Hepatitis B virus (HBV) reactivation after cytotoxic or immunosuppressive therapy — pathogenesis and management

✍ Scribed by Luo Xunrong; Au Wing Yan; Raymond Liang; George K. K. Lau

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 115 KB
• Volume: 11
• Category: Article
• ISSN: 1052-9276
• DOI: 10.1002/rmv.322

✦ Synopsis

Abstract

In an endemic area for chronic hepatitis B infection, reactivation of this virus is a serious cause of morbidity and mortality in patients undergoing cytotoxic or immunosuppressive therapy. Careful prospective serological testing has shown that hepatitis B virus reactivation is a two‐staged process. The initial stage occurs during intense cytotoxic or immunosuppressive therapy and is characterised by enhanced viral replication, as reflected by increases in the serum levels of hepatitis B virus DNA, hepatitis B e antigen, hepatitis B virus DNA polymerase and infection of naïve hepatocytes with hepatitis B virus. The second stage is related to restoration of immune function following withdrawal of cytotoxic or immunosuppressive therapy, which causes rapid immune‐mediated destruction of infected hepatocytes. Clinically, this can lead to hepatitis, hepatic failure and even death. The occurrence and severity of hepatitis B virus reactivation after various cytotoxic or immunosuppressive therapy is unpredictable and treatment has been disappointing, largely due to the late administration of therapy. Recently, pre‐emptive treatment of chronic hepatitis B patients undergoing cytotoxic or immunosuppressive therapy, with potent nucleoside analogues has shown some promising results. Further controlled studies are needed to define the incidence and risk factors of hepatitis B reactivation so that pre‐emptive treatment with nucleoside analogues could be administered to those patients at high risk of disease. Copyright © 2001 John Wiley & Sons, Ltd.