The most severe complication of NAIT is intracranial haemorrhage, said to occur in 15-30% of cases, up to 50% in utero. Recently, antenatal administration of high dose gammaglobulin has been shown to be useful in preventing intrauterine cerebral haemorrhage NAIT. We here report a case of NAIT due to anti HPA-IA in which intrauterine cerebal haemorrhage was probably prevented by this therapy. The patient was a 24 year old G4P3. Her first pregnancy had resulted in stillbirth and the second in neonatal death due to a massive cerebral haemorrhage. The third child developed petechiae soon after birth, was severely thrombocytopaenic {Pit count 8 × 10 /L) and had intracranial calcification presumably secondary to intrauterine cerebral haemorrhage. The platelet count recovered without therapy but the infant shows developmental delay. The patient typed as HPA-IA negative and her husband as HPA - 1A positive. No HPA-IA antibody was identified at this time but was detected on a 6 months follow up. Presence of the HPA-IA antibody was confirmed early in the fourth pregnancy and the patient was given IVIG lg/Kg/week from week 29 to 37 (Intragam CSL). The strength of the HPA-IA antibody rapidly reached a titre of N/4 in mid pregnancy, dropping to N/2 after IVIG. Prior to delivery by elective caesarean, maternal platelets we re harvested, divided into two aliquots and resuspended in AB plasma. The baby platelet count at birth was 8 × 109 / L). Maternal platelets were transfused with a one hour increment 64 × 109/L. A further transfusion was given at 40 hours of age. The platelet count recovered without further therapy and the child is developing normally. The successful outcome in this case with the history of severely affected children suggests that IVIG given weekly can protect against intracerebral haemorrhage. The most severe complication of NAIT is intracranial haemorrhage, said to occur in 15-30% of cases, up to 50% in utero. Recently, antenatal administration of high dose gammaglobulin has been shown to be useful in preventing intrauterine cerebral haemorrhage NAIT. We here report a case of NAIT due to anti HPA-IA in which intrauterine cerebal haemorrhage was probably prevented by this therapy. The patient was a 24 year old G4P3. Her first pregnancy had resulted in stillbirth and the second in neonatal death due to a massive cerebral haemorrhage. The third child developed petechiae soon after birth, was severely thrombocytopaenic {Pit count 8 × 10 /L) and had intracranial calcification presumably secondary to intrauterine cerebral haemorrhage. The platelet count recovered without therapy but the infant shows developmental delay. The patient typed as HPA-IA negative and her husband as HPA - 1A positive. No HPA-IA antibody was identified at this time but was detected on a 6 months follow up. Presence of the HPA-IA antibody was confirmed early in the fourth pregnancy and the patient was given IVIG lg/Kg/week from week 29 to 37 (Intragam CSL). The strength of the HPA-IA antibody rapidly reached a titre of N/4 in mid pregnancy, dropping to N/2 after IVIG. Prior to delivery by elective caesarean, maternal platelets we re harvested, divided into two aliquots and resuspended in AB plasma. The baby platelet count at birth was 8 × 109 / L). Maternal platelets were transfused with a one hour increment 64 × 109/L. A further transfusion was given at 40 hours of age. The platelet count recovered without further therapy and the child is developing normally. The successful outcome in this case with the history of severely affected children suggests that IVIG given weekly can protect against intracerebral haemorrhage.