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Japanese Journal of Clinical Oncology 21:360-363 (1991)
© 1991 Foundation for Promotion of Cancer Research


research-article

Activation of Hepatitis B Virus Infection by Chemotherapy Containing Glucocorticoid in Hepatitis B Virus Carriers with Hematologic Malignancies

Tomoko Ohtsu1,*, Toshiaki Sai1, Masayuki Oka1, Yoshiki Sugai1 and Kensei Tobinai2

1Department of Internal Medicine, Iwaki Kyoritsu General Hospital 16 Kusehara, Mimaya-machi, Uchigo, Iwaki 973
2Hematology-Oncology and Medical Oncology Division, National Cancer Center Hospital 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104

*For reprints and all correspondence

Received January 24, 1991; accepted June 3, 1991

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.

Key Words: Hematologic malignancies • HBV carriers • Glucocorticoid • Activation of HBV infection


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