Published online Jan 7, 2022. doi: 10.3748/wjg.v28.i1.96
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
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.