Editorial
Copyright ©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.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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
Abstract

Our understanding of hepatitis B virus (HBV) reactivation during immunosuppresive therapy has increased remarkably during recent years. HBV reactivation in hepatitis B surface antigen (HBsAg)-positive individuals has been well-described in certain immunosuppressive regimens, including therapies containing corticosteroids, anthracyclines, rituximab, antibody to tumor necrosis factor (anti-TNF) and hematopoietic stem cell transplantation (HSCT). HBV reactivation could also occur in HBsAg-negative, antibody to hepatitis B core antigen (anti-HBc) positive individuals during therapies containing rituximab, anti-TNF or HSCT.For HBsAg-positive patients, prophylactic antiviral therapy is proven to the effective in preventing HBV reactivation. Recent evidence also demonstrated entecavir to be more effective than lamivudine in this aspect. For HBsAg-negative, anti-HBc positive individuals, the risk of reactivations differs with the type of immunosuppression. For rituximab, a prospective study demonstrated the 2-year cumulative risk of reactivation to be 41.5%, but prospective data is still lacking for other immunosupressive regimes. The optimal management in preventing HBV reactivation would involve appropriate risk stratification for different immunosuppressive regimes in both HBsAg-positive and HBsAg-negative, anti-HBc positive individuals.

Keywords: Hepatitis B virus; Antibody to hepatitis B core antigen; Hepatitis B surface antigen; Rituximab; Antigen CD20; Hematopoietic stem cell transplantation; Antibody to tumor necrosis factor; Occult

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.