Effect of occult hepatitis B virus infection on the early-onset of hepatocellular carcinoma in patients with hepatitis C virus infection

Oncol Rep. 2013 Nov;30(5):2049-55. doi: 10.3892/or.2013.2700. Epub 2013 Aug 27.

Abstract

Although overt hepatitis B virus (HBV) infection promotes the onset of hepatocellular carcinoma (HCC) in hepatitis C virus (HCV)-infected patients, the effect of occult HBV infection remains unclear. The aim of this study was to investigate the effect of occult HBV infection on the early-onset of HCC in HCV-infected patients. A total of 173 HCC patients with HCV infection were enrolled and classified into 2 groups according to the median age of HCC onset: the early-onset group (n=91; 61.1±5.6 years) and the late-onset group (n=82; 73.8±3.7 years). Independent factors associated with the early-onset of HCC were assessed by multivariate analysis. In the overall analysis, independent risk factors for the early-onset of HCC were the white blood cell count and alanine aminotransferase level, but not the presence of HBV DNA. In a stratification analysis according to albumin levels of ≥3.5 g/dl, the presence of HBV DNA was a significant independent risk factor for the early-onset of HCC (OR 145.18, 95% CI 1.38-15296.61, P=0.036), whereas the presence of antibodies against hepatitis B core antigen was not found to be a risk factor. The presence of HBV DNA was not a risk factor for the early-onset of HCC in the overall analysis. However, its presence was an independent factor for the early-onset of HCC in HCV-infected patients with an albumin level of ≥3.5 g/dl. Thus, occult HBV infection may accelerate hepatocarcino-genesis in HCV-infected patients with relatively low carcinogenic potential.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Alanine Transaminase / blood
  • Carcinoma, Hepatocellular / blood
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / pathology*
  • DNA, Viral / blood
  • DNA, Viral / immunology
  • Female
  • Hepacivirus / genetics
  • Hepacivirus / pathogenicity
  • Hepatitis B / blood
  • Hepatitis B / genetics
  • Hepatitis B / pathology*
  • Hepatitis B Surface Antigens / blood
  • Hepatitis B Surface Antigens / immunology
  • Hepatitis B virus / genetics
  • Hepatitis B virus / pathogenicity
  • Hepatitis C / blood
  • Hepatitis C / genetics
  • Hepatitis C / pathology*
  • Humans
  • Liver Neoplasms / blood
  • Liver Neoplasms / genetics
  • Liver Neoplasms / pathology*
  • Male
  • Middle Aged
  • Risk Factors

Substances

  • DNA, Viral
  • Hepatitis B Surface Antigens
  • Alanine Transaminase