关于代谢功能障碍相关脂肪肝病 (MASLD) 患者使用直接作用抗病毒药物 (DAA) 治疗丙型肝炎病毒 (HCV) 获得持续病毒学应答 (SVR12) 后发生新发肝细胞癌 (HCC) 的风险的数据有限.1598 名符合条件的患者接受了一年两次的甲胎蛋白 (AFP) 和肝脏成像监测，以检测达到 SVR12 的新生 HCC。 MASLD 定义为存在受控衰减参数 (CAP) ≥ 248 dB/m 且≥ 1 个心脏代谢危险因素 (CMRF)。比较患有/不患有 MASLD 的患者之间的累积 HCC 发病率。我们建立了单变量和多变量 Cox 比例风险模型来评估与 HCC 相关的因素。使用细灰色次分布风险模型进行敏感性分析。此外，我们使用自举中介分析评估了 MASLD 对 CMRF 以及 CMRF 对 MASLD 对 HCC 的中介作用。HCC 的发病率为每 100 人年随访 (PYFU) 1.44 [95% 置信区间 (CI) ）：1.19-1.74]。患有 MASLD 的患者比没有患有 MASLD 的患者具有更高的累积 HCC 发病率（对数秩检验，p < 0.001）。多变量 Cox 回归分析显示，除了年龄、性别、LSM、血小板计数和 AFP 之外，MASLD（调整后风险比 (aHR)：2.07 [95% CI：1.36-3.16]，p < 0.001）与 HCC 独立相关。 Fine-Gray 模型证实了这一发现，该模型显示 MASLD 的子分布 HR (sHR) 为 2.07（95% CI：1.34-3.19，p < 0.001）。 MASLD 显着介导 HCC 发展的 CMRF。在达到 SVR12 后，与没有 MASLD 的患者相比，患有 MASLD 的患者表现出 HCC 风险增加。警惕 HCC 监测和控制 CMRF 以减轻 MASLD 对 HCC 的影响对于该人群仍然至关重要。MASLD（脂肪肝病 (SLD) 的一种新命名法）患者在使用 DAA 达到 SVR12 后，新发 HCC 的风险仍然存在有待确认。在这项招募了 1598 名台湾患者的研究中，与没有 MASLD 的患者相比，在达到 SVR12 后，患有 MASLD 的个体患新发 HCC 的风险增加了大约两倍。 MASLD 显着介导 HCC 发展的 CMRF。我们的研究结果强调了药物干预和积极生活方式改变对控制 MASLD 患者 CMRF 的至关重要性，以及需要进行警惕的 HCC 监测以确保 HCV 根除后获得良好的结果。版权所有 © 2024 欧洲肝脏研究协会。由 Elsevier B.V. 出版。保留所有权利。

Data are limited on the risk of de novo hepatocellular carcinoma (HCC) in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) after achieving sustained virologic response (SVR12) using direct-acting antivirals (DAAs) for hepatitis C virus (HCV).1598 eligible patients received biannual alpha-fetoprotein (AFP) and liver imaging surveillance to detect de novo HCC beyond achieving SVR12. MASLD was defined as presence of controlled attenuation parameter (CAP) ≥ 248 dB/m and ≥ one cardiometabolic risk factor (CMRF). Cumulative HCC incidence was compared between patients with/without MASLD. We built univariable and multivariable Cox proportional hazards models to evaluate factors associated with HCC. Sensitivity analysis was performed using the Fine-Gray subdistribution hazards model. Additionally, we evaluated the mediation effect of MASLD on CMRFs and of CMRFs on MASLD for HCC using mediation analysis with bootstrapping.The incidence rate of HCC was 1.44 per 100 person-years of follow-up (PYFU) [95% confidence interval (CI): 1.19-1.74]. Patients with MASLD had a higher cumulative HCC incidence than those without MASLD (log-rank test, p < 0.001). Multivariable Cox regression analysis revealed that in addition to age, sex, LSM, platelet count, and AFP, MASLD (adjusted hazard ratio (aHR): 2.07 [95% CI:1.36-3.16], p < 0.001) was independently associated with HCC. This finding was confirmed by the Fine-Gray model, which showed a subdistribution HR (sHR) of 2.07 (95% CI: 1.34-3.19, p < 0.001) for MASLD. MASLD significantly mediated CMRFs for HCC development.After achieving SVR12, patients with MASLD exhibited an increased HCC risk compared to those without MASLD. Vigilant HCC surveillance and control of CMRFs to mitigate the effect MASLD on HCC remain crucial for this population.The risk of de novo HCC among patients with MASLD, a novel nomenclature of steatotic liver disease (SLD), after the attaining of SVR12 using DAAs remains to be confirmed. In this study recruiting 1598 patients in Taiwan, individuals with MASLD exhibited approximately a two-fold increased risk of de novo HCC, compared to those without MASLD after achieving SVR12. MASLD significantly mediated CMRFs for HCC development. Our findings underscore the critical importance of pharmacological interventions and proactive lifestyle modifications to control CMRFs in patients with MASLD, as well as the need for vigilant HCC surveillance to ensure favorable outcomes following HCV eradication.Copyright © 2024 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.