Neonatal alloimmune thrombocytopenia: current considerations.

Some mothers produce antibodies to the platelet antigens of their fetuses. Exposure to these antigens may occur owing to prior transfusions or through feto-maternal hemorrhage during gestation or delivery. The sensitizing antigen is usually an epitope of one of the glycoproteins (GP) found on the platelet membrane. Specific GPs act as receptors for factors important in hemostasis, such as von Willebrand's Factor (vWF), fibrinogen, fibronectin, and collagen. Molecular biological techniques have identified single base pair substitutions resulting in antigenic specificity owing to one amino acid difference in a particular GP. Human platelet antigen (HPA) 1a is the most antigenic of the GPs. Neonatal alloimmune thrombocytopenia (NAT) results when a mother lacking an antigen present on fetal platelets develops the specific antibody. The incidence of NAT ranges from 1/1,500 to 1/5,000 births. An affected child is born with thrombocytopenia and may suffer consequences varying from petechiae and minor bleeding to central nervous system hemorrhage and death. Approximately 50 percent of the time, NAT is evident with the first pregnancy. Recent advances in obstetrical care permit percutaneous umbilical blood sampling (PUBS) early in pregnancy to determine whether or not the fetus is being adversely affected. Treatment through the use of cordocentesis and infusion of the mother's platelets or other compatible platelets may be performed. Clear identification of antibodies against platelets remains problematic for the routine clinical laboratory. Reagents to identify platelet antigens and antibodies are not readily available. Postnatal treatment of NAT requires infusion of the mother's platelets or platelets which are antigenetically compatible with the mother.