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©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Apr 28, 2015; 7(6): 825-830
Published online Apr 28, 2015. doi: 10.4254/wjh.v7.i6.825
Hepatitis B virus reactivation during immunosuppressive therapy: Appropriate risk stratification
Wai-Kay Seto
Wai-Kay Seto, Department of Medicine, the University of Hong Kong, Queen Mary Hospital, Hong Kong, China
Wai-Kay Seto, Department of Medicine, the University of Hong Kong-Shenzhen Hospital, Shenzhen 518053, China
Wai-Kay Seto, State Key Laboratory for Liver Research, the University of Hong Kong, Hong Kong, China
Author contributions: Seto WK solely contributed to this manscript.
Conflict-of-interest: Seto WK is an advisory board member of Gilead Sciences and received speaker’s fees from Bristol-Myers Squibb.
Correspondence to: Dr. Wai-Kay Seto, Department of Medicine, the University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong, China. wkseto@hku.hk
Telephone: +852-2-2553994 Fax: +852-2-8162863
Received: January 13, 2015
Peer-review started: January 15, 2015
First decision: February 7, 2015
Revised: February 14, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: April 28, 2015
Processing time: 108 Days and 2.6 Hours
Core Tip

Core tip: Hepatitis B virus (HBV) reactivation not only occurs in hepatitis B surface antigen (HBsAg)-positive, but also in HBsAg-negative, antibody to hepatitis B core antigen positive individuals. Immunosuppressive therapies with increased risk of HBV reactivation include corticosteroids, anthracyclines, rituximab, antibody to tumor necrosis factor and hematopoietic stem cell transplantation. The decision between prophylactic antiviral therapy vs routine clinical monitoring would involve appropriate risk stratification for individual types of immunosuppressives regimes.