晚期纤维化/肝硬化的 HIV/HCV 合并感染者使用 DAA 清除 HCV 后的临床结果和预后因素。

IF 12.9 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Hepatology Pub Date : 2025-01-01 Epub Date: 2024-03-07 DOI:10.1097/HEP.0000000000000838
Juan Berenguer, Teresa Aldámiz-Echevarría, Víctor Hontañón, Chiara Fanciulli, Carmen Quereda, Carmen Busca, Lourdes Domínguez, Cristina Hernández, Jorge Vergas, Gabriel Gaspar, Lucio J García-Fraile, Cristina Díez, Marta De Miguel, José M Bellón, Rafael Bañares, Juan González-García
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引用次数: 0

摘要

目的和背景:我们评估了晚期肝纤维化(AdF)或肝硬化的HIV/HCV合并感染患者使用直接作用抗病毒药物(DAAs)获得持续病毒应答(SVR)后的长期临床结果和肝病进展的预后因素:2014年至2017年期间,西班牙共纳入了1300名使用DAAs获得SVR的患者:1145例慢性晚期肝病(cACLD)患者(384例AdF和761例代偿性肝硬化[CoC])和155例失代偿性肝硬化(DeC)患者。中位随访时间为 40.9 个月。总共有 85 人死亡,其中 61 人死于非肝病非艾滋病相关原因 (NLNA),这是所有肝病阶段的主要死因。每百人年(py)失代偿发生率(95% 置信区间 [CI]):AdF 患者为 0,CoC 患者为 1.01(0.68-1.51),DeC 患者为 8.35(6.05-11.53)。AdF 患者每 100 py 的肝细胞癌 (HCC) 发生率(95% CI)为 0.34(0.13-0.91),CoC 患者为 0.73(0.45-1.18),DeC 患者为 1.92(1.00-3.70)/100 py。cACLD患者失代偿的预后因素包括血清白蛋白、肝硬度测量(LSM)和FIB-4。在这一人群中,基于LSM和LSM的治疗后风险分层模型显示了其对失代偿和HCC的预测能力:NLNA事件是AdF/肝硬化合并感染患者在DAA治愈后发病和死亡的主要原因。在 cACLD 患者中,基于基线 LSM 和治疗后 LSM 的模型有助于评估失代偿和 HCC 风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clinical outcomes and prognostic factors after HCV clearance with DAA in HIV/HCV-coinfected patients with advanced fibrosis/cirrhosis.

Background and aims: We assessed long-term clinical outcomes and prognostic factors for liver disease progression after sustained viral response with direct-acting antivirals in patients coinfected with HIV/HCV with advanced fibrosis or cirrhosis.

Approach and results: A total of 1300 patients who achieved sustained viral response with direct-acting antivirals from 2014 to 2017 in Spain were included: 1145 with compensated advanced chronic liver disease (384 advanced fibrosis and 761 compensated cirrhosis) and 155 with decompensated cirrhosis. The median follow-up was 40.9 months. Overall, 85 deaths occurred, 61 due to non-liver non-AIDS-related causes that were the leading cause of death across all stages of liver disease. The incidence (95% CI) of decompensation per 100 person-years (py) was 0 in patients with advanced fibrosis, 1.01 (0.68-1.51) in patients with compensated cirrhosis, and 8.35 (6.05-11.53) in patients with decompensated cirrhosis. The incidence (95% CI) of HCC per 100 py was 0.34 (0.13-0.91) in patients with advanced fibrosis, 0.73 (0.45-1.18) in patients with compensated cirrhosis, and 1.92 (1.00-3.70) per 100 py in patients with decompensated cirrhosis. Prognostic factors for decompensation in patients with compensated advanced chronic liver disease included serum albumin, liver stiffness measurement (LSM), and fibrosis 4. In this population, LSM and LSM-based posttreatment risk stratification models showed their predictive ability for decompensation and HCC.

Conclusions: Non-liver non-AIDS-related events were the leading causes of morbidity and mortality after direct-acting antiviral cure among coinfected patients with advanced fibrosis/cirrhosis. Among those with compensated advanced chronic liver disease, baseline LSM and posttreatment LSM-based models helped to assess decompensation and HCC risk.

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来源期刊
Hepatology
Hepatology 医学-胃肠肝病学
CiteScore
27.50
自引率
3.70%
发文量
609
审稿时长
1 months
期刊介绍: HEPATOLOGY is recognized as the leading publication in the field of liver disease. It features original, peer-reviewed articles covering various aspects of liver structure, function, and disease. The journal's distinguished Editorial Board carefully selects the best articles each month, focusing on topics including immunology, chronic hepatitis, viral hepatitis, cirrhosis, genetic and metabolic liver diseases, liver cancer, and drug metabolism.
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