Reactivation of Chronic Hepatitis B Virus Infection by Cancer Chemotherapy

TLDR

Reactivation likely results from increased HBV synthesis during chemotherapy and a subsequent rebound of host immune responses after treatment cessation. In two asymptomatic HBsAg carriers, chemotherapy triggered acute hepatitis with marked HBV replication, but both patients recovered and became seronegative, indicating that chemotherapeutic agents can reactivate chronic HBV infection.

Abstract

Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HBsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.