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Red cell aplasia due to host type isohemagglutinins with exuberant red cell progenitor production of donor type in an ABO-mismatched allogeneic bone marrow transplant recipient.

作者信息

Cockerill K J, Lyding J, Zander A R

机构信息

Division of Bone Marrow Transplantation, Pacific Presbyterian Medical Center, San Francisco, California.

出版信息

Eur J Haematol. 1989 Sep;43(3):195-200. doi: 10.1111/j.1600-0609.1989.tb00282.x.

DOI:10.1111/j.1600-0609.1989.tb00282.x
PMID:2509237
Abstract

ABO-mismatched bone marrow transplants have resulted in delayed red cell production in patients who have persistently elevated anti-ABO isohemagglutinin titers. We present a patient with chronic myelogenous leukemia who received an HLA-matched, ABO-incompatible bone marrow transplant from his sister. Post-transplant, he developed pure red cell aplasia with exuberant production of donor red cell precursors by in vitro BFU-E assay. Restriction fragment length polymorphism (RFLP) analysis of bone marrow, peripheral blood and BFU-E colonies demonstrated only donor type DNA post-transplant. However, the patient had persistently elevated isohemagglutinin titer and Ph1 chromosome-positive metaphases on chromosome analysis, indicating the presence of persistent host lymphocytes. With onset of acute graft vs. host disease (GVHD), the isohemagglutinin titer dropped, Ph1 chromosome-positive metaphases disappeared, and full hematopoietic recovery ensued. Longitudinal analysis of RFLP's, isohemagglutinin titers and chromosomes may be helpful in understanding the immunological interplay following allogeneic bone marrow transplantation.

摘要

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引用本文的文献

1
Prevention of pure red cell aplasia after major or bidirectional ABO blood group incompatible hematopoietic stem cell transplantation by pretransplant reduction of host anti-donor isoagglutinins.通过移植前降低宿主抗供体同种凝集素预防主要或双向ABO血型不相合造血干细胞移植后的纯红细胞再生障碍。
Haematologica. 2009 Feb;94(2):239-48. doi: 10.3324/haematol.13356. Epub 2009 Jan 14.