Infectious Diseases Unit, Hospital General Universitario de Elche, Department of Clinical Medicine, University Miguel Hernández, Elche, Alicante, Spain.
BMC Infect Dis. 2011 Feb 4;11:40. doi: 10.1186/1471-2334-11-40.
Abacavir has been associated with an increased risk of acute myocardial infarction, but the pathogenic mechanisms remain unknown. We evaluated longitudinal changes in pro-atherosclerotic biomarkers in patients initiating abacavir or tenofovir.
Consecutive patients initiating antiretroviral therapy (ART) with abacavir/lamivudine or tenofovir/emtricitabine were included. Plasma levels of high sensitivity C reactive protein (hsCRP), interleukin-6 (IL-6), intercellular adhesion molecule-1, vascular cell adhesion molecule-1 (sVCAM-1) and plasminogen activator inhibitor-1 (PAI-1) were measured at baseline and at different time points throughout 48 weeks. Comparisons were adjusted for age, sex, ART status at inclusion, viral load, lipodystrophy, Framingham score and hepatitis C virus co-infection status.
50 patients were analyzed, 28 initiating abacavir and 22 tenofovir. The endothelial biomarker sVCAM-1 declined significantly in both treatment groups. hsCRP tended to increase soon after starting therapy with abacavir, a trend that was not seen in those initiating tenofovir. IL-6 significantly increased only at week 24 from baseline in patients on abacavir (+225%, p < 0.01) although the differences were not significant between groups. The procoagulant biomarker PAI-1 plasma levels increased from baseline at week 12 (+57%; p = 0.017), week 24 (+72%; p = 0.008), and week 48 (+149%; p < 0.001) in patients on tenofovir, but differences between groups were not statistically significant.
Changes in biomarkers of inflammation, coagulation, and endothelial function are not different in viremic patients starting ART with abacavir/lamivudine or tenofovir/emtricitabine. These changes occur in the early phases of treatment and include anti- and pro-atherosclerotic effects with both drugs.
阿巴卡韦与急性心肌梗死风险增加有关，但发病机制尚不清楚。我们评估了开始使用阿巴卡韦或替诺福韦的患者中促动脉粥样硬化生物标志物的纵向变化。
连续纳入开始使用阿巴卡韦/拉米夫定或替诺福韦/恩曲他滨的抗逆转录病毒治疗（ART）的患者。在基线和 48 周的不同时间点测量高敏 C 反应蛋白（hsCRP）、白细胞介素-6（IL-6）、细胞间黏附分子-1、血管细胞黏附分子-1（sVCAM-1）和纤溶酶原激活物抑制剂-1（PAI-1）的血浆水平。比较调整了年龄、性别、纳入时的 ART 状态、病毒载量、脂肪营养不良、弗雷明汉评分和丙型肝炎病毒合并感染状态。
分析了 50 例患者，其中 28 例开始使用阿巴卡韦，22 例开始使用替诺福韦。两组内皮生物标志物 sVCAM-1 均显著下降。hsCRP 在开始阿巴卡韦治疗后不久即呈上升趋势，而开始替诺福韦治疗的患者则没有这种趋势。仅在开始阿巴卡韦治疗后 24 周时，IL-6 较基线显著增加（+225%，p <0.01），但两组间差异无统计学意义。在开始替诺福韦治疗后 12 周（+57%，p = 0.017）、24 周（+72%，p = 0.008）和 48 周（+149%，p <0.001）时，促凝生物标志物 PAI-1 血浆水平从基线升高，但两组间差异无统计学意义。
在开始阿巴卡韦/拉米夫定或替诺福韦/恩曲他滨治疗的病毒血症患者中，炎症、凝血和内皮功能生物标志物的变化没有差异。这些变化发生在治疗的早期阶段，包括两种药物的抗动脉粥样硬化和促动脉粥样硬化作用。
