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Hepatitis B virus (HBV) reactivation following immunosuppression is defined by an abrupt rise in HBV replication followed by laboratory signs of hepatocellular injury in a "silent" hepatitis B surface antigen (HBsAg) carrier. Reactivation can also occur, albeit at a lower rate, in patients with occult HBV infection. The clinical presentation of reactivation is variable ranging from an asymptomatic course to severe hepatitis, liver failure, and death. It is most frequently observed in patients with lymphoma treated with rituximab and corticosteroids as well as in patients undergoing stem cell and bone marrow transplantation. Other risk groups include patients with solid tumors, subjects infected with human immunodeficiency virus, organ transplant recipients, and those with autoimmune diseases (i.e., inflammatory bowel disease, rheumatoid arthritis). In cancer patients, HBV reactivation can lead to interruption of chemotherapy with serious impact on prognosis. In HBsAg-positive patients who are candidates for chemotherapy or treatment with biologic agents, preemptive treatment with an antiviral agent such as lamivudine, and lately with the more potent tenofovir or entecavir, has become a standard of care, effectively preventing HBV reactivation. Patients with occult HBV should be monitored for alanine aminotransferase and HBV DNA during the course of immunosuppression. Prompt administration of a potent antiviral agent upon diagnosis of reactivation may be lifesaving in such patients.
Shibolet et al. (Sat,) studied this question.