Reactivation of hepatitis B virus in rheumatologic patients receiving immunosuppressive agents.

摘要

Reactivation of hepatitis B virus (HBV) replication in patients receiving cytotoxic or immunosuppressive therapy is a well-recognized complication . The reactivation is characterized by an elevation of serum HBV-DNA levels and abnormal liver biochemistry tests, with a wide variety of clinical manifestations, ranging from mild, transient raised levels of serum aminotransferase to fulminant hepatitis . The mechanism of liver injury in HBV reactivation is still not fully understood. It has been suggested that immunosuppressive agents result in increased viral replication. Following withdrawal of the agents, the function of the immune system is restored and immune-mediated destruction of hepatocytesensues [3-5]. In addition, glucocorticoids and doxorubicin might directly stimulate HBV replication in vitro, and there is a specific glucocorticoid-response element in the HBV genome .