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Urinary corticosteriod and diphenylhydantoin metabolite patterns in neonates exposed to anticonvulsant drugs in utero
Author(s) -
Reynolds John W.,
Mirkin Bernard L.
Publication year - 1973
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt1973145891
Subject(s) - barbiturate , metabolite , urinary system , endocrinology , anticonvulsant , medicine , excretion , in utero , chemistry , pregnenolone , dehydroepiandrosterone , fetus , steroid , epilepsy , pregnancy , pharmacology , hormone , biology , psychiatry , genetics , androgen
Five newborn infants, whose mothers had received anticonvulsant therapy throughout gestation (diphenylhydantoin and a barbiturate [4] or diphenylhydantoin alone [1]), were studied. Urinary steroids (6β‐OH‐cortisol, tetrahydrocortisone, 16α‐OH‐pregnenolone, and 16α‐OH‐dehydroepiandrosterone) and urinary 5‐parahydroxyphenyl, 5‐phenylhydantoin (HPPH, conjugated and unconjugated) were quantitatively assayed during the early neonatal period. The urinary steroid excretions were found not to be significantly different from those of normal full‐term newborn infants. Total HPPH excretion and the unconjugated/total metabolite ratios showed no correlation with urinary steroid excretion. Thus, the enhanced 6β‐hydroxylation of cortisol seen in adults after barbiturate or diphenylhydantoin was not observed in newborns exposed to these drugs in utero.