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Epilepsy Res. 1989 Sep-Oct;4(2):147-55.

A transient retardation of early postnatal growth in drug-exposed children of epileptic mothers.

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I Clinic of Pediatrics, University of Helsinki, Finland.


Increase of length and weight during the first 6 months of life, and height at 1 and 5.5 years of age were investigated in 132 children of epileptic mothers (the study group) and 103 control children born after 37 completed gestational weeks. One hundred and seventeen children had been exposed to antiepileptic drugs in utero: 48 to phenytoin monotherapy, 16 to carbamazepine monotherapy, 24 to barbiturates (23 in combination with other drugs), 27 to drug combinations including phenytoin and/or carbamazepine but not barbiturates, and 2 to other drugs. There was no evidence of intrauterine drug exposure causing prenatal growth retardation. The mean length increment in the first postnatal month was significantly smaller in the drug-exposed children than in the non-exposed study children or controls. The drug-exposed children also gained significantly less weight during the first postnatal month than non-exposed study group children. A normal growth rate was already resumed in the drug-exposed group in the second postnatal month. Sedative drug effects on the neonate probably partly explain the transient weight lag, especially in the barbiturate-exposed subgroup. The marked delay in length gain suggests that a hormonal mechanism, perhaps a reversible suppression of thyroid function, might also be involved. The transient growth retardation was not associated with an excess of minor anomalies or impaired intelligence at 5.5 years of age. As only 1 drug-exposed child had persistent postnatal growth deficiency combined with other signs suggesting a prenatal disorder, the risk of teratogenic growth deficiency caused by antiepileptic drug exposure seems to be very low.

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