丙型肝炎持续病毒学应答后肝癌发生的危险因素及预测模型

许姗姗; 仇丽霞; 柳雅立; 张晶

doi:10.12449/JCH240629

丙型肝炎持续病毒学应答后肝癌发生的危险因素及预测模型

DOI: 10.12449/JCH240629

首都医科大学附属北京佑安医院肝病中心三科，北京 100069

基金项目:

2022年度院内中青年人才孵育项目 (BJYAYY-YN2022-02)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：许姗姗负责撰写和修改论文；仇丽霞，柳雅立负责参与文献的收集和整理；张晶负责拟定写作思路，指导撰写文章并最后定稿。

详细信息

通信作者:
张晶， drzhangjing@163.com （ORCID： 0000-0002-3082-8330）

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出版历程
- 收稿日期: 2023-11-12
- 录用日期: 2023-12-01
- 出版日期: 2024-06-25

Risk factors and predictive models for liver cancer after sustained virologic response in hepatitis C

Third Department of Liver Disease Center，Beijing YouAn Hospital，Capital Medical University，Beijing 100069，China

Research funding:

Scientific Research Project of Beijing Youan Hospital, CCMU, 2022 (BJYAYY-YN2022-02)

More Information

Corresponding author: ZHANG Jing， drzhangjing@163.com （ORCID： 0000-0002-3082-8330）

摘要

摘要: 丙型肝炎是肝癌发生的主要病因之一。随着直接抗病毒药物的应用，95%以上的患者可根除HCV，获得持续病毒学应答（SVR）。有效的抗病毒治疗可以改变丙型肝炎的自然病程，降低肝癌发生风险，但仍有一部分患者会受到年龄、性别、肝纤维化、糖尿病、肝脂肪变、饮酒和遗传因素等影响，成为肝癌高危人群。因此，如何识别和预测丙型肝炎SVR后肝癌高危人群需进一步明确与完善。本文通过系统综述丙型肝炎患者SVR后肝癌发生的危险因素和肝癌预测模型，旨在为临床识别丙型肝炎SVR后肝癌高风险人群提供依据。
- 丙型肝炎 /
- 持续病毒学应答 /
- 肝肿瘤 /
- 危险因素
Abstract: Hepatitis C is one of the main causes of liver cancer. With the application of direct-acting antiviral agents， more than 95% of patients can achieve the eradication of hepatitis C virus and obtain sustained virologic response （SVR）. Effective antiviral therapy can change the natural course of hepatitis C and reduce the risk of liver cancer； however， some patients are still affected by age， sex， liver fibrosis， diabetes， hepatic steatosis， alcohol consumption， and genetic factors and become the high-risk population of liver cancer. Therefore， it is needed to further clarify and improve the identification and prediction of high-risk populations of liver cancer after SVR of hepatitis C. This article reviews the risk factors and predictive models for liver cancer after SVR in patients with hepatitis C， in order to provide a basis for identifying the high-risk population of liver cancer after SVR of hepatitis C in clinical practice.
- Hepatitis C /
- Sustained Virologic Response /
- Liver Neoplasms /
- Risk Factors

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参考文献(37)

[1]	Chinese Society of Hepatology and Chinese Society of Infectious Diseases, Chinese Medical Association. Guidelines for the prevention and treatment of hepatitis C(2022 version)[J]. Chin J Infect Dis, 2023, 41( 1): 29- 46. DOI: 10.3760/cma.j.cn311365-20230217-00045. 中华医学会肝病学分会, 中华医学会感染病学分会. 丙型肝炎防治指南(2022年版)[J]. 中华传染病杂志, 2023, 41( 1): 29- 46. DOI: 10.3760/cma.j.cn311365-20230217-00045.
[2]	World Health Organization. Global progress report on HIV, viral hepatitis and sexually transmitted Global progress report on HIV, viral hepatitis and sexually transmitted infections, 2021[EB/OL]. Accountability for the global health sector strategies 2016- 2021: actions for impact, 2021, Geneva: World Health Organization.
[3]	PIÑERO F, MENDIZABAL M, RIDRUEJO E, et al. Treatment with direct-acting antivirals for HCV decreases but does not eliminate the risk of hepatocellular carcinoma[J]. Liver Int, 2019, 39( 6): 1033- 1043. DOI: 10.1111/liv.14041.
[4]	EUropean Association for the Study of the Liver. EASL recommendations on treatment of hepatitis C: Final update of the series[J]. J Hepatol, 2020, 73( 5): 1170- 1218. DOI: 10.1016/j.jhep.2020.08.018.
[5]	Professional Committee for Prevention and Control of Hepatobiliary and Pancreatic Diseases of Chinese Preventive Medicine Association; Professional Committee for Hepatology, Chinese Research Hospital Association; Chinese Society of Hepatology, Chinese Medical Association, et al. Guideline for stratified screening and surveillance of primary liver cancer(2020 edition)[J]. J Clin Hepatol, 2021, 37( 2): 286- 295. DOI: 10.3969/j.issn.1001-5256.2021.02.009. 中华预防医学会肝胆胰疾病预防与控制专业委员会, 中国研究型医院学会肝病专业委员会, 中华医学会肝病学分会, 等. 原发性肝癌的分层筛查与监测指南(2020版)[J]. 临床肝胆病杂志, 2021, 37( 2): 286- 295. DOI: 10.3969/j.issn.1001-5256.2021.02.009.
[6]	JÍLKOVÁ ZM, SEIGNEURIN A, COPPARD C, et al. Circulating IL-13 is associated with de novo development of HCC in HCV-infected patients responding to direct-acting antivirals[J]. Cancers, 2020, 12( 12): 3820. DOI: 10.3390/cancers12123820.
[7]	HAMOIR C, HORSMANS Y, STÄRKEL P, et al. Risk of hepatocellular carcinoma and fibrosis evolution in hepatitis C patients with severe fibrosis or cirrhosis treated with direct acting antiviral agents[J]. Acta Gastroenterol Belg, 2021, 84( 1): 25- 32. DOI: 10.51821/84.1.420.
[8]	RAVAIOLI F, CONTI F, BRILLANTI S, et al. Hepatocellular carcinoma risk assessment by the measurement of liver stiffness variations in HCV cirrhotics treated with direct acting antivirals[J]. Dig Liver Dis, 2018, 50( 6): 573- 579. DOI: 10.1016/j.dld.2018.02.010.
[9]	PREVEDEN T, VERES B, RUZIC M, et al. Triglyceride-Glucose Index and Hepatic Steatosis Index for the assessment of liver steatosis in HCV patients[J]. Minerva Gastroenterol, 2023, 69( 2): 254- 260. DOI: 10.23736/S2724-5985.22.03168-0.
[10]	MORADPOUR D, ENGLERT C, WAKITA T, et al. Characterization of cell lines allowing tightly regulated expression of hepatitis C virus core protein[J]. Virology, 1996, 222( 1): 51- 63. DOI: 10.1006/viro.1996.0397.
[11]	MORIYA K, FUJIE H, SHINTANI Y, et al. The core protein of hepatitis C virus induces hepatocellular carcinoma in transgenic mice[J]. Nat Med, 1998, 4( 9): 1065- 1067. DOI: 10.1038/2053.
[12]	NOUREDDIN M, WONG MM, TODO T, et al. Fatty liver in hepatitis C patients post-sustained virological response with direct-acting antivirals[J]. World J Gastroenterol, 2018, 24( 11): 1269- 1277. DOI: 10.3748/wjg.v24.i11.1269.
[13]	PELEG N, ISSACHAR A, SNEH ARBIB O, et al. Liver steatosis is a major predictor of poor outcomes in chronic hepatitis C patients with sustained virological response[J]. J Viral Hepat, 2019, 26( 11): 1257- 1265. DOI: 10.1111/jvh.13167.
[14]	KANWAL F, KRAMER J, ASCH SM, et al. Risk of hepatocellular cancer in HCV patients treated with direct-acting antiviral agents[J]. Gastroenterology, 2017, 153( 4): 996- 1005. e 1. DOI: 10.1053/j.gastro.2017.06.012.
[15]	DEGASPERI E, D’AMBROSIO R, IAVARONE M, et al. Factors associated with increased risk of de novo or recurrent hepatocellular carcinoma in patients with cirrhosis treated with direct-acting antivirals for HCV infection[J]. Clin Gastroenterol Hepatol, 2019, 17( 6): 1183- 1191. e 7. DOI: 10.1016/j.cgh.2018.10.038.
[16]	LU M, LI J, RUPP LB, et al. Hepatitis C treatment failure is associated with increased risk of hepatocellular carcinoma[J]. J Viral Hepat, 2016, 23( 9): 718- 729. DOI: 10.1111/jvh.12538.
[17]	KUKLA M, PIOTROWSKI D, WALUGA M, et al. Insulin resistance and its consequences in chronic hepatitis C[J]. Clin Exp Hepatol, 2015, 1( 1): 17- 29. DOI: 10.5114/ceh.2015.51375.
[18]	KARAGOZIAN R, DERDÁK Z, BAFFY G. Obesity-associated mechanisms of hepatocarcinogenesis[J]. Metabolism, 2014, 63( 5): 607- 617. DOI: 10.1016/j.metabol.2014.01.011.
[19]	TSAI PC, KUO HT, HUNG CH, et al. Metformin reduces hepatocellular carcinoma incidence after successful antiviral therapy in patients with diabetes and chronic hepatitis C in Taiwan[J]. J Hepatol, 2023, 78( 2): 281- 292. DOI: 10.1016/j.jhep.2022.09.019.
[20]	JACOB R, PRINCE DS, KENCH C, et al. Alcohol and its associated liver carcinogenesis[J]. J Gastroenterol Hepatol, 2023, 38( 8): 1211- 1217. DOI: 10.1111/jgh.16248.
[21]	EL-SERAG HB, MASON AC. Risk factors for the rising rates of primary liver cancer in the United States[J]. Arch Intern Med, 2000, 160( 21): 3227. DOI: 10.1001/archinte.160.21.3227.
[22]	ALLEN NE, BERAL V, CASABONNE D, et al. Moderate alcohol intake and cancer incidence in women[J]. J Natl Cancer Inst, 2009, 101( 5): 296- 305. DOI: 10.1093/jnci/djn514.
[23]	TRÉPO E, PRADAT P, POTTHOFF A, et al. Impact of patatin-like phospholipase-3(rs738409 C>G) polymorphism on fibrosis progression and steatosis in chronic hepatitis C[J]. Hepatology, 2011, 54( 1): 60- 69. DOI: 10.1002/hep.24350.
[24]	BALASUS D, WAY M, FUSILLI C, et al. The association of variants in PNPLA3 and GRP78 and the risk of developing hepatocellular carcinoma in an Italian population[J]. Oncotarget, 2016, 7( 52): 86791- 86802. DOI: 10.18632/oncotarget.13558.
[25]	OHTA A, OGAWA E, MURATA M, et al. Impact of the PNPLA3 genotype on the risk of hepatocellular carcinoma after hepatitis C virus eradication[J]. J Med Virol, 2022, 94( 10): 5007- 5014. DOI: 10.1002/jmv.27904.
[26]	BURLONE ME, BELLAN M, BARBAGLIA MN, et al. HSD17B13 and other liver fat-modulating genes predict development of hepatocellular carcinoma among HCV-positive cirrhotics with and without viral clearance after DAA treatment[J]. Clin J Gastroenterol, 2022, 15( 2): 301- 309. DOI: 10.1007/s12328-021-01578-1.
[27]	DEGASPERI E, GALMOZZI E, PELUSI S, et al. Hepatic fat-genetic risk score predicts hepatocellular carcinoma in patients with cirrhotic HCV treated with DAAs[J]. Hepatology, 2020, 72( 6): 1912- 1923. DOI: 10.1002/hep.31500.
[28]	IOANNOU GN. HCC surveillance after SVR in patients with F3/F4 fibrosis[J]. J Hepatol, 2021, 74( 2): 458- 465. DOI: 10.1016/j.jhep.2020.10.016.
[29]	ALONSO LÓPEZ S, MANZANO ML, GEA F, et al. A model based on noninvasive markers predicts very low hepatocellular carcinoma risk after viral response in hepatitis C virus-advanced fibrosis[J]. Hepatology, 2020, 72( 6): 1924- 1934. DOI: 10.1002/hep.31588.
[30]	DAJTI E, MARASCO G, RAVAIOLI F, et al. Risk of hepatocellular carcinoma after HCV eradication: Determining the role of portal hypertension by measuring spleen stiffness[J]. JHEP Rep, 2021, 3( 3): 100289. DOI: 10.1016/j.jhepr.2021.100289.
[31]	TANI J, MORISHITA A, SAKAMOTO T, et al. Simple scoring system for prediction of hepatocellular carcinoma occurrence after hepatitis C virus eradication by direct-acting antiviral treatment: All Kagawa Liver Disease Group Study[J]. Oncol Lett, 2020, 19( 3): 2205- 2212. DOI: 10.3892/ol.2020.11341.
[32]	SHIHA G, WAKED I, SOLIMAN R, et al. GES: A validated simple score to predict the risk of HCC in patients with HCV-GT4-associated advanced liver fibrosis after oral antivirals[J]. Liver Int, 2020, 40( 11): 2828- 2833. DOI: 10.1111/liv.14666.
[33]	IOANNOU GN, GREEN PK, BESTE LA, et al. Development of models estimating the risk of hepatocellular carcinoma after antiviral treatment for hepatitis C[J]. J Hepatol, 2018, 69( 5): 1088- 1098. DOI: 10.1016/j.jhep.2018.07.024.
[34]	FAN R, PAPATHEODORIDIS G, SUN J, et al. aMAP risk score predicts hepatocellular carcinoma development in patients with chronic hepatitis[J]. J Hepatol, 2020, 73( 6): 1368- 1378. DOI: 10.1016/j.jhep.2020.07.025.
[35]	QIU LX, XU SS, QIU YD, et al. Comparison of acknowledged hepatocellular carcinoma risk scores in high-risk hepatitis C patients with sustained virological response[J]. J Viral Hepat, 2023, 30( 6): 559- 566. DOI: 10.1111/jvh.13829.
[36]	NAHON P, BAMBA-FUNCK J, LAYESE R, et al. Integrating genetic variants into clinical models for hepatocellular carcinoma risk stratification in cirrhosis[J]. J Hepatol, 2023, 78( 3): 584- 595. DOI: 10.1016/j.jhep.2022.11.003.
[37]	IOANNOU GN, TANG WJ, BESTE LA, et al. Assessment of a deep learning model to predict hepatocellular carcinoma in patients with hepatitis C cirrhosis[J]. JAMA Netw Open, 2020, 3( 9): e2015626. DOI: 10.1001/jamanetworkopen.2020.15626.