Volume 7, Issue 10 , Pages 1130-1137, October 2009
Reactivation of Hepatitis B With Reappearance of Hepatitis B Surface Antigen After Chemotherapy and Immunosuppression
Background & Aims
HBV infection may reactivate in the setting of immunosuppression, although the frequency and consequences of HBV reactivation are not well known. We report 6 patients who experienced loss of serologic markers of hepatitis B immunity and reappearance of HBsAg in the serum as a result of a variety of acquired immune deficiencies.
Methods
Between 2000 and 2005, six patients with reactivation of hepatitis B were seen in consultation by the Liver Diseases Branch at the Clinical Center, National Institutes of Health. The course and outcome of these 6 patients were reviewed.
Results
All 6 patients developed reappearance of HBsAg and evidence of active liver disease after stem cell transplantation (n = 4), immunosuppressive therapy (n = 1), or change in human immunodeficiency virus antiretroviral regimen (n = 1), despite having antibody to HBsAg (anti-HBs) or antibody to hepatitis B core antigen (anti-HBc) without HBsAg before. All 6 patients developed chronic hepatitis B, 2 patients transmitted hepatitis B to their spouses, and 1 patient developed cirrhosis. The diagnosis of hepatitis B reactivation was frequently missed or delayed and often required interruption of the therapy for the underlying condition. None of the patients received antiviral prophylaxis against HBV reactivation.
Conclusions
Serologic evidence of recovery from hepatitis B infection does not preclude its reactivation after immunosuppression. Screening for serologic evidence of hepatitis B and prophylaxis of those with positive results by using nucleoside analogue antiviral therapy should be provided to individuals in whom immunosuppressive therapy is planned.
Abbreviations used in this paper: ALP, alkaline phosphatase, anti-HBc, antibody to hepatitis B core antigen, anti-HBs, antibody to hepatitis B surface antigen, CML, chronic myelogenous leukemia, GVHD, graft-versus-host disease, HIV, human immunodeficiency virus
Conflicts of interest The authors disclose the following: Dr Uri Lopatin runs the HBV translational medicine program at Roche Pharmaceuticals. He made his contributions to the manuscript 3 years ago, when he was an NIH fellow. The remaining authors disclose no conflicts.
Funding This research was supported by the Intramural Research Programs of the NIDDK (Z01 DK054514-02), NIAID, NHLBI, and NCI, NIH.
PII: S1542-3565(09)00600-4
doi:10.1016/j.cgh.2009.06.027
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
Volume 7, Issue 10 , Pages 1130-1137, October 2009


