Journal of the Japan Society of Blood Transfusion
Online ISSN : 1883-8383
Print ISSN : 0546-1448
ISSN-L : 0546-1448
PLATELET TRANSFUSION REFRACTORINESS ASSOCIATED WITH IGM-HLA-CLASS I ANTIBODIES
IMMUNOGLOBULIN CLASS HETEROGENEITY OF HLA CLASS I ANTIBODIES IN PTR PATIENTS
Satoshi SaitoToyohiro TamaiMasao OtaSatoshi OtaMasayoshi KomatsuMorito HirabayashiKeiko TamakiHideyuki SeshimoHisashi ShimizuHideki AsamuraHirofumi FukushimaSetsuo Nomura
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2006 Volume 52 Issue 3 Pages 405-413

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Abstract

Although HLA-class I antibodies (Abs) are considered one of the major obstacles in posttransfusion platelet increments for platelet transfusion refractory (PTR) patients, whether IgM-HLA-class I Abs are associated with accelerated platelet destruction and transfusion failure remains unclear. Accordingly, we assessed the frequency of IgM-HLA-class I Abs development in 121 PTR patients using the magnetic-mixed passive hemagglutination assay (M-MPHA), flow cytometric reagents for detection of panel-reactive antibody against HLA Class I antigens (FlowPRA) and the anti-human immunoglobulin lymphocyte cytotoxity test (AHG-LCT). The relationship between IgM-HLA-class I Abs and PTR was assessed by calculating 24h post-transfusion corrected platelet count increments (CCI24hours). Result showed that IgM-HLA-class I Abs were detected in 48 of 121 patients using the M-MPHA. Only 20 and 35 of these 48 IgM-HLA-class I Abs were detected using the AHG-LCT and FlowPRA respectively. In 7 of 48 patients positive for IgM-HLA-class I Abs, 74 transfusions without corresponding antigen for specificities of IgM-HLA-class I Abs had CCI24hours of 19.7±4.7(×109/L). In contrast, 38 transfusions with corresponding antigens for specificities of the same Abs had CCI24hours of 2.0±1.9(×109/L). Collectively, IgM-HLA-class I Abs were detected in 39.7% of PTR patients, and were considered to play a role in mediating refractoriness to platelet transfusions. In 28 of 48 cases, IgM-HLA-class I Abs could not be detected by the AHG-LCT. Detection of IgM-HLA-class I Abs using the M-MPHA may clarify the as yet unknown mechanism of the pathogenesis of PTR.

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© The Japan Society of Transfusion Medicine and Cell Therapy
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