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Risk stratification for hepatitis B virus related hepatocellular carcinoma
Author(s) -
Lin ChihLin,
Kao JiaHorng
Publication year - 2013
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12010
Subject(s) - hepatocellular carcinoma , medicine , hbsag , hepatitis b virus , cirrhosis , hepatitis b , liver disease , liver cancer , cohort , gastroenterology , immunology , virology , virus
Hepatitis B virus ( HBV ) infection is the major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma ( HCC ) worldwide, especially in the A sia– P acific region. Several hepatitis B viral factors predictive of clinical outcomes in HBV carriers have been identified. The Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer‐HBV ( REVEAL ‐ HBV ) study from T aiwan illustrated the strong association between HBV ‐ DNA level at study entry and risk of HCC over time. In this community‐based cohort study, male gender, older age, high serum alanine aminotransferase level, positive hepatitis B e antigen, higher HBV ‐ DNA level, HBV genotype C infection, and core promoter mutation are independently associated with a higher risk of HCC . Another large hospital‐based Elucidation of Risk Factors for Disease Control or Advancement in T aiwanese Hepatitis B Carriers cohort of Taiwanese patients further validated the findings of REVEAL ‐ HBV . The risk of HCC started to increase when HBV ‐ DNA level was higher than 2000 IU/mL. Both HBV ‐ DNA and HBsAg levels were shown to be associated with HCC development. While HBV ‐ DNA level had better predictive accuracy than HBsAg level, when investigating the overall cohort in patients with HBV ‐ DNA level < 2000 IU/mL, HBsAg level ≥ 1000 IU/mL was identified as a new independent risk factor for HCC . With the results from REVEAL ‐ HBV , a risk calculation for predicting HCC in non‐cirrhotic patients has been developed and validated by independent cohorts ( R isk E stimation for H epatocellular C arcinoma in C hronic H epatitis B ).Taken together, ample evidence indicates that HBsAg level can complement HBV ‐ DNA level in predicting HCC development, especially in HBV carriers with low viral load. In conclusion, HBV treatment guidelines should include the risk stratification of HCC to individualize the management of HBV carriers with different levels of HCC risk.