Abstract
Alloantigenic determinants on platelet membrane glycoproteins can be targets for alloimmune antibody responses that cause bleeding disorders such as neonatal alloimmune thrombocytopenic purpura, post-transfusion purpura (PTP), and refractoriness to platelet transfusion therapy [1]. In PTP, a transfused patient forms alloantigen-specific antibodies that, for still unknown reasons, may cause destruction of autologous platelets often resulting in life-threatening thrombocytopenia. In feto-maternal alloimmune thrombocytopenia, designated as neonatal alloimmune thrombocytopenic purpura (NATP), fetal thrombocytopenia is caused by maternal alloimmunization against one or more paternal platelet alloantigens with similar life-threatening complications. Severe NATP may lead to either prenatal or neonatal intracranial haemorrhage that may cause fetal death or psychomoter impairment.
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