Yoshiba M, Sekiyama K, Sugata F, Okamoto H, Yamamoto K, Yotsumoto S
Division of Gastroenterology, Showa University, Fujigaoka Hospital, Yokohama, Japan.
Dig Dis Sci. 1992 Aug;37(8):1253-9. doi: 10.1007/BF01296569.
Three hepatitis B virus carriers who were HB(e)Ag negative and having normal liver function developed fulminant hepatitis with evidence of HBV replication following intensive chemotherapy for non-Hodgkin's lymphoma. Each was continuously negative for HB(e)Ag. Analysis of the precore region of HBV isolated from each demonstrated that the HBV of each had a point mutation in the precore region that inhibited the synthesis and the release of hepatitis B(e) antigen. This observation suggests that all HB carriers receiving either immunosuppressive or cytotoxic therapy should be monitored closely even if standard assays suggest that viral replication is not present. Sudden enhanced replication of a HBV mutant as a result of such therapy can be a cause of either very severe hepatitis or occasionally fulminant hepatitis.
三名乙肝病毒携带者，乙肝e抗原（HBeAg）阴性且肝功能正常，在接受非霍奇金淋巴瘤强化化疗后发生暴发性肝炎，并有乙肝病毒复制的证据。三人的HBeAg均持续呈阴性。对从每个人身上分离出的乙肝病毒前核心区进行分析表明，每个人的乙肝病毒在前核心区都有一个点突变，该突变抑制了乙肝e抗原的合成与释放。这一观察结果表明，所有接受免疫抑制或细胞毒性治疗的乙肝携带者都应密切监测，即便标准检测表明不存在病毒复制。此类治疗导致乙肝病毒突变体突然增强复制，可能是引发极其严重肝炎的原因，偶尔也会导致暴发性肝炎。
