Summary:Purpose: To determine whether anticonvulsant exposure during human pregnancy caused an increase of the abnormal form of prothrombin, known as PIVKA-I1 (prothrombin induced by vitamin K absence for factor 11), and a decrease in total prothrombin, in the blood of the newborn.Methods: Cord blood was collected from the placenta at the time of parturition from 12 women who had received anticonvulsant therapy during pregnancy and from 11 control women.Results: PIVKA-I1 was present in cord blood from control mothers at low or nondetectable levels. In the same samples, total prothrombin concentrations were -50% of adult levels, but there was wide variation between individuals. Exposure to carbamazepine (CBZ) alone during pregnancy was associated It has been known for a number of years that maternal use of the anticonvulsants (AEDs) phenobarbital (PB; and derivatives), phenytoin (PHT), and carbamazepine (CBZ) is sometimes associated with bleeding in the neonate (1-5). Furthermore, each of these drugs is associated with an abnormal facial appearance in some of the exposed neonates. Typically there is a small, depressed nose and midfacial hypoplasia (6-8). The similarity between this facial appearance and the facies of children exposed to warfarin prenatally (9), and the tendency for both groups to have neonatal bleeding, has led to the suggestion that these defects are the result of AEDinduced vitamin K deficiency in the embryo (9,lO). The primary pharmacologic effect of warfarin is to block vitamin K recycling, which results in an effective vitamin K deficiency.There is some evidence that vitamin K may be necessary for normal prenatal midfacial growth (1 1 ) as well as