Luna-Cuadros MA, Chen HW, Hanif H, Ali MJ, Khan MM, Lau DTY. Risk of hepatocellular carcinoma after hepatitis C virus cure. World J Gastroenterol 2022; 28(1): 96-107 [PMID: 35125821 DOI: 10.3748/wjg.v28.i1.96]
Corresponding Author of This Article
Daryl Tan-Yeung Lau, MD, MSc, Associate Professor, Liver Center, Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis Street, Suite 4A, Boston, MA 02215, United States. dlau@bidmc.harvard.edu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jan 7, 2022; 28(1): 96-107 Published online Jan 7, 2022. doi: 10.3748/wjg.v28.i1.96
Risk of hepatocellular carcinoma after hepatitis C virus cure
Maria Alejandra Luna-Cuadros, Hao-Wei Chen, Hira Hanif, Mukarram Jamat Ali, Muzammil Muhammad Khan, Daryl Tan-Yeung Lau
Maria Alejandra Luna-Cuadros, Hao-Wei Chen, Hira Hanif, Mukarram Jamat Ali, Muzammil Muhammad Khan, Daryl Tan-Yeung Lau, Liver Center, Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States
Author contributions: Luna-Cuadros MA, Chen HW contributed equally to this work; Luna-Cuadros MA, Chen HW organized and wrote significant sections and revision of the manuscript; Hanif H, Khan MM contributed to the literature search and manuscript writing; Ali AJ designed the figures and contributed to the edit and revision of the manuscript; Lau DTY provided guidance on the overall concept and execution of the manuscript.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Daryl Tan-Yeung Lau, MD, MSc, Associate Professor, Liver Center, Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis Street, Suite 4A, Boston, MA 02215, United States. dlau@bidmc.harvard.edu
Received: May 29, 2021 Peer-review started: May 29, 2021 First decision: June 22, 2021 Revised: July 12, 2021 Accepted: December 25, 2021 Article in press: December 25, 2021 Published online: January 7, 2022 Processing time: 216 Days and 10.7 Hours
Abstract
Hepatitis C virus (HCV) is a significant cause of hepatocellular carcinoma (HCC). The direct-acting antivirals marked a new era of HCV therapy and are associated with greater than 95% cure rate. Successful treatment of chronic hepatitis C greatly reduces the risk of HCC. A proportion of patients, especially those with pre-existing cirrhosis, remain at risk for HCC despite sustained virologic response (SVR). Diabetes mellitus, hepatic steatosis, alcohol consumption and lack of fibrosis regression are associated with risks of HCC after HCV cure. Noninvasive modalities such as aspartate aminotransferase to platelet ratio index and fibrosis-4 index and transient elastography have been used to monitor hepatic fibrosis. More recently, various fibrosis scores have been combined with clinical parameters and other novel biomarkers to predict risks of HCC for patients who achieved SVR. These models still need to be validated and standardized prior to applying to routine clinical care.
Core Tip: Direct-acting antivirals (DAA) therapy has revolutionized the treatment for chronic hepatitis C. However, the development of hepatocellular carcinoma (HCC) after achieving DAA-induced sustained virologic response remains a significant concern, especially those with advanced fibrosis. It is critically important to monitor hepatic fibrosis and continue HCC surveillance for patients with pre-existing cirrhosis. Lack of hepatic regression and several comorbid conditions are associated with HCC risks. Some promising models for predicting HCC risks after hepatitis C virus cure are in development.
