Development of hepatocellular carcinoma in treated and untreated patients with chronic hepatitis B virus infection

Lin, Chih-Lin; Kao, Jia-Horng

doi:.0.0.0

Clin Mol Hepatol > Epub ahead of print

Review

Development of hepatocellular carcinoma in treated and untreated patients with chronic hepatitis B virus infection

Chih-Lin Lin^1,2, Jia-Horng Kao^3,4,5,6

¹Department of Gastroenterology, Renai branch, Taipei City Hospital, Taipei, Taiwan
²Department of Psychology, National Chengchi University, Taipei, Taiwan
³Graduate Institute of Clinical Medicine, National Taiwan University, College of Medicine, Taipei, Taiwan
⁴Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
⁵Hepatitis Research Center, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan
⁶Department of Medical Research, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan

Correspondence :

Jia-Horng Kao ,
Tel: +886-2-23123456 ext. 67307, Fax: +886-2-23825962, Email: kaojh@ ntu.edu.tw

Received: October 31, 2022 Revised: January 2, 2023 Accepted: February 12, 2023

ABSTRACT

Hepatitis B virus (HBV) is responsible for more than 50% of hepatocellular carcinoma (HCC) in HBV hyperendemic areas, such as the Asia-Pacific region. Several hepatitis B viral factors are involved in HBV-related hepatocarcinogenesis. Hepatitis B viral load is the most important risk factor of HCC development. In addition, HBV integration, HBV genotype C, and core-promoter mutations are also associated with a risk of HCC development. For untreated chronic hepatitis B (CHB) patients, the estimated HCC incidence rates per 100 patient-years were 0.03–0.17 in inactive carriers, 0.07–0.42 in asymptomatic carriers, 0.12–0.49 in chronic hepatitis, and 2.03–3.37 in cirrhosis. Complementary to HBV DNA, serum levels of the hepatitis B surface antigen and hepatitis B core-related antigen (HBcrAg) can predict the occurrence of HCC for untreated patients with low and intermediate viral loads, respectively. For patients receiving antiviral therapy, the risks of HCC occurrence 40–60% lower than those for untreated patients. Patients treated with residual detectable HBV DNA or intrahepatic cccDNA still have a risk of HCC. Serum levels of HBcrAg, M2BPGi and fibrosis-4 are predictive of the risk of HCC development in treated patients. Several well-developed HCC risk scores can help clinicians identify high-risk CHB patients for HCC surveillance, regardless of treatment status. These strategies can help minimize the threat of HCC and prolong survival in CHB patients.

KeyWords: Chronic hepatitis B; Cirrhosis; Hepatocellular carcinoma