Abstract

The hypothesis to be tested is that persistence of the fetal zone of the adrenal gland after preterm birth is due to continuing stimulation by ACTH. 22 infants of mean gestation 27.6 weeks and mean birth weight 946g were studied longitudinally between 170-360 days postconceptional age (PCA). Circulating DHEAS and its urin;try metabolites were used as a measure of adrenal fetal zone function. Mean plasma DHEAS fell form 12.3 μmol 1− at 176 days PCA to < 1.0 μmol 1− at 350 days PCA. During the same period the plasma ACTH increased from 9 pg ml− to 48 pg ml−. After term (280 days) the plasma DHEAS became barely detectable. In individual babies urinary excretion of DHEAS metabolites remained elevated but declined between 280-300 days PCA. Dexanieihasone given to one infant completely suppressed plasma Cortisol and ACTH, but the plasma DHEAS and its metabolites in the urine were not suppressed to the same extent. We conclude that the adrenal fetal zone in preterm infants continues to secrete 3β-OH-5ene steroids following delivery and after term these decline. Because of the observed changes in plasma ACTH and DHEAS and the failure of dexamethasone to fully suppress the fetal zone it is likely that ACTH is not the sole regulator of the fetal zone of the adrenal gland in preterm infants.

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