摘要
Our understanding of hepatitis B virus(HBV) reactivation during immunosuppresive therapy has increased remarkably during recent years. HBV reactivation in hepatitis B surface antigen(HBs Ag)-positive individuals has been well-described in certain immunosuppressive regimens, including therapies containing corticosteroids, anthracyclines, rituximab, antibody to tumor necrosisfactor(anti-TNF) and hematopoietic stem cell transplantation(HSCT). HBV reactivation could also occur in HBs Ag-negative, antibody to hepatitis B core antigen(anti-HBc) positive individuals during therapies containing rituximab, anti-TNF or HSCT.For HBs Ag-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 HBs Ag-negative, antiHBc 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 HBs Ag-positive and HBs Ag-negative, anti-HBc positive individuals.
Our understanding of hepatitis B virus （HBV） reactivationduring immunosuppresive therapy has increasedremarkably during recent years. HBV reactivation inhepatitis B surface antigen （HBsAg）-positive individualshas been well-described in certain immunosuppressiveregimens, including therapies containing corticosteroids,anthracyclines, rituximab, antibody to tumor necrosisfactor （anti-TNF） and hematopoietic stem cell transplantation（HSCT）. HBV reactivation could also occur inHBsAg-negative, antibody to hepatitis B core antigen（anti-HBc） positive individuals during therapies containingrituximab, anti-TNF or HSCT.For HBsAg-positive patients,prophylactic antiviral therapy is proven to the effectivein preventing HBV reactivation. Recent evidence alsodemonstrated entecavir to be more effective thanlamivudine in this aspect. For HBsAg-negative, anti-HBc positive individuals, the risk of reactivations differswith the type of immunosuppression. For rituximab, aprospective study demonstrated the 2-year cumulativerisk of reactivation to be 41.5%, but prospective datais still lacking for other immunosupressive regimes. Theoptimal management in preventing HBV reactivationwould involve appropriate risk stratification for differentimmunosuppressive regimes in both HBsAg-positive andHBsAg-negative, anti-HBc positive individuals.
