Reactivation of hepatitis B virus during rituximab treatment of a patient with follicular lymphoma

Dear Editor, It has been demonstrated that reactivation of hepatitis B (HBV) replication can occur during either the natural course of HBV infection or immunosuppression. Whether the clinical course of HBV reactivation is a self-limiting hepatitis or a fatal fulminating hepatitis, its early detection and emergency management is mandatory, especially in lymphoma patients who are also carriers of HBV (HBV surface antigen [HBsAg]-positive) and recipients of chemotherapy or immunosuppressive treatment. Treatment of B cell non-Hodgkin’s lymphomas (NHL) with rituximab, a chimeric anti-CD20 monoclonal antibody, has greatly improved the outcome of these patients. However, sporadic cases of HBV reactivation have been reported in lymphoma patients treated with the combination of rituximab, multiagent chemotherapy, and steroid. Whether HBV reactivation is caused by rituximab itself has not been determined because both chemotherapy and steroid individually have this capability. In this paper, we report that HBV was reactivated in a HBsAg-positive follicular lymphoma patient who was treated with rituximab monotherapy. A 41-year-old woman with stage IVA, grade I follicular lymphoma, presented with cervical, axillary, and paraaortic lymphadenopathy and bone marrow involvement in Dec. 2003. She was a HBsAg-positive, hepatitis B envelope antigen (HBeAg)-negative, and anti-HBeAg-positive HBV carrier. To avoid reactivation of HBV, she was treated with chlorambucil monotherapy but no steroid drugs. A partial remission was achieved. However, after 4 months of chemotherapy, HBV reactivation occurred with elevated