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Posttransplant immune‐mediated hemolysis
Author(s) -
Sokol Robert J.,
Stamps Robert,
Booker David J.,
Scott Fiona M.,
Laidlaw Stuart T.,
Vandenberghe Elisabeth A.,
Barker Helen F.
Publication year - 2002
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.2002.00026.x
Subject(s) - hemolysis , medicine , autoantibody , autoimmune hemolytic anemia , immunology , bone marrow , hemolytic anemia , immune system , anemia , aplastic anemia , antibody
BACKGROUND: Immune‐mediated hemolysis is a well‐recognized complication of transplantation, but few reports have drawn together the different mechanisms that could be involved. STUDY DESIGN AND METHODS: The clinical and laboratory records of three patients are used to illustrate different types and complexities of posttransplant immune‐mediated RBC destruction. RESULTS: Patient 1 received bone marrow from an HLA‐matched, unrelated donor. At 7 months after transplant, his Hb level fell to 50 g per L. The serum contained warm autoantibodies, and the DAT was strongly positive for IgG, IgM, and C3d; an eluate yielded IgG and IgM autoantibodies. Autoimmune hemolytic anemia was diagnosed. Patient 2, blood group A, experienced severe hemolysis 14 days after receiving a lung from a group O donor. The DAT was positive for IgG. Serum and RBC eluate contained anti‐A produced by immunocompetent B cells in the transplanted lung‐this was the passenger lymphocyte syndrome. Patient 3 experienced posttransplant hemolysis caused by two different immune mechanisms. Originally group A, D‐ with anti‐C, ‐D, ‐E, she received a peripheral blood progenitor cell (PBPC) transplant from her HLA‐identical group A, D+ son. Six months later, chimerism was evident; the remaining recipient marrow was still producing antibodies that destroyed D+ RBCs made by the transplant. Later, autoimmune hemolytic anemia also developed; the DAT became positive for IgG, and warm autoantibodies were eluted from D‐ RBCs. CONCLUSION: An understanding of the causes and circumstances under which posttransplant immune hemolysis arises is required for proper management. As more patients become long‐term survivors of unrelated bone marrow and/or PBPC transplants, chimerism and complex serologic problems will become more common.