The difficulties of managing severe hepatitis B virus reactivation
Version of Record online: 4 JAN 2011
© 2011 John Wiley & Sons A/S
Special Issue: Proceedings of the 4th Paris Hepatitis Conference. The publication of this supplement was supported by an unrestricted educational grant from F. Hoffmann-Laroche Ltd.
Volume 31, Issue Supplement s1, pages 104–110, January 2011
How to Cite
Roche, B. and Samuel, D. (2011), The difficulties of managing severe hepatitis B virus reactivation. Liver International, 31: 104–110. doi: 10.1111/j.1478-3231.2010.02396.x
- Issue online: 4 JAN 2011
- Version of Record online: 4 JAN 2011
- Received 10 November 2010Accepted 26 November 2010
- Liver failure;
- Nucleoside analogue
Reactivation of hepatitis B is characterized by a sudden increase in hepatitis B virus (HBV) replication in a patient with prior evidence of resolved or inactive HBV infection. Although HBV reactivation can occur spontaneously, it usually occurs after chemotherapy, immunosuppression (organ transplantation) or an alteration in immune function (therapy for autoimmune disease, human immunodeficiency virus infection). The clinical presentation cases can vary, ranging from a subclinical, asymptomatic course to severe acute hepatitis and even death. Although reactivation of HBV is mainly found in HBsAg-positive patients, it can be observed in serologically recovered anti-hepatitis B core antibody (HBc)-positive, HBsAg-negative patients. Serum HBV DNA typically increases during immune suppression, followed by a disease flare and HBV DNA clearance following immune restoration after immune suppression is stopped. In organ transplant recipients, without immune reconstitution, high HBV DNA levels can lead to fibrosing cholestatic hepatitis related to the direct cytopathic effect of HBV. Several randomized, controlled trials and meta-analyses have shown that reactivation can be prevented by lamivudine prophylaxis. Screening for HBsAg and anti-HBc should be performed before beginning immunosuppressive treatment and routine prophylaxis is recommended in HBsAg-positive patients. The optimal duration of prophylaxis remains to be determined. In anti-HBc-positive patients with or without anti-hepatitis B surface antigen, alanine transaminase and HBV DNA levels should be closely monitored and antiviral therapy should be started when HBV reactivation is confirmed. The use of new more potent nucleos(t)ides analogues with lower resistance rates would seem to be logical; however, experience with these drugs in the prophylaxis and treatment of severe HBV reactivation is limited.