Published online Apr 28, 2015. doi: 10.4254/wjh.v7.i6.825
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
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.
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.