Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Department of Occupational Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; Faculty of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
J Hepatol. 2014 Jul;61(1):67-74. doi: 10.1016/j.jhep.2014.02.022. Epub 2014 Mar 5.
BACKGROUND & AIMS: Hepatitis C virus (HCV)-infected patients with cirrhosis remain at risk of hepatocellular carcinoma (HCC) even after achieving sustained virological response (SVR). The aim of the study was to explore the incidence and risk for HCC among non-cirrhotic patients with an SVR.
A total of 642 patients with an SVR after peginterferon/ribavirin therapy were enrolled with a median follow-up period of 53.0 months (range: 6-133 months).
Thirty-three of the 642 (5.1%) patients developed HCC over 2324.8 person-years of follow-up. Cox regression analysis revealed that the strongest predictive factor of HCC occurrence was liver cirrhosis (HR 4.98, 95% CI 2.32-10.71, p<0.001), followed by age (HR 1.06, 95% CI 1.02-1.11, p=0.005) and γGT levels (HR 1.008, 95% CI 1.004-1.013, p<0.001). The incidence of HCC did not differ between patients with high and low baseline γGT levels among patients with cirrhosis (p=0.53), but the incidence of HCC was significantly higher in non-cirrhotic patients with high γGT levels compared with those with low γGT levels (p=0.001). Cox regression analysis revealed that the strongest factors associated with HCC development in non-cirrhotic sustained responders were baseline γGT levels (HR 6.44, 95% CI 2.20-18.89, p=0.001) and age (HR 3.68, 95% CI 1.33-10.17, p=0.012). The incidence of HCC was not different between older non-cirrhotic patients with high γGT levels and cirrhotic patients (p=0.34).
HCC remains a threat in non-cirrhotic patients with an SVR. Serum γGT levels helped to identify potential patients at high risk.
即使丙型肝炎病毒（HCV）感染患者实现了持续病毒学应答（SVR），他们仍有发生肝细胞癌（HCC）的风险。本研究旨在探讨 SVR 后非肝硬化患者 HCC 的发生率和风险。
共纳入 642 例接受聚乙二醇干扰素/利巴韦林治疗后获得 SVR 的患者，中位随访时间为 53.0 个月（范围：6-133 个月）。
642 例患者中有 33 例（5.1%）在 2324.8 人年的随访中发生 HCC。Cox 回归分析显示，HCC 发生的最强预测因素是肝硬化（HR 4.98，95%CI 2.32-10.71，p<0.001），其次是年龄（HR 1.06，95%CI 1.02-1.11，p=0.005）和γGT 水平（HR 1.008，95%CI 1.004-1.013，p<0.001）。在肝硬化患者中，基线γGT 水平较高和较低的患者 HCC 发生率无差异（p=0.53），但在非肝硬化患者中，基线γGT 水平较高的患者 HCC 发生率明显高于γGT 水平较低的患者（p=0.001）。Cox 回归分析显示，非肝硬化持续应答者 HCC 发生的最强因素是基线γGT 水平（HR 6.44，95%CI 2.20-18.89，p=0.001）和年龄（HR 3.68，95%CI 1.33-10.17，p=0.012）。在γGT 水平较高的老年非肝硬化患者和肝硬化患者中，HCC 的发生率无差异（p=0.34）。
HCC 仍是 SVR 后非肝硬化患者的威胁。血清γGT 水平有助于识别高危患者。
