Northwestern University Center for Global Health, Northwestern University, Chicago, Illinois 60611, USA.
AIDS. 2010 Mar 27;24(6):885-90. doi: 10.1097/QAD.0b013e3283352ed5.
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.
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.
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.
Twenty-six patients switched to atazanavir (all continued on ritonavir); 24 remained on their protease inhibitor regimen. Median CD4 cell count was 499 cells/mul, total cholesterol 204 mg/dl, low-density lipoprotein cholesterol 122 mg/dl, and triglycerides 244 mg/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. +1.5 mg/dl, P = 0.009), triglycerides (-58 vs. +3.5 mg/dl, P = 0.013), and nonhigh-density lipoprotein cholesterol (-27 vs. -0.5 mg/dl, P = 0.014).
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.
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谱；我们研究了其对动脉功能和其他代谢和炎症性心血管疾病危险因素的影响。
在接受稳定的基于蛋白酶抑制剂治疗的 HIV 感染患者中进行的前瞻性、随机、多国试验，这些患者的血浆 HIV RNA 小于 500 拷贝/ml，空腹低密度脂蛋白胆固醇大于 130mg/dl，或甘油三酯大于 200mg/dl。
患者被随机分配继续服用当前的蛋白酶抑制剂或将蛋白酶抑制剂换为阿扎那韦，如果给予蛋白酶抑制剂增效剂，则继续服用利托那韦，持续 24 周。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、炎症和代谢标志物。计算了（符号秩检验）和（Wilcoxon 检验）臂内的中位数变化。
26 例患者换用阿扎那韦（均继续服用利托那韦）；24 例患者继续服用蛋白酶抑制剂方案。中位 CD4 细胞计数为 499 个/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，血流介导的扩张无显著变化。在 24 周时，与继续蛋白酶抑制剂组相比，阿扎那韦组的总胆固醇（-25 对 +1.5mg/dl，P=0.009）、甘油三酯（-58 对 +3.5mg/dl，P=0.013）和非高密度脂蛋白胆固醇（-27 对-0.5mg/dl，P=0.014）有显著变化。
在稳定治疗中 HIV RNA 受抑制的血脂异常患者中，将蛋白酶抑制剂换为阿扎那韦/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变化。
