Change to atazanavir/ritonavir treatment improves lipids but not endothelial function in patients on stable antiretroviral therapy
Change to atazanavir/ritonavir treatment improves lipids but not endothelial function in patients on stable antiretroviral therapy
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DOI：
10.1097/qad.0b013e3283352ed5
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发表时间：
2010-03-27
期刊：
影响因子：
3.8
通讯作者：
Stein, James H.
中科院分区：
文献类型：
--
作者：
Murphy, Robert L.;Berzins, Baiba;Stein, James H.
目的：蛋白酶抑制剂和其他抗逆转录病毒药物与血脂异常、内皮功能障碍和心血管疾病风险增加有关。蛋白酶抑制剂阿扎那韦具有有利的血脂特征；我们研究了它对动脉功能以及其他代谢和炎症性心血管疾病危险因素的影响。设计：对接受稳定蛋白酶抑制剂治疗的 HIV 感染患者进行前瞻性、随机、多国试验，血浆 HIV RNA 低于 500 拷贝/ml，空腹低密度脂蛋白胆固醇超过 130 mg/dl，或甘油三酯超过 200 mg/dl。方法：患者被随机分配继续使用当前的蛋白酶抑制剂或更换蛋白酶如果作为蛋白酶抑制剂加强剂给予 24 周，则继续服用阿扎那韦抑制剂并继续利托那韦。在基线、第 12 周和第 24 周测量肱动脉血流介导的扩张、脂蛋白以及炎症和代谢标志物。计算臂内（符号秩检验）和臂间（Wilcoxon 检验）的中位变化。结果：26 名患者转用阿扎那韦（全部继续使用利托那韦）； 24 人继续接受蛋白酶抑制剂治疗。中位CD4细胞计数为499个细胞/μl，总胆固醇204mg/dl，低密度脂蛋白胆固醇122mg/dl，甘油三酯244mg/dl。 12 周和 24 周后血流介导的扩张没有显着变化。 24 周时，观察到阿扎那韦组与持续蛋白酶抑制剂组的总胆固醇（-25 vs. +1.5mg/dl，P = 0.009）、甘油三酯（-58 vs. +3.5mg/dl，P = 0.013）和非高密度脂蛋白胆固醇（-27 vs. -0.5mg/dl，P = 0.013）发生显着变化。 0.014). 结论：在稳定治疗后 HIV RNA 受到抑制的血脂异常个体中，将蛋白酶抑制剂改为阿扎那韦/利托那韦 24 周，可改善血脂；然而，内皮功能、炎症和代谢标志物没有改变。 (C) 2010 年 Wolters Kluwer Health 垂直条 Lippincott Williams & Wilkins
Objective: Protease inhibitors and other antiretroviral drugs have been associated with dyslipidemia, endothelial dysfunction, and increased cardiovascular disease risk. The protease inhibitor atazanavir has an advantageous lipid profile; we studied its effects on arterial function and other metabolic and inflammatory cardiovascular disease risk factors.Design: Prospective, randomized, multinational trial in HIV-infected patients receiving stable protease inhibitor-based therapy with plasma HIV RNA less than 500 copies/ml and fasting low-density lipoprotein cholesterol more than 130 mg/dl, or triglycerides more than 200 mg/dl.Methods: Patients were randomized to continue their current protease inhibitor or switch the protease inhibitor to atazanavir and continue ritonavir if given as a protease inhibitor booster for 24 weeks. Brachial artery flow-mediated dilation, lipoproteins, and inflammatory and metabolic markers were measured at baseline, week 12, and week 24. Median changes within (signed rank test) and between (Wilcoxon test) arms were calculated.Results: Twenty-six patients switched to atazanavir (all continued on ritonavir); 24 remained on their protease inhibitor regimen. Median CD4 cell count was 499 cells/mu l, total cholesterol 204mg/dl, low-density lipoprotein cholesterol 122 mg/dl, and triglycerides 244mg/dl. There were no significant changes in flow-mediated dilation after 12 and 24 weeks. At 24 weeks, significant changes in the atazanavir vs. continued protease inhibitor group were observed for total cholesterol (-25 vs. +1.5mg/dl, P = 0.009), triglycerides (-58 vs. +3.5mg/dl, P = 0.013), and nonhigh-density lipoprotein cholesterol (-27 vs. -0.5mg/dl, P = 0.014).Conclusion: In dyslipidemic individuals with suppressed HIV RNA on stable therapy, changing the protease inhibitor to atazanavir/ritonavir for 24 weeks improved lipids; however, endothelial function, inflammatory, and metabolic markers did not change. (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins