Sammendrag
A 42 year old Norwegian male patient with myelodysplastic syndrome underwent allogeneic bone marrow transplantation in December 1992.He had markers of an earlier hepatitis B virus (HBV) infection (anti-HBs and anti-HBc positive) and HBsAg and HBV-DNA negative. His anti-HBs titer declined and disappeared 12 months after the transplantation. No HBV-DNA could be detected by PCR during the first 12 months. However, 17 months after the transplantation, while still on ciclosporin A, free circulating HBV-DNA as well as detectable HBsAg and HBeAg appeared in his sera. The bone marrow donor, blood donors and the family members had no HBV markers, and other risk factors for contracting an HBV infection were excluded. The reactivation of HBV in our case was probably secondary to the impaired cellular immunity caused by the immunoablative and immunosuppressive treatment, the fact that the B cells from the donor did not produce antibodies against HBsAg and GVHD. A logical approach to prevent reactivation of HBV in patients with markers of resolved HBV infection would be to vaccinate anti-HBs negative donors prior to transplantation.
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