Reactivation of chronic hepatitis B virus infection by cancer chemotherapy.
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 HGsAg 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.
D000328:Adult; D000970:Antineoplastic Agents / Q000009:adverse effects*; D002353:Carrier State; D002908:Chronic Disease; D004279:DNA, Viral / Q000097:blood; D004259:DNA-Directed DNA Polymerase / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D006509:Hepatitis B / Q000139:chemically induced*; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006801:Humans; D008223:Lymphoma / Q000188:drug therapy; D008297:Male; D012008:Recurrence; D013736:Testicular Neoplasms / Q000188:drug therapy
D000970:Antineoplastic Agents; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D004259:DNA-Directed DNA Polymerase