Abstract

In fetal alloimmune thrombocytopenia, maternal IgG antibodies directed against platelets pass into the fetal circulation and lead to the destruction of fetal platelets. Fetal thrombocytopenia is usually first noted postnatally, but the maternal alloantibodies may lead to severe fetal haemorrhage in utero in the second or, more commonly, third trimester. Platelet-specific antibodies appear to play the major role in the pathogenesis of fetal alloimmune thrombocytopenia. Antenatal serological diagnosis is complicated by the fact that no platelet-specific alloantibodies are detectable in untreated maternal serum in about 20% of cases. Even when antibodies are detected, repeated estimation of the titre in the mother gives no indication of the severity of the fetal thrombocytopenia. Therefore, when the diagnosis of fetal alloimmune thrombocytopenia is suspected, it should be confirmed and subsequently monitored by cordocentesis. The intrauterine transfusion of compatible platelets and the administration of high dose IgG infusions to the mother and/or fetus are currently being used as approaches to treatment. Despite advances in the antenatal diagnosis and therapy of fetal alloimmune thrombocytopenia, the clinical effects on the fetus remain unpredictable.

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