HLA antibodies and neonatal alloimmune thrombocytopenia.

A female baby with a severe thrombocytopenia at 18 x 10(9)/l was born to a 29-year-old (gestation 2/partum 2) mother. Scattered petechiae were present on her legs, arms, chest and face, but there was no bleeding, infection, fever or hepatosplenomegaly. A platelet antibody screening immunocapture test was positive, which was performed on the mother's serum 3, 12 and 38 days after delivery, but no platelet-specific antibodies were found by the monoclonal-antibody-specific immobilization of platelet antigen assay. The baby's platelets and lymphocytes and the father's platelets reacted strongly with the HLA antibodies present in the mother's serum. The neonate was treated with intravenous human immunoglobulin (Tegeline), 1 g/kg per day) 1, 2 and 3 days after delivery. The platelet count rose from 18 x 10(9)/l on day 0 to 37 x 10(9)/l on day 3 and to 227 x 10(9)/l on day 12. No platelet transfusion was needed. Several factors which developed hereafter lead us to think that this neonatal alloimmune thrombocytopenia is due to the transplacental passage of maternal HLA antibodies to the baby.

[In utero fetal death in multiple pregnancies during the second and third trimesters. A series of 21 cases]. / Mort foetale in utero dans les grossesses multiples au cours des deuxième et troisième trimestres. A propos de 21 cas.

OBJECTIVE: Recall the maternal and fetal risks in multiple pregnancies with in utero death during the second and third trimester. METHODS: From january 1, 1984 through December 31, 1994 21 cases of in utero death occurred among 405 multiple pregnancies followed in our unit. The frequency and circumstances of maternal and fetal complications were established according to type of placenta implantation, etiology, term at death of the twin and delay from death to delivery. RESULTS: The rate of in utero death was 5.2%. Various etiologies were observed, but the main cause was intra-uterine growth retardation. Maternal complications were marked by moderate asymptomatic disorders in hemostasis which resolved rapidly. Fetal complications included premature delivery (20/25 infants) and multicystic encephalopathy in one surviving twin. In monochorial pregnancies there is either tromboplastin release or hypotension-hypoxia phenomena which lead to neurological lesions. CONCLUSION: Fetal prognosis depends essentially on the type of placenta implantation. The most severe fetal complications are caused by neurological damage occurring in monochorial pregnancies. Screening for this anomaly is difficult, limiting the antenatal evaluation to the prognosis of the surviving twin. In bichorial pregnancies, and even more so in monochorial pregnancies. It is important to prevent premature delivery and maintain regular obstetrical care. The ultrasound-Doppler examination is the key to follow-up in pregnancy.