Department of Epidemiology and Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
J Acquir Immune Defic Syndr. 2012 Aug 1;60(4):359-68. doi: 10.1097/QAI.0b013e31825b03be.
Inflammation and hemostasis perturbation may be involved in vascular complications of HIV infection. We examined atherogenic biomarkers and subclinical atherosclerosis in HIV-infected adults before and after beginning highly active antiretroviral therapy (HAART).
In the Women's Interagency HIV Study, 127 HIV-infected women studied pre and post HAART were matched to HIV-uninfected controls. Six semiannual measurements of soluble CD14, tumor necrosis factor (TNF) alfa, soluble interleukin (IL) 2 receptor, IL-6, IL-10, monocyte chemoattractant protein 1, D-dimer, and fibrinogen were obtained. Carotid artery intima-media thickness was measured by B-mode ultrasound.
Relative to HIV-uninfected controls, HAART-naive HIV-infected women had elevated levels of soluble CD14 (1945 vs 1662 ng/mL, Wilcoxon signed rank P < 0.0001), TNF-α (6.3 vs 3.4 pg/mL, P < 0.0001), soluble IL-2 receptor (1587 vs 949 pg/mL, P < 0.0001), IL-10 (3.3 vs 1.9 pg/mL, P < 0.0001), monocyte chemoattractant protein 1 (190 vs 163 pg/mL, P < 0.0001), and D-dimer (0.43 vs 0.31 μg/mL, P < 0.01). Elevated biomarker levels declined after HAART. Although most biomarkers normalized to HIV-uninfected levels, in women on effective HAART, TNF-α levels remained elevated compared with HIV-uninfected women (+0.8 pg/mL, P = 0.0002). Higher post-HAART levels of soluble IL-2 receptor (P = 0.02), IL-6 (P = 0.05), and D-dimer (P = 0.03) were associated with increased carotid artery intima-media thickness.
Untreated HIV infection is associated with abnormal hemostasis (eg, D-dimer), proatherogenic (eg, TNF-α), and antiatherogenic (eg, IL-10) inflammatory markers. HAART reduces most inflammatory mediators to HIV-uninfected levels. Increased inflammation and hemostasis are associated with subclinical atherosclerosis in recently treated women. These findings have potential implications for long-term risk of cardiovascular disease in HIV-infected patients, even with effective therapy.
炎症和止血紊乱可能与 HIV 感染的血管并发症有关。我们在开始高效抗逆转录病毒治疗（HAART）之前和之后，检查了 HIV 感染成年人的动脉粥样硬化生物标志物和亚临床动脉粥样硬化。
在妇女艾滋病研究机构间合作研究中，127 名接受 HAART 治疗的 HIV 感染妇女与 HIV 未感染对照者进行了匹配。在 6 次半年度测量中，测量了可溶性 CD14、肿瘤坏死因子（TNF）alfa、可溶性白细胞介素（IL）2 受体、IL-6、IL-10、单核细胞趋化蛋白 1、D-二聚体和纤维蛋白原。通过 B 型超声测量颈动脉内膜中层厚度。
与 HIV 未感染对照者相比，HAART 初治 HIV 感染妇女可溶性 CD14 水平升高（1945 与 1662ng/ml，Wilcoxon 符号秩检验 P <0.0001）、TNF-α（6.3 与 3.4pg/ml，P <0.0001）、可溶性 IL-2 受体（1587 与 949pg/ml，P <0.0001）、IL-10（3.3 与 1.9pg/ml，P <0.0001）、单核细胞趋化蛋白 1（190 与 163pg/ml，P <0.0001）和 D-二聚体（0.43 与 0.31μg/ml，P <0.01）。HAART 后升高的生物标志物水平下降。尽管大多数生物标志物恢复到 HIV 未感染水平，但在接受有效 HAART 的妇女中，TNF-α水平仍高于 HIV 未感染妇女（+0.8pg/ml，P=0.0002）。HAART 后可溶性 IL-2 受体（P=0.02）、IL-6（P=0.05）和 D-二聚体（P=0.03）水平升高与颈动脉内膜中层厚度增加有关。
未经治疗的 HIV 感染与异常止血（如 D-二聚体）、促动脉粥样硬化（如 TNF-α）和抗动脉粥样硬化（如 IL-10）炎症标志物有关。HAART 将大多数炎症介质降低到 HIV 未感染水平。最近接受治疗的妇女中，炎症和止血增加与亚临床动脉粥样硬化有关。这些发现可能对 HIV 感染患者的心血管疾病长期风险具有重要意义，即使接受了有效的治疗。
