Department of Epidemiology, Robert Stempel College of Public Health and Social Work, Florida International University, Miami, Florida, USA.
Center for Healthcare Advancement and Outcomes, Baptist Health South Florida, Miami, Florida, USA.
Rev Med Virol. 2018 Jan;28(1). doi: 10.1002/rmv.1953. Epub 2017 Nov 14.
The incidence of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) coinfection has been increasing with over 10 million people affected globally. The role biomarkers play as predictors of cardiovascular disease (CVD) risk among coinfected individuals is not well defined. We aimed to systematically review current evidence describing CVD biomarkers among individuals with HIV/HCV coinfection. We searched EMBASE, CINAHL, Google Scholar, PubMed, and Web of Science from inception to June 2017. MeSH terms and keywords were used to identify studies with information on HIV/HCV coinfection and CVD biomarkers (structural, functional, and serological) such as carotid intima-media thickness (CIMT), endothelial markers, C-reactive protein (CRP), homocysteine, and lipids. Among 332 articles screened, 28 were included (39,498 participants). Study designs varied: 18 cross-sectional, 9 cohort, and 1 clinical trial. Compared with healthy controls and people with HIV or HCV monoinfection, individuals with HIV/HCV coinfection had statistically significant lower levels of lipids and CRP and higher levels of endothelial markers (sICAM-1 and sVCAM-1), CIMT, homocysteine, and IL-6. One study found the odds of carotid plaque in coinfected individuals was 1.64 (0.91-2.94) compared with healthy controls, and another study showed the prevalence of vascular plaques (carotid and femoral) in coinfected individuals was higher compared with HIV monoinfected individuals (44% vs 14%, P = 0.04). Biomarkers of CVD have different patterns of association with HIV/HCV coinfection compared with monoinfection and healthy controls. Prospective studies are needed to confirm the predictive value of these biomarkers for clinical CVD risk among coinfected individuals.
人类免疫缺陷病毒（HIV）和丙型肝炎病毒（HCV）合并感染的发病率在全球范围内已超过 1000 万人，呈上升趋势。目前尚不清楚生物标志物在合并感染个体心血管疾病（CVD）风险预测中的作用。我们旨在系统地回顾目前描述 HIV/HCV 合并感染个体 CVD 生物标志物的证据。我们从建库开始至 2017 年 6 月在 EMBASE、CINAHL、Google Scholar、PubMed 和 Web of Science 中进行了检索。使用 MeSH 术语和关键词来确定关于 HIV/HCV 合并感染和 CVD 生物标志物（结构、功能和血清学标志物）的研究，如颈动脉内膜中层厚度（CIMT）、内皮标志物、C 反应蛋白（CRP）、同型半胱氨酸和脂质。在筛选出的 332 篇文章中，有 28 篇被纳入（39498 名参与者）。研究设计各不相同：18 项横断面研究，9 项队列研究和 1 项临床试验。与健康对照组和 HIV 或 HCV 单感染组相比，HIV/HCV 合并感染个体的脂质和 CRP 水平显著降低，而内皮标志物（sICAM-1 和 sVCAM-1）、CIMT、同型半胱氨酸和 IL-6 水平较高。一项研究发现，与健康对照组相比，合并感染个体发生颈动脉斑块的几率为 1.64（0.91-2.94），另一项研究表明，合并感染个体的血管斑块（颈动脉和股动脉）患病率高于 HIV 单感染个体（44% vs 14%，P = 0.04）。与单感染和健康对照组相比，CVD 生物标志物与 HIV/HCV 合并感染的相关性模式不同。需要前瞻性研究来证实这些生物标志物对合并感染个体临床 CVD 风险的预测价值。
