Abstract

GLUCOCORTICOIDS are commonly used in obstetric practice, both for maternal immunosuppression and for shortterm treatment of the fetus, usually to accelerate lung maturation when there is threatened preterm delivery. The immediate benefits of short-term prepartum glucocorticoid therapy in maturing the fetal lung and reducing neonatal mortality are clearly supported by controlled studies. 1,2 Recently, long-term prenatal therapy of fetuses potentially affected with congenital adrenal hyperplasia (CAH) has been advocated, 3,4 but the safety of this experimental therapy has not been established in rigorously controlled trials. See also p 1073. Congenital adrenal hyperplasia is a recessively inherited disease in which a disordered steroidogenic enzyme, usually P450c21 (21-hydroxylase), diverts adrenal steroid synthesis away from cortisol toward androgens. 5 In utero, low fetal plasma cortisol levels stimulate increased corticotropin (ACTH) secretion, which in turn stimulates further adrenal steroidogenesis, resulting in even more androgen synthesis. In an XY male fetus, these adrenal androgens have

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