Abstract

Human platelet alloantigens (HPAs) and their correspondingalloantibodies (alloabs) play an essential rolein fetal and neonatal alloimmune thrombocytopenia,posttransfusion purpura and platelet transfusion refractoriness.Emerging genotyping methods (e.g. microarraytechnology) will allow an automated throughput for HPAtyping of large donor cohorts in the near future. For theclinical diagnosis of alloimmune thrombocytopenia,however, the proof of pathogenic alloabs still remains aprerequisite. Nowadays, monoclonal antibody-basedantigen capture assays are the state of the art in manylaboratories. This technique seems to come up againstlimiting factors. In a certain number of cases that arehighly suspicious for alloimmune thrombocytopenia,platelet-specific alloabs are not detectable. Current observationsindicate that these alloabs are heterogeneousin terms of their alloantigenic determinants as well as theconsequences on platelet function. This heterogeneitymay correlate to the severe bleeding complicationssometimes seen in patients with alloimmune thrombocytopenia.New insights on the role of pathogenic alloabswill help us to improve diagnostic and therapeutic approachesfor the adequate treatment of affected patients.

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