| [ Summary ] |
cccDNA of HBV inevitably remains in the nuclei of hepatocytes for life once infected by HBV. Thus, serum HBV‒DNA may become detectable during and after immunosuppressive therapies and/or antineoplastic chemotherapies in patients with previously resolved HBV infection, thereby manifesting positive anti‒HBc and/or anti‒HBs despite negative HBsAg, as is in HBV carriers positive for HBsAg; such phenomenon is called as "HBV reactivation". The outcome of patients with de novo HBV hepatitis, defined as liver injuries due to HBV reactivation in patients with previously resolved HBV infection, is in general unfavorable. Such fatal hepatitis can be prevented when immunosuppressive therapies and/or antineoplastic chemotherapies are done according to the guideline proposed by the Japan Society of Hepatology (JSH). Patients diagnosed as having acute liver failure due to de novo HBV hepatitis, however, have still been enrolled in the nationwide survey conducted by the study group sponsored by the Ministry of Health, Labor and Welfare of Japan, and the percentage of such patients among HBV carriers manifesting acute liver failure was about 50 % in the recent years. Although HBV reactivation develops frequently in patients receiving chemotherapies for myeloproliferative and lymphoproliferative diseases, fatal de novo HBV hepatitis may occur even in patients receiving immunosuppressive therapies for rheumatoid diseases. Therefore, all physicians who may perform immunosuppressive therapies and/or antineoplastic chemotherapies should be educated on HBV reactivation. |