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直接作用抗病毒药物未能降低丙型肝炎病毒相关性肝硬化中肝细胞癌的发生率:一项真实世界研究。

Direct-acting antivirals failed to reduce the incidence of hepatocellular carcinoma occurrence in hepatitis C virus associated cirrhosis: A real-world study.

作者信息

Tao Xue-Mei, Zeng Ming-Hui, Zhao You-Fei, Han Jia-Xin, Mi Yu-Qiang, Xu Liang

机构信息

Clinical School of the Second People's Hospital, Tianjin Medical University, Tianjin 300192, China.

Department of Hepatology, Tianjin Second People's Hospital, Tianjin 300192, China.

出版信息

World J Hepatol. 2024 Jan 27;16(1):41-53. doi: 10.4254/wjh.v16.i1.41.

DOI:10.4254/wjh.v16.i1.41
PMID:38313240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10835484/
Abstract

BACKGROUND

Direct-acting antivirals (DAAs) revolutionized the treatment of chronic hepatitis C virus (HCV)-associated disease achieving high rates of sustained virological response (SVR). However, whether DAAs can reduce the occurrence of hepatocellular carcinoma (HCC) in patients with HCV-associated cirrhosis who are at high risk have not been concluded.

AIM

To investigate the effect of DAAs on the occurrence of HCC in patients with HCV-associated cirrhosis after achieving SVR.

METHODS

Of 427 inpatients with HCV-associated cirrhosis were enrolled in Tianjin Second People's Hospital from January 2014 to April 2020. 118 patients weren't received antiviral treatment with any reasons named non-antiviral treatment group, and 236 patients obtained from the 309 DAAs treatment patients according to the propensity score matching named DAAs treatment group. Demographic information and laboratory data were collected from baseline and the following up. Kaplan-Meier curve and Log-Rank test were used to compare the incidence and cumulative incidence of HCC between the two groups. Cox proportional risk regression was used to re-evaluate the risk factors for HCC.

RESULTS

HCC incidence was 4.68/100PY (95%CI, 3.09-6.81) in the DAAs treatment group, while it was 3.00/100PY (95%CI, 1.50-5.37) in the non-antiviral treatment group, and the relative risk was 1.82 (95%CI, 0.93-3.53, > 0.05). The incidence of HCC at 12, 24, 36 and 48 months was 3.39%, 6.36%, 8.47% and 10.17% in the DAAs treatment group, and it was 0%, 0%, 3.39% and 9.32% in the non-antiviral treatment group, respectively. Age > 58 [hazard ratio (HR) = 1.089; 95%CI, 1.033-1.147; = 0.002] and liver stiffness measurement > 27.85 kPa (HR = 1.043; 95%CI, 1.022-1.065; = 0.000) were risk factors for HCC in all patients ( = 427), and DAAs treatment didn't show protective efficacy.

CONCLUSION

DAAs treatment seems failed to reduce the incidence of HCC occurrence in HCV-associated cirrhosis in 48 months, and even increased the incidence of HCC in 36 months.

摘要

背景

直接作用抗病毒药物(DAAs)彻底改变了慢性丙型肝炎病毒(HCV)相关疾病的治疗方式,实现了高持续病毒学应答率(SVR)。然而,DAAs能否降低HCV相关肝硬化高危患者肝细胞癌(HCC)的发生率尚无定论。

目的

探讨DAAs对HCV相关肝硬化患者实现SVR后HCC发生情况的影响。

方法

选取2014年1月至2020年4月在天津市第二人民医院住院的427例HCV相关肝硬化患者。118例因各种原因未接受抗病毒治疗的患者作为非抗病毒治疗组,从309例接受DAAs治疗的患者中根据倾向评分匹配出236例作为DAAs治疗组。收集基线及随访时的人口统计学信息和实验室数据。采用Kaplan-Meier曲线和Log-Rank检验比较两组HCC的发病率和累积发病率。采用Cox比例风险回归重新评估HCC的危险因素。

结果

DAAs治疗组HCC发病率为4.68/100人年(95%CI,3.09 - 6.81),非抗病毒治疗组为3.00/100人年(95%CI,1.50 - 5.37),相对风险为1.82(95%CI,0.93 - 3.53,P>0.05)。DAAs治疗组在12、24、36和48个月时HCC的发病率分别为3.39%、6.36%、8.47%和10.17%,非抗病毒治疗组分别为0%、0%、3.39%和9.32%。年龄>58岁[风险比(HR)=1.089;95%CI,1.033 - 1.147;P = 0.002]和肝脏硬度测量值>27.85 kPa(HR = 1.043;95%CI,1.022 - 1.065;P = 0.000)是所有患者(n = 427)发生HCC的危险因素,DAAs治疗未显示出保护作用。

结论

DAAs治疗在48个月内似乎未能降低HCV相关肝硬化患者HCC的发生率,甚至在36个月时增加了HCC的发生率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/61bc9e2b592d/WJH-16-41-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/42f2d55c8893/WJH-16-41-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/29c58eee3fe6/WJH-16-41-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/357b8ba2a26e/WJH-16-41-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/61bc9e2b592d/WJH-16-41-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/42f2d55c8893/WJH-16-41-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/29c58eee3fe6/WJH-16-41-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/357b8ba2a26e/WJH-16-41-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ed/10835484/61bc9e2b592d/WJH-16-41-g004.jpg

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