Case Report
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World J Gastroenterol. May 7, 2014; 20(17): 5165-5170
Published online May 7, 2014. doi: 10.3748/wjg.v20.i17.5165
Hepatitis B surface antigen seroconversion after HBV reactivation in non-Hodgkin’s lymphoma
Wei-Ping Liu, Wen Zheng, Yu-Qin Song, Ling-Yan Ping, Gui-Qiang Wang, Jun Zhu
Wei-Ping Liu, Wen Zheng, Yu-Qin Song, Ling-Yan Ping, Jun Zhu, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Lymphoma, Peking University Cancer Hospital and Institute, Beijing 100142, China
Gui-Qiang Wang, Department of Infectious Diseases, Center for Liver Diseases, Peking University First Hospital, Beijing 100142, China
Author contributions: Liu WP, Wang GQ and Zhu J designed the study; Liu WP, Zheng W and Song YQ performed the research; Ping LY analyzed the data; and Liu WP and Zhu J wrote the paper.
Supported by National Natural Science Foundation of China, Grant No. 81241073; and Peking University Cancer Hospital Foundation for Scientific Research, Grant No. 2013-Autonomous-9
Correspondence to: Jun Zhu, MD, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Lymphoma, Peking University Cancer Hospital and Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China. zhu-jun@bjcancer.org
Telephone: +86-10-88196596 Fax: +86-10-88196115
Received: September 12, 2013
Revised: February 24, 2014
Accepted: March 4, 2014
Published online: May 7, 2014
Processing time: 236 Days and 20.3 Hours
Abstract

Reactivation of hepatitis B virus (HBV) can occur in lymphoma patients infected with HBV when they receive chemotherapy or immunotherapy. Prophylactic administration of lamivudine (LAM) reduces the morbidity and mortality associated with HBV reactivation. However, what defines HBV reactivation and the optimal duration of treatment with LAM have not yet been clearly established. HBV reactivation may occur due to the cessation of prophylactic LAM, although re-treatment with nucleoside analogs may sometimes result in hepatitis B surface antigen (HBsAg) seroconversion, which is a satisfactory endpoint for the management of HBV infection. We report a case of HBV reactivation in a 68-year-old HBsAg-positive patient who received rituximab-based immunochemotherapy for follicular lymphoma. HBV reactivation developed following cessation of prophylactic LAM therapy. The patient subsequently received treatment with entecavir (ETV), which led to a rapid and sustained suppression of HBV replication and HBsAg seroconversion. We also appraised the literature concerning HBV reactivation and the role of ETV in the management of HBV reactivation in lymphoma patients. A total of 28 cases of HBV reactivation have been reported as having been treated with ETV during or after immunosuppressive chemotherapy in lymphoma patients. We conclude that ETV is an efficacious and safe treatment for HBV reactivation following LAM cessation in lymphoma patients treated with rituximab-based immunochemotherapy.

Keywords: Hepatitis B surface antigen; Seroconversion; Non-Hodgkin’s lymphoma; Rituximab; Entecavir

Core tip: We describe the case of a 68-year-old hepatitis B surface antigen (HBsAg)-positive male patient who received rituximab-based immunochemotherapy for follicular lymphoma, and experienced hepatitis B virus (HBV) reactivation following cessation of lamivudine prophylaxis. Subsequent entecavir treatment produced rapid, sustained viral suppression and HBsAg seroconversion. Lamivudine prevents HBV reactivation but resistance rates may be as high as 17% in lymphoma patients. Available data suggest that entecavir is effective and safe for the treatment of HBV reactivation in lymphoma patients. Prophylactic antiviral therapy is recommended for patients with active or occult HBV infection following chemotherapy or immunochemotherapy. Potent antiviral drugs with a high genetic barrier to resistance should be considered in these cases.