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直接作用抗病毒药物时代的未满足需求:丙型肝炎病毒清除后肝细胞癌的风险和分子机制。

Unmet needs in the post-direct-acting antivirals era: The risk and molecular mechanisms of hepatocellular carcinoma after hepatitis C virus eradication.

机构信息

Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

College of Medicine and Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical University, Kaohsiung, Taiwan.

出版信息

Clin Mol Hepatol. 2024 Jul;30(3):326-344. doi: 10.3350/cmh.2024.0155. Epub 2024 Apr 26.

Abstract

Hepatitis C virus (HCV) infection is one of the major etiologies of hepatocellular carcinoma (HCC) with approximately 30% of HCC being due to HCV infection worldwide. HCV eradication by antivirals greatly reduces the risk of HCC; nevertheless, HCC remains to occur in chronic hepatitis C (CHC) patients who have achieved a sustained virological response (SVR). The proportion of post-SVR HCC among newly diagnosed HCC patients is increasing in the direct-acting antiviral (DAA) era and might be due to preexisting inflammatory and fibrotic liver backgrounds, immune dysregulation between host and virus interactions, as well as host epigenetic scars, genetic predispositions and alternations. By means of applying surrogate markers and adopting risk stratification, HCC surveillance should be consistently performed in high-risk populations. In this review, we discuss the possible molecular mechanism, risk factors, and HCC surveillance strategy for HCC development after HCV eradication in CHC patients.

摘要

丙型肝炎病毒 (HCV) 感染是肝细胞癌 (HCC) 的主要病因之一,全球约有 30%的 HCC 归因于 HCV 感染。抗病毒药物清除 HCV 可大大降低 HCC 的风险;然而,在获得持续病毒学应答 (SVR) 的慢性丙型肝炎 (CHC) 患者中仍会发生 HCC。在直接作用抗病毒药物 (DAA) 时代,新诊断 HCC 患者中 post-SVR HCC 的比例在增加,这可能归因于先前存在的炎症和纤维化肝脏背景、宿主与病毒相互作用之间的免疫失调,以及宿主表观遗传痕迹、遗传易感性和改变。通过应用替代标志物和采用风险分层,可以在高危人群中持续进行 HCC 监测。在这篇综述中,我们讨论了 CHC 患者 HCV 清除后 HCC 发展的可能分子机制、危险因素和 HCC 监测策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a73c/11261227/edcba50dc1c6/cmh-2024-0155f1.jpg

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