Patel Pragna, Bush Tim, Overton Turner, Baker Jason, Hammer John, Kojic Erna, Conley Lois, Henry Keith, Brooks John T
Division of HIV/AIDS Prevention, Centers for Disease Control and Prevention, Atlanta, GA, USA.
Antivir Ther. 2012;17(4):755-61. doi: 10.3851/IMP2020. Epub 2011 Dec 16.
This study examined the effect of abacavir on acute changes in biomarkers associated with cardiovascular dysfunction.
Among the Study to Understand the Natural History of HIV/AIDS in the Era of Effective therapy (SUN) participants, we identified 25 individuals (cases) who were HLA-B5701-negative and who had ≥ 2 weeks without abacavir exposure at one visit and ≥ 2 weeks with abacavir exposure at the consecutive visit while maintaining viral suppression. We identified 43 individuals (controls) similarly unexposed and exposed to tenofovir. We assessed concentrations of prothrombin fragment F(1+2), D-dimer, high-sensitivity C-reactive protein, interleukin-8, intercellular adhesion molecule-1, vascular adhesion molecule-1, E-selectin, P-selectin, serum amyloid A and serum amyloid P. We examined the median percentage change of these biomarkers from the unexposed to exposed state among cases and controls compared with the expected assay variability using a sign test, and compared changes among cases with controls using the Wilcoxon rank-sum test.
Baseline characteristics were similar between cases and controls: median age 45 versus 46 years, 80% versus 81% male, 64% versus 63% non-Hispanic White and median CD4(+) T-cell count 538 versus 601 cells/mm(3), respectively. Mean exposure times were 65 and 15 weeks for abacavir and tenofovir, respectively. We observed no significant changes in biomarkers from the unexposed to exposed state among cases or controls compared with the expected assay variability. We found that no biomarkers were significantly increased among cases compared with controls; however, prothrombin fragment F(1+2) was significantly lower among controls (P=0.035).
In virologically suppressed contemporary HIV-infected patients, abacavir exposure was not associated with increases in biomarkers associated with increased cardiovascular risk.
本研究检测了阿巴卡韦对与心血管功能障碍相关生物标志物急性变化的影响。
在“了解高效治疗时代HIV/AIDS自然史研究”（SUN）的参与者中，我们确定了25名个体（病例组），他们HLA - B5701阴性，在一次访视时未接触阿巴卡韦≥2周，而在连续访视时接触阿巴卡韦≥2周，同时维持病毒抑制状态。我们确定了43名个体（对照组），他们同样未接触和接触了替诺福韦。我们评估了凝血酶原片段F(1+2)、D - 二聚体、高敏C反应蛋白、白细胞介素 - 8、细胞间黏附分子 - 1、血管黏附分子 - 1、E - 选择素、P - 选择素、血清淀粉样蛋白A和血清淀粉样蛋白P的浓度。我们使用符号检验比较了病例组和对照组中这些生物标志物从未接触状态到接触状态的中位百分比变化与预期检测变异性，并使用Wilcoxon秩和检验比较了病例组与对照组之间的变化。
病例组和对照组的基线特征相似：中位年龄分别为45岁和46岁，男性分别为80%和81%，非西班牙裔白人分别为64%和63%，CD4(+) T细胞计数中位数分别为538和601个细胞/mm³。阿巴卡韦和替诺福韦的平均暴露时间分别为65周和15周。与预期检测变异性相比，我们未观察到病例组或对照组中生物标志物从未接触状态到接触状态有显著变化。我们发现与对照组相比，病例组中没有生物标志物显著升高；然而，对照组中凝血酶原片段F(1+2)显著更低（P = 0.035）。
在病毒学抑制的当代HIV感染患者中，接触阿巴卡韦与心血管风险增加相关生物标志物的升高无关。
