Yang Caiyun, Lv Fengxiang, Yang Jiaqi, Ding Dawei, Cui Lina, Han Ying
Xi'an Medical University, Xi'an 710021, Shannxi, PR China; National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Xijing Hospital, Air Force Military Medical University, Xi'an 710032, PR China.
National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Xijing Hospital, Air Force Military Medical University, Xi'an 710032, PR China.
Ann Hepatol. 2024 Sep 12;30(2):101582. doi: 10.1016/j.aohep.2024.101582.
Hepatitis C virus (HCV) belongs to the Flaviviridae family, and is a single-stranded RNA virus with positive polarity. It is the primary cause of hepatocellular carcinoma (HCC) worldwide. The treatment of HCV has entered a new era with the advent of direct-acting antiviral drugs (DAAs) and is associated with cure rates of more than 95 %, making HCV the only curable viral disease. The successful treatment of chronic hepatitis C has greatly reduced, but not eliminated, the risk of HCC. Certain individuals, especially those with cirrhosis already present, remain vulnerable to HCC after achieving a sustained virological response (SVR). This article systematically reviews the recent studies on the risk and mechanisms of HCC development after HCV viral cure, the screening and predictive value of biological markers, and patient surveillance. Factors such as older age, diabetes, hepatic fat accumulation, alcohol use, and lack of fibrosis reversal are linked to increased HCC risk after HCV cure. The mechanism of HCC development after DAAs treatment remains unclear, but the possible mechanisms include immune cell dysfunction during HCV infection, cytokine network imbalance, epigenetic alterations, and host factors. Several biological markers and risk prediction models have been used to monitor the risk of HCC in CHC patients who have achieved SVR, but most still require validation and standardization. The implementation of risk-stratified surveillance programs is becoming urgent from a cost-effective point of view, but the availability of validated biomarkers to predict HCC in cured patients remains an unmet clinical need. Additionally, managing CHC patients who achieve SVR is becoming a growing challenge as an increasing number of HCV patients are cured.
丙型肝炎病毒（HCV）属于黄病毒科，是一种正链单链RNA病毒。它是全球肝细胞癌（HCC）的主要病因。随着直接作用抗病毒药物（DAAs）的出现，HCV治疗进入了一个新时代，治愈率超过95%，使HCV成为唯一可治愈的病毒性疾病。慢性丙型肝炎的成功治疗大大降低了但并未消除HCC的风险。某些个体，尤其是那些已经存在肝硬化的个体，在实现持续病毒学应答（SVR）后仍易患HCC。本文系统综述了HCV病毒治愈后HCC发生风险及机制、生物标志物的筛查和预测价值以及患者监测的最新研究。年龄较大、糖尿病、肝脏脂肪堆积、饮酒和纤维化未逆转等因素与HCV治愈后HCC风险增加有关。DAAs治疗后HCC发生的机制尚不清楚，但可能的机制包括HCV感染期间免疫细胞功能障碍、细胞因子网络失衡、表观遗传改变和宿主因素。几种生物标志物和风险预测模型已被用于监测已实现SVR的CHC患者发生HCC的风险，但大多数仍需要验证和标准化。从成本效益的角度来看，实施风险分层监测计划变得迫在眉睫，但在治愈患者中预测HCC的经过验证的生物标志物的可用性仍然是未满足的临床需求。此外，随着越来越多的HCV患者被治愈，管理已实现SVR的CHC患者正成为一个日益严峻的挑战。
