Neonatal alloimmune thrombocytopenia (NAITP), defined as thrombocytopenia (
platelet count < 150 x 10(9)/l) due to transplacentally acquired maternal p
latelet alloantibodies, occurs in approximately I per 1200 live births in a
Caucasian population. In such a population, the majority (>75 percent) of
cases are due to fetomaternal incompatibility for the platelet specific all
oantigen, HPA-la (Pl(Al), Zw(a)). Incompatibility for the HPA-5b (Br-a) all
oantigen is the next most frequent cause of NAITP in Caucasians; much less
common is NAITP due to incompatibility for HLA, blood group ABO or other pl
atelet-specific antigens. In non-Caucasian populations (e.g. Orientals) HPA
-la incompatibility is a rare cause of NAITP and other alloantigens e.g. HP
A-4b (Pen(b), Yuk(a)) are implicated. The greatest clinical challange relat
es to the antenatal management of pregnant women alloimmunized to the HPA-l
a (Pl(Al), Zw(a)) antigen, and particularly the subset of such women who ha
ve a history of a previously affected infant with severe thrombocytopenia a
nd/or intracranial hemorrhage (ICH). The risk of antenatal ICH in the fetus
of such women is high enough to merit intervention, either weekly infusion
of high-dose intravenous immunoglobulin G (IVIG) with or without corticost
eroids given to the mother (the preferred approach in North American centre
s), or repeated in-utero fetal platelet transfusions (the preferred treatme
nt approach in some European centres). Post-natal management of severely af
fected infants centres on the rapid provision of compatible antigen-negativ
e platelets harvested from the mother or a phenotyped donor. The value of a
ntenatal screening programs to detect 'at risk' alloimmunized women during
pregnancy continues to be debated.