{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:34:54Z","timestamp":1773308094964,"version":"3.50.1"},"reference-count":20,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,4,25]],"date-time":"2006-04-25T00:00:00Z","timestamp":1145923200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> Under immunosuppressive conditions after hematopoietic stem cell transplantation (HSCT), even if hepatitis B virus (HBV) antigen is negative but hepatitis B surface antibody (HBsAb) or hepatitis B core antibody (HBcAb) is presented, HBV reactivates and sometimes causes fulminant hepatitis. However, it remains unclear which patients will develop fulminant hepatitis, or whether fulminant hepatitis is caused by host\u2010related factors or by virus\u2010related factors. A 30\u2010yr\u2010old man with a history of aplastic anemia since 3\u2003yr of age underwent allogenic BMT, when HBsAb and HBcAb were positive but HBs antigen (HBsAg) was negative. The donor was negative for HBsAg, HBsAb and HBcAb. After transplantation, the patient was complicated by acute graft\u2010vs.\u2010host disease (GVHD), cytomegalovirus infection, intestinal thrombotic microangiopathy and aspergillus colitis. Chronic GVHD was well controlled by FK506 and prednisolone. Twenty months after transplantation, the patient was admitted with general fatigue and liver dysfunction and was found to be positive for HBsAg and HBeAg. His serum HBV\u2010DNA level was &gt;8.8\u2003log of the genome equivalent (LGE)\/mL. Therefore, he was diagnosed as having hepatitis B caused by HBV reactivation and 100\u2003mg\/d lamivudine treatment was started. However, jaundice and hepatic failure deteriorated and became fatal. On analysis of the HBV\u2010DNA, two adjacent gene mutations in the core promoter region (T1762\/A1764) were detected. Increased replication of the mutated HBV might have caused HBV reactivation which progressed to fulminant hepatitis.<\/jats:p>","DOI":"10.1111\/j.1600-0609.2006.00678.x","type":"journal-article","created":{"date-parts":[[2006,4,25]],"date-time":"2006-04-25T17:48:13Z","timestamp":1145987293000},"page":"255-258","source":"Crossref","is-referenced-by-count":27,"title":["Fulminant hepatitis after allogenic bone marrow transplantation caused by reactivation of hepatitis B virus with gene mutations in the core promotor 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