96IN - How to deal with patients with active hepatitis B & C

Date 01 October 2012
Event ESMO Congress 2012
Session Key topics in supportive care
Topics Supportive measures
Presenter John Lubel
Authors J. Lubel
  • Eastern Health, 3128 - Melbourne/AU


Chronic viral hepatitis is a global problem with approximately 350 million people infected with hepatitis B virus (HBV) and 170 million people infected with hepatitis C virus (HCV) worldwide. It is estimated that one-third of the worlds population (over 2 billion people) have been infected with HBV. In Europe the prevalence of HBV ranges between 0.1% and 7% whereas the prevalence of HCV ranges between 0.4% and 22%. These two viruses account for the majority of cases of chronic viral hepatitis and contribute to the development of cirrhosis and hepatocellular carcinoma, yet differ markedly in virology, natural history and management. In chronic viral hepatitis, equilibrium exists between the host's immunity and viral replication. Immunosuppression allows viral replication to continue unchecked. In non-cirrhotic patients with HCV infection this rarely results in significant clinical sequelae and patients embarking on immunosuppressive therapy can generally be monitored. In contrast, patients infected with hepatitis B may have significant hepatitis ‘flares’ following periods of immunosuppression which can result in hepatic failure, need for liver transplant and occasionally death. The hepatitis B virus itself is not cytopathic; hepatic inflammation occurs as a result of immune-mediated injury and therefore generally occurs after maximal immunosuppression. The cornerstone to management of HBV in patients receiving chemotherapy is identification of currently or previously infected patients with appropriate requesting and interpretation of hepatitis B serology. In order to prevent HBV reactivation, all patients with chronic hepatitis B (CHB) should be started on antiviral prophylaxis before commencing immunosuppressive chemotherapy and for a period of 12 months after chemotherapy has been completed. In patients with high viral loads the use of antiviral agents with a high genetic barrier to resistance should be considered (eg entecavir and tenofovir). In those with low or undetectable viral loads lamivudine is an acceptable alternative. In patients who have apparently cleared hepatitis B (surface antigen negative, core antibody positive), HBV can reactivate with subsequent reappearance of surface antigen (seroreversion). This can be followed by clinically significant HBV flares. The risk of this occurring seems particularly high for regimens containing Rituximab. Patients unable to be monitored closely for reactivation with monthly HBV DNA quantification and liver function tests should receive antiviral prophylaxis.


The author has declared no conflicts of interest.