Antivirals and chemotherapy: Managing cancer patients with hepatitis
Active hepatitis B virus (HBV) and hepatitis C virus (HCV) are highly prevalent around the world.
- Date: 02 Oct 2012
- Topic: Gastrointestinal cancers
Approximately one third of the world’s population (over 2 billion people) has been infected with HBV and 350 million have chronic HBV infection. Around 150 million people have chronic HCV infection and 350,000 people die annually from HCV-related liver diseases.
According to the World Health Organization (WHO), 1 million people a year die from HBV- and HCV- related liver disease.
In a special symposium at ESMO 2012 Vienna on ‘Key topics in supportive care’, Dr John Lubel of Eastern Health, Melbourne, Australia, presented strategies and approaches to dealing with patients infected by HBV and HCV who are undergoing chemotherapy. Different strategies are necessary for their effective treatment, he said, because the two viruses differ significantly in virology, natural history and therefore management approaches.
In chronic viral hepatitis there is equilibrium between the host’s immunity and viral replication, resulting in immunosuppression that doesn’t inhibit viral replication. In non-cirrhotic HCV patients, this rarely results in significant complications; HCV patients undergoing immunosuppressive therapy, such as chemotherapy, generally just require monitoring.
In contrast, patients with HBV may have significant hepatitis ‘flares’ following periods of immunosuppression which may lead to hepatic failure, the need for liver transplant or death in the most extreme cases. Although HBV does not kill cells, inflammation results from immune-mediated injury and therefore generally occurs following periods of maximal immunosuppression. To prevent such reactivation, Dr Lubel recommended that patients with chronic HBV take antiviral prophylaxis prior to immunosuppressive chemotherapy and remain on antivirals for a year after chemotherapy is finished.
Patients with high viral loads should take antiviral agents such as entecavir and tenofovir; these drugs have a high genetic barrier to viral resistance. Lamivudine is acceptable for patients with low or undetectable viral loads.
Dr Lubel warned that in patients who seem to have cleared their hepatitis B infection, reactivation of the virus can occur with the subsequent reappearance of surface antigen (seroreversion) followed by clinically significant HBV flares. He also noted that the risk of this seems to be particularly high for chemotherapy regimens containing the anti CD20 antibody, Rituximab. Thus, patients who cannot be closely monitored for virus reactivation through monthly HBV DNA quantification and liver function tests should also receive antiviral prophylaxis.
Dr Lubel advised that the management of HBV and HCV should be in the domain of the hepatologist. “The essential role of the oncologist is to be aware of the problem and screen appropriately”, said Dr Lubel.