肝脏 ›› 2024, Vol. 29 ›› Issue (2): 182-188.

• 肝癌 • 上一篇    下一篇

不同抗病毒治疗方案对慢性丙型肝炎持续应答患者肝细胞癌发生的影响

赵雅琳, 申川, 魏梦平, 赵彩彦   

  1. 050051 石家庄 河北医科大学第三医院感染科
  • 收稿日期:2023-03-05 出版日期:2024-02-29 发布日期:2024-03-18
  • 通讯作者: 赵彩彦,Email: zhaocy2005@163.com

The impact of different antiviral therapy on the development of hepatocellular carcinoma in patients with chronic hepatitis C

ZHAO Ya-lin, SHEN Chuan, WEI Meng-ping, ZHAO Cai-yan   

  1. Department of Infectious Disease, the Third Hospital of Heibei Medical University, Shijiazhuang 101151, China
  • Received:2023-03-05 Online:2024-02-29 Published:2024-03-18
  • Contact: ZHAO Cai-yan, Email: zhaocy2005@163.com

摘要: 目的 研究直接抗病毒药物(DAAs)与利巴韦林(PR)方案治疗慢性丙型肝炎患者获得持续病毒学应答后肝细胞癌发生率的差异,并分析其危险因素。方法 回顾性分析河北医科大学第三医院2006年1月以来符合纳入标准的慢性丙型肝炎住院患者的临床病例资料,根据患者治疗方案将其分为DAAs组和PR组。使用倾向性匹配分析均衡两组间基线资料。采用Kaplan-Meier法估计发生率,并用Log-rank法比较两组间差异,单因素和多因素Cox比例风险模型分析肝细胞癌发生的危险因素。结果 在369名符合纳入条件的患者中,229(62.1%)例应用PR方案治疗,140(37.9%)例应用DAAs治疗,经倾向性匹配后每组各106例。两组肝细胞癌的4年发生率分别为:7.9%和10.2%,无统计学意义(P=0.070)。多因素分析显示:丙肝初治时的年龄(HR=1.093, 95%CI: 1.007, 1.186)、合并糖尿病(HR=9.988, 95%CI: 2.093, 47.662)、肝硬化(HR=9.422, 95%CI: 1.079, 82.250)、基线AFP水平≥10 ng/mL(HR=5.683, 95%CI: 1.100, 29.369)以及HCV RNA高水平复制(HR=2.877, 95%CI: 1.203, 6.878)为获得持续病毒学应答后慢性丙型肝炎患者发生肝细胞癌的独立危险因素。结论 经不同抗病毒治疗方案获得持续病毒性应答的丙肝患者,肝细胞癌4年发生率无差异。

关键词: 慢性丙型肝炎, 肝细胞癌, 直接抗病毒药物, 聚乙二醇干扰素, 持续病毒学应答

Abstract: Objective To compare the occurrence of hepatocellular carcinoma in patients with chronic hepatitis C who achieved sustained virologic response after direct-acting antiviral agents (DAAs) or pegylated interferon combined with ribavirin (PR regimen), and to analyze the risk factors for developing hepatocellular carcinoma. Methods We retrospectively analyzed the clinical data of patients with chronic hepatitis C who met the inclusion criteria at the Third Hospital of Hebei Medical University from January 2006. Patients were divided into the DAAs group and the PR group based on the treatment regimens. Propensity Scores Matching was utilized to mitigate the confounding bias between the two groups. The Kaplan-Meier method was employed to estimate the incidience rate, and the Log-rank test was used to assess the differences. Cox proportional hazard regression analysis was conducted to identify the risk factors for HCC occurence. Results A total of 369 patients were enrolled, with 229 (62.1%) patients receiving PR regimen and 140 (37.9%) patients receiving DAAs. After propensity matching, 106 patients in each group were further analyzed. The 4-year incidence of hepatocellular carcinoma in the two groups was 7.9% and 10.2% respectively, with no statistical significance (P=0.070). Multivariate analysis revealed that age at the initiation of treatment (HR=1.093, 95%CI: 1.007, 1.186), diabetes mellitus (HR=9.988, 95%CI: 2.093, 47.662), liver cirrhosis (HR=9.422, 95%CI: 1.079, 82.250), baseline AFP ≥10 ng/mL (HR=5.683, 95%CI: 1.100, 29.369), and high HCV RNA level (HR=2.877, 95%CI: 1.203, 6.878) were independent predictors of HCC occurence in patients with chronic hepatitis C who achieved sustained virologic response. Conclusion There was no significant difference in the 4-year incidence of hepatocellular carcinoma in patients with sustained virologic response to different antiviral treatment regimens.

Key words: Chronic hepatitis C, Hepatocellular carcinoma, Direct antiviral agents, Peg-interferon, Sustained virologic response