| Theme |
Liver and Immunity |
| Title |
De novo Hepatitis B Virus (HBV)-Related Hepatitis |
| Author |
Makoto Oketani |
Department of Digestive and Life-style Related Disease, Kagoshima University Graduate School of Medical and Dental Sciences |
| Author |
Hirofumi Uto |
Department of Digestive and Life-style Related Disease, Kagoshima University Graduate School of Medical and Dental Sciences |
| Author |
Akio Ido |
Department of Digestive and Life-style Related Disease, Kagoshima University Graduate School of Medical and Dental Sciences |
| Author |
Hirohito Tsubouchi |
Department of Digestive and Life-style Related Disease, Kagoshima University Graduate School of Medical and Dental Sciences |
| [ Summary ] |
De novo hepatitis B virus(HBV)-related hepatitis develops in patients who are considered to be in post-hepatitis B status after immuno-suppressive therapy or chemotherapy. Negative HBsAg status and positive HBcAb and/or HBsAb status is an indication of post-hepatitis B status. The causes of de novo HBV-related hepatitis are diverse. The risk of developing de novo HBV-related hepatitis and the clinical course of hepatitis differ in relation to the extent of immune suppression. De novo HBV-related hepatitis induced by rituximab plus a regimen incorporating steroids is associated with a higher risk of fulminant hepatitis and mortality. In de novo HBV-related hepatitis, the interval between cessation of therapy and HBV DNA elevation, and HBV DNA elevation and onset of hepatitis are longer than those observed in HBV reactivation from HBsAg positive inactive carriers. When HBV DNA is detectable during or after immuno-suppressive therapy, prompt administration of a nucleoside analog is efficacious for prevention of de novo HBV-related hepatitis. |