HEPATITIS-B VIRUS-INFECTION IN ALLOGENEIC BONE-MARROW TRANSPLANTATION

Fourty-four patients who underwent allogeneic bone marrow transplantat ion (alloBMT) were studied for hepatitis B virus (HBV)-related complic ations, The mean follow-up period was 15.3 months, Positivity for HBV surface antigen (HBsAg) was observed in 10 patients (22.7%) throughout the study, Four of the 10 patients were HBsAg carriers before alloBMT , while the remaining six became HBsAg(+) after alloBMT, During the fo llow-up period (from 6 months to 45 months), an elevation in serum ALT activity was observed in the four carriers when immunosuppression was reduced or withdrawn, All of the four HBsAg carriers developed hepati tis, but none of them died of liver failure due to HBV, Only one death due to GVHD and diabetic ketoacidosis was observed in this group, Two of the four carriers received marrow from anti-HBs positive donors an d one of them cleared HBsAg from his serum via adoptive immunity 8 mon ths after transplantation. The remaining six patients acquired HBV aft er alloBMT, but we were unable to demonstrate the source of HBV, Five of them had a moderate increase in serum ALT activity while the other patient had a normal ALT. Two patients seroconverted to anti-HBs spont aneously, Two patients died during the follow-up, one due to intracran ial hemorrhage and the other due to GVHD and accompanying pulmonary in fection, The rest of the study group (34 patients) remained HBsAg(-) t hroughout the study, Two of them had an HBsAg(+) donor, but neither de veloped HBV infection in their follow-up period, The acquisition rate of HBV infection was relatively low in recipients who were positive fo r anti-HBs compared to those who were negative for anti-HBs (8 vs 19%) . Anti-HBs positivity remained for a longer period in recipients who r eceived marrow from anti-HBs positive donors compared to those recipie nts who had anti-HBs negative donors (median 12 vs 3 months), We think that HBV is a frequent cause of liver dysfunction in alloBMT patients where HBV infection is endemic, Whether the disease is in the form of reactivation of HBsAg-positive recipients, or is acquired from unknow n sources in recipients who never had contact with the virus, the cour se of the disease Is not fatal. Silent serologic changes can be demons trated if viral serologic markers are sought serially, Among them, the disappearance of serum anti-HBs may be important as it increases the risk of HBV contamination in recipients.