BONE MARROW TRANSPLANTATION

M. Lindemann¹, M. Fiedler², A. Elmaagacli³, A. Schumann⁴, M. Roggendorf², P.A. Horn¹, D.W. Beelen^3
1Institute For Transfusion Medicine, University Hospital Essen, Essen/GERMANY, ²Institute Of Virology, University Hospital Essen, Essen/GERMANY, ³Department Of Bone Marrow Transplantation, University Hospital Essen, Essen/GERMANY, ⁴Institute For Transfusion Medicine And Institute Of Virology, University Hospital Essen, Essen/GERMANY

Body: Introduction: After having shown that immune transfer can occur via hematopoietic stem cell transplantation and – depending on the strength of donor immunity – also after liver transplantation we implemented this knowledge in clinical patient care. Methods: We here describe two patients who suffered from non-Hodgkin lymphoma or acute myeloid leukemia plus either acute or chronic hepatitis B (HBV) infection, respectively, prior to peripheral blood stem cell transplantation (PBSCT). Results: In the patient with acute HBV infection occurring at month 6 prior to PBSCT, we actively immunized the HLA-identical sister 4 times (day 0, week 2, week 4, and month 5) using Bio-Hep-B, an HBV vaccine containing PreS1, PreS2 and S antigens (Berna Biotech, Switzerland) and thereby obtained humoral and cellular HBV immunity prior to PBSCT (anti-HBs titer: 347 IU/L, HBV-specific stimulation index (SI): 8.5, and HBV-specific interferon-gamma production as determined by ELISpot: 12 spots increment). The corresponding recipient was transplanted after HBV DNA became undetectable. He was followed up for 19 months and remained HBV DNA negative. At month 19, anti-HBs and HBV-specific cellular immunity were still measurable (1483 IU/L, SI of 4.8, and 8.5 spots increment) indicating that HBV infection was controlled by donor immunity. The patient with chronic HBV infection received a graft from an unrelated donor who had been immunized using a German standard HBV vaccine containing the S antigen (anti-HBs titer >10 IU/L). She was furthermore treated by antiviral drugs prior to and post transplantation. After PBSCT the patient cleared her chronic HBV infection and became HBV DNA negative. Furthermore, she displayed humoral and cellular HBV immunity at month 1 after transplantation (anti-HBs titer 588497 IU/L, SI of 5.4, and 8 spots increment). Most likely, after PBSCT HBs antigen had persisted outside the peripheral blood and “boostered” anti-HBs production. Conclusion: The data demonstrate that in PBSCT recipients the reactivation of acute HBV infection could be prevented and chronic HBV infection could be cleared if donors were immunized against HBV. *This study was partly supported by the DFG [Project A-III of the clinical research group (KFO)-117].

Disclosure: All authors have declared no conflicts of interest.