Human platelet antigen (HPA)-specific immunoglobulin M antibodies in neonatal alloimmune thrombocytopenia can inhibit the binding of HPA-specific immunoglobulin G antibodies

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A term baby with unexplained thrombocytopenia and a platelet (PLT) count of 14 × 109/L (maternal PLT count was 200 × 109/L) was investigated for neonatal alloimmune thrombocytopenia.


Serologic investigations were performed using the PLT immunofluorescence test (PIFT), monoclonal antibody immobilization of PLT antigens (MAIPA), and a bead-based assay (BBA) with maternal sera taken up to 56 days postdelivery. One serum sample was also separated into “immunoglobulin (Ig)M-rich” and “IgM-depleted” fractions and tested for PLT-specific antibodies. The family was genotyped for HPA.


HPA-3a–specific IgM antibodies were detected in the PIFT and confirmed in the BBA. PLT-specific IgG HPA-3a antibodies were not detected in the MAIPA assay and BBA in the initial sample but were detected in both techniques in subsequent serum samples. Testing of IgM-rich and IgM-depleted fractions in the MAIPA assay revealed that IgG antibody binding of the IgM-depleted fraction was inhibited by approximately 50% when it was reconstituted with the IgM-rich fraction suggesting that the IgM antibodies blocked the binding of the IgG antibodies. This effect was not observed when the IgM-depleted fraction or untreated serum was diluted with elution buffer. Incompatibility for HPA-3 was identified between the mother and the infant. The infant received one HPA-1a, −5b negative neonatal PLT transfusion, and one random PLT transfusion, with satisfactory outcomes. Both units were later found to be HPA-3b3b.


HPA-3a IgM antibodies can inhibit PLT-specific HPA-3a IgG antibodies in the MAIPA assay.

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