aDepartment of Epidemiology, Columbia University, Mailman School of Public Health, New York, USA bInserm U-738 and École des Hautes Études en Santé Publique cAP-HP Department of Cardiology, Hôpital Saint-Antoine, F-75012, Paris, France dUPMC Univ Paris 06, Paris F75012 eAPHP Department of Infectious and Tropical Diseases, Hôpital Saint-Antoine fAPHP Hôpital Tenon, Service de biochimie et hormonologie, Paris F75020 gInserm UMR_S938, Paris F-75012 hInserm U970, Paris-Cardiovascular Research Center, and Paris-Descartes University iAP-HP Centre d'Investigation Clinique Paris-EST (9304), Hôpital Pitié-Salpêtrière, Paris, France jDepartment of Medicine, University of Cambridge, Cambridge, UK kInserm UMR-S707, Paris, France.
AIDS. 2013 Oct 23;27(16):2603-14. doi: 10.1097/QAD.0b013e3283634819.
To determine whether the reported increased atherosclerotic risk among HIV-infected individuals is related to antiretroviral therapy (ART) or HIV infection, whether this risk persists in never-smokers, and whether inflammatory profiles are associated with higher risk.
Matched cross-sectional study.
A total of 100 HIV-infected patients (50 ART-treated >4 years, 50 ART-naive but HIV-infected >2 years) and 50 HIV-negative controls were recruited in age-matched never-smoking male triads (mean age 40.2 years). Carotid intima-media maximal thickness (c-IMT) was measured across 12 sites. Pro-inflammatory [highly sensitive C-reactive protein (hs-CRP), resistin, interleukin-6, interleukin-18, insulin, serum amyloid A, D-dimer) and anti-inflammatory (total and high molecular weight adiponectin, interleukin-27, interleukin-10) markers were dichotomized into high/low scores (based on median values). c-IMT was compared across HIV/treatment groups or inflammatory profiles using linear regression models adjusted for age, diabetes, hypertension, and, for HIV-infected patients, nadir CD4 cell counts.
Although adjusted c-IMT initially tended to be thicker in ART-exposed patients (P=0.2), in post-hoc analyses stratifying by median HIV duration we observed significantly higher adjusted c-IMT in patients with longer (>7.9 years: 0.760±0.008 mm) versus shorter prevalent duration of known HIV infection (<7.9 years: 0.731±0.008 mm, P=0.02), which remained significant after additionally adjusting for ART (P=0.04). Individuals with low anti-inflammatory profile (
Known HIV duration is related to thicker c-IMT, irrespective of ART, in these carefully selected age-matched never-smoking HIV-treated and ART-naive male individuals. Higher levels of anti-inflammatory markers appeared protective for atherosclerosis.
确定 HIV 感染者中报告的动脉粥样硬化风险增加是与抗逆转录病毒治疗（ART）还是 HIV 感染有关，这种风险是否在从不吸烟的人群中持续存在，以及炎症特征是否与更高的风险相关。
配对的横断面研究。
共招募了 100 名 HIV 感染患者（50 名接受 ART 治疗>4 年，50 名未接受 ART 治疗但 HIV 感染>2 年）和 50 名 HIV 阴性对照者，他们均为年龄匹配的从不吸烟的男性三胞胎（平均年龄 40.2 岁）。在 12 个部位测量颈动脉内膜-中层最大厚度（c-IMT）。将促炎标志物[高敏 C 反应蛋白（hs-CRP）、抵抗素、白细胞介素-6、白细胞介素-18、胰岛素、血清淀粉样蛋白 A、D-二聚体]和抗炎标志物[总和高分子量脂联素、白细胞介素-27、白细胞介素-10]分为高低分数（基于中位数）。使用线性回归模型比较 HIV/治疗组或炎症特征，该模型调整了年龄、糖尿病、高血压以及 HIV 感染患者的最低 CD4 细胞计数。
尽管接受 ART 暴露的患者的调整后 c-IMT 最初倾向于更厚（P=0.2），但在根据中位 HIV 持续时间进行事后分析时，我们观察到患有较长（>7.9 年：0.760±0.008mm）而非较短（<7.9 年：0.731±0.008mm，P=0.02）已知 HIV 感染持续时间的患者具有更高的调整后 c-IMT，即使在进一步调整 ART 后仍具有显著差异（P=0.04）。抗炎特征较低的个体（<中位数与>中位数评分）的 c-IMT 更厚（0.754±0.006mm 与 0.722±0.006mm，P<0.001），随着 HIV 感染的流行持续时间增加，抗炎标志物下降（线性趋势 P<0.001）。
在这些精心挑选的年龄匹配的从不吸烟的 HIV 治疗和未接受 ART 治疗的男性个体中，已知的 HIV 持续时间与更厚的 c-IMT 相关，无论 ART 如何。更高水平的抗炎标志物似乎对动脉粥样硬化有保护作用。
