A. M. and A. Migliavacca Center for Liver Disease, Division of Gastroenterology and Hepatology, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy.
Department of Biomedical Sciences, Humanitas University, Rozzano-Milan, Italy.
Liver Int. 2018 Aug;38(8):1459-1467. doi: 10.1111/liv.13707. Epub 2018 Mar 12.
In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN.
In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints.
During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0).
Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.
在 HCV 相关肝硬化患者中，持续病毒学应答可能导致肝硬化消退。组织学变化是否能转化为预防长期并发症，特别是肝细胞癌，目前仍不清楚。本研究在一组接受 IFN 治疗后获得持续病毒学应答的组织学肝硬化患者中进行，这些患者在获得持续病毒学应答后前瞻性随访了 10 年。
所有 38 名获得持续病毒学应答的肝硬化患者在 SVR 后 5 年内接受了肝活检，并前瞻性随访以评估肝硬化消退对临床终点的影响。
在肝活检后 86（30-96）个月的随访期间，没有患者发生临床失代偿，而 5 名（13%）在 79（7-88）个月后发生肝细胞癌。8 年累积肝细胞癌发生率为 17%，无肝硬化消退患者与无肝硬化消退患者之间无差异（19%[95%CI 6%-50%] vs 14%[95%CI 4%-44%]，P=0.88）。发生或未发生肝细胞癌的患者残留肝硬化率相似（P=1.0）、胶原含量（P=0.48）、METAVIR 活动度（P=0.34）、门脉炎症（P=0.06）和脂肪变性（P=0.17）。基线时，发生肝细胞癌的患者 γGT（HR 1.03，95%CI 1.00-1.06；P=0.014）和葡萄糖（HR 1.02，95%CI 1.00-1.02；P=0.012）值更高；此外，他们的 Forns 评分（HR 12.8，95%CI 1.14-143.9；P=0.039）、Lok 指数（HR 6.24，95%CI 1.03-37.6；P=0.046）和 PLF（HR 19.3，95%CI 1.72-217.6；P=0.016）值更高。1 名回归患者死于肺癌。8 年累积生存率为 97%，与肝硬化消退（96%比 100%，P=1.0）或肝细胞癌（100%比 97%，P=1.0）无关。
SVR 后肝硬化消退不能预防肝细胞癌的发生。
