Reactivation of hepatitis B virus (HBV) infection in adult T-cell leukemia–lymphoma patients with resolved HBV infection following systemic chemotherapy
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Reactivation of hepatitis B virus (HBV) infection may occur in adult T-cell leukemia–lymphoma (ATL) patients with resolved HBV infection who receive monotherapy with the anti-CC chemokine receptor 4 monoclonal antibody, mogamulizumab. However, there is little evidence regarding the incidence and characteristics of HBV reactivation in ATL patients receiving systemic chemotherapy, including the use of this antibody. We conducted a retrospective study for 24 ATL patients with resolved HBV infection underwent regular HBV DNA monitoring to assess HBV reactivation in Nagoya City University Hospital between January 2005 and June 2013. With median HBV DNA follow-up of 238 days (range 57–1420), HBV reactivation (defined as the detection of HBV DNA) was observed in three (12.5 %) of 24 patients with resolved HBV infection. No hepatitis due to HBV reactivation occurred in those patients who were diagnosed with HBV DNA levels below 2.1 log copies/mL and who received antiviral drugs. Mogamulizumab was administered prior to HBV reactivation in two of three HBV-reactivated patients. In the mogamulizumab era, further well-designed prospective studies are warranted to estimate the incidence of HBV reactivation and to establish regular HBV DNA monitoring-guided preemptive antiviral therapy for such patients.
KeywordsReactivation HBV CCR4 Mogamulizumab ATL
Hepatitis B virus
Adult T-cell leukemia–lymphoma
Hepatitis B surface antigen
Antibodies against hepatitis B core antigen
Antibodies against hepatitis B surface antigen
CC chemokine receptor 4
We would like to thank staff as follows: Ms. Chiori Fukuyama and Dr. Shintaro Ogawa (Nagoya City University Graduate School of Medical Sciences, Nagoya) for keeping and measurement of specimens on this study. We also thank Dr. Shiro Akinaga (Kyowa Hakko Kirin Co., Ltd., Tokyo) for his enlightening advice on this article. This study was supported in part by the Ministry of Health, Labour and Welfare of Japan (grant-in-aid H24-kanen-004 to M.M.) and the Ministry of Education, Culture, Sports Science and Technology of Japan (grant-in-aid for Scientific Research (C) No. 24591428 to S.K.) and grant-in-aid for National Cancer Center Research and Development Fund (No. 26-A-4 to T.I.).
Conflict of interest
Shigeru Kusumoto received Research funding and honoraria from Kyowa Hakko Kirin Co., Ltd., and honoraria from Bristol-Myers Squibb. Takashi Ishida received research funding from Kyowa Hakko Kirin Co., Ltd., Bayer Pharma AG, and Celgene K.K. Ryuzo Ueda received research funding from Kyowa Hakko Kirin Co., Ltd. Yasuhito Tanaka received research funding from Bristol-Myers Squibb, and honoraria from Bristol-Myers Squibb. Shinsuke Iida received research funding from Kyowa Hakko Kirin Co., Ltd.
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