无明显变化，提示这些药物在 HIV 感染者中的生物学特性不同。
