Sokol Robert J, Stamps Robert, Booker David J, Scott Fiona M, Laidlaw Stuart T, Vandenberghe Elisabeth A, Barker Helen F
National Blood Service, Trent Center, Sheffield, UK.
Transfusion. 2002 Feb;42(2):198-204. doi: 10.1046/j.1537-2995.2002.00026.x.
Immune-mediated hemolysis is a well-recognized complication of transplantation, but few reports have drawn together the different mechanisms that could be involved.
The clinical and laboratory records of three patients are used to illustrate different types and complexities of posttransplant immune-mediated RBC destruction.
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.
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.
免疫介导的溶血是移植中一种公认的并发症，但很少有报告汇总可能涉及的不同机制。
使用3例患者的临床和实验室记录来说明移植后免疫介导的红细胞破坏的不同类型和复杂性。
患者1接受了来自HLA匹配的无关供者的骨髓移植。移植后7个月，他的血红蛋白水平降至50 g/L。血清中含有温自身抗体，直接抗人球蛋白试验（DAT）对IgG、IgM和C3d呈强阳性；洗脱液中检测到IgG和IgM自身抗体。诊断为自身免疫性溶血性贫血。患者2血型为A，在接受来自O型供者的肺移植14天后发生严重溶血。DAT对IgG呈阳性。血清和红细胞洗脱液中含有移植肺中免疫活性B细胞产生的抗A抗体，即过客淋巴细胞综合征。患者3移植后溶血由两种不同的免疫机制引起。她原本血型为A、Rh阴性，有抗-C、-D、-E抗体，接受了来自与其HLA相同的A型、Rh阳性儿子的外周血祖细胞（PBPC）移植。6个月后，嵌合体明显；剩余的受者骨髓仍在产生破坏移植产生的Rh阳性红细胞的抗体。后来，自身免疫性溶血性贫血也发生了；DAT对IgG呈阳性，温自身抗体从Rh阴性红细胞中洗脱出来。
为了进行恰当的处理，需要了解移植后免疫溶血发生的原因和情况。随着越来越多的患者成为无关骨髓和/或PBPC移植的长期存活者，嵌合体和复杂的血清学问题将变得更加常见。
