Eradication of Hepatitis C Virus Infection in Patients With Cirrhosis Reduces Risk of Liver and Non-Liver Complications
Eradication of Hepatitis C Virus Infection in Patients With Cirrhosis Reduces Risk of Liver and Non-Liver Complications
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DOI：
10.1053/j.gastro.2016.09.009
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发表时间：
2017-01-01
期刊：
影响因子：
29.4
通讯作者：
Roudot-Thoraval, Francoise
中科院分区：
文献类型：
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作者：
Nahon, Pierre;Bourcier, Valerie;Roudot-Thoraval, Francoise
背景与目的：我们进行了一项前瞻性研究，旨在调查持续病毒应答 (SVR) 对丙型肝炎病毒 (HCV) 感染和代偿性肝硬化患者预后的影响。方法：我们收集了 2006 年至 2012 年从法国 35 个临床中心招募的前瞻性国家 SIDA 和病毒性肝炎研究机构 (ANRS) 病毒性肝硬化 (CirVir) 队列中的 1323 名患者的数据。所有患者均患有 HCV 感染和活检证实的肝硬化，属于 Child-Pugh A 级，并且既往没有肝脏并发症。所有患者在纳入之前或之后均接受抗 HCV 治疗（先使用干扰素，然后使用直接抗病毒药物），并每 6 个月接受一次超声检查以及内窥镜评估。 SVR 被认为是一个依赖于时间的协变量；通过 Cox 比例风险回归方法评估其对结果的影响。我们使用倾向评分来最大程度地减少治疗指示和实现 SVR 能力的混淆。结果：中位随访期 58.2 个月后，668 名患者 (50.5%) 实现了 SVR。 SVR 与肝细胞癌发病率降低（与未获得 SVR 的患者相比，风险比 [HR] 为 0.29；95% 置信区间 [CI]，0.19-0.43；P < .001）和肝代偿失调（HR，0.26；95% CI，0.17-0.39；P < .001）相关。获得 SVR 的患者心血管事件（HR，0.42；95% CI，0.25-0.69；P = .001）和细菌感染（HR，0.44；95% CI，0.29-0.68；P < .001）的风险也较低。在 SVR 患者中，代谢特征与较高的肝细胞癌风险相关，但在病毒血症患者中则不然。 SVR 影响总体死亡率（与无 SVR 的患者相比，HR 为 0.27；95% CI，0.18-0.42；P < .001）以及肝脏相关和非肝脏相关原因导致的死亡。在倾向评分匹配的人群中也获得了类似的结果。结论：在一项针对 CirVir 队列中 HCV 感染和代偿性肝硬化患者的前瞻性研究中，我们证实了与肝脏相关或无关的危急事件的减少，这些患者实现了 SVR。我们发现 SVR 可以降低总体死亡率以及肝脏相关和非肝脏相关原因导致的死亡风险。需要更长时间的随访评估来准确描述和评估该人群并发症的具体危险因素。
BACKGROUND & AIMS: We performed a prospective study to investigate the effects of a sustained viral response (SVR) on outcomes of patients with hepatitis C virus (HCV) infection and compensated cirrhosis. METHODS: We collected data from 1323 patients included in the prospective Agence Nationale pour la Recherche sur le SIDA et les hepatites virales (ANRS) viral cirrhosis (CirVir) cohort, recruited from 35 clinical centers in France from 2006 through 2012. All patients had HCV infection and biopsy-proven cirrhosis, were Child-Pugh class A, and had no prior liver complications. All patients received anti-HCV treatment before or after inclusion (with interferon then with direct antiviral agents) and underwent an ultrasound examination every 6 months, as well as endoscopic evaluations. SVR was considered as a time-dependent covariate; its effect on outcome was assessed by the Cox proportional hazard regression method. We used a propensity score to minimize confounding by indication of treatment and capacity to achieve SVR. RESULTS: After a median follow-up period of 58.2 months, 668 patients (50.5%) achieved SVR. SVR was associated with a decreased incidence of hepatocellular carcinoma (hazard ratio [HR] compared with patients without an SVR, 0.29; 95% confidence interval [CI], 0.19-0.43; P < .001) and hepatic decompensation (HR, 0.26; 95% CI, 0.17-0.39; P < .001). Patients with SVRs also had a lower risk of cardiovascular events (HR, 0.42; 95% CI, 0.25-0.69; P = .001) and bacterial infections (HR, 0.44; 95% CI, 0.29-0.68; P < .001). Metabolic features were associated with a higher risk of hepatocellular carcinoma in patients with SVRs, but not in patients with viremia. SVR affected overall mortality (HR, 0.27 compared with patients without SVR; 95% CI, 0.18-0.42; P < .001) and death from liver-related and non-liver-related causes. Similar results were obtained in a propensity score-matched population. CONCLUSIONS: We confirmed a reduction in critical events, liver-related or not, in a prospective study of patients with HCV infection and compensated cirrhosis included in the CirVir cohort who achieved an SVR. We found an SVR to reduce overall mortality and risk of death from liver-related and non-liver-related causes. A longer follow-up evaluation is required to accurately describe and assess specific risk factors for complications in this population.