Abstract 1364 Neonatology: Clinical Studies in the Premature Infant Platform, Tuesday, 5/4

Background: Premature infants have increased cortisol precursors, compared to term infants. Infants who develop CLD have decreased cortisol values, both basal and stimulated, compared to infants who recover without CLD. We hypothesized that infants develo** CLD have impairment or immaturity of adrenal function, resulting in increased cortisol precursors and precursor to product ratios, but decreased cortisol values and decreased cortisol response to ACTH. Methods: Forty infants 500-999 grams birth weight were enrolled in a prospective trial of hydrocortisone (HC) to prevent CLD at 36 weeks postconception. Three days after therapy (day 14 - 19), specimens were obtained before and 30 minutes after IV ACTH (3.5µg/kg). Cortisol, 11-deoxycortisol, 17OH progesterone, and dehydroepiandrosterone sulfate (DHEAS) were assayed by RIA. Differences between groups (HC-treated vs placebo; CLD vs No-CLD) were analyzed by multiple regression after log transformation of hormone values, and included gestational age. Results: Values were similar between HC-treated and placebo infants. DHEAS values were similar in CLD vs no-CLD groups. Table, below, shows glucocorticoid values and precursor to product ratios as median [25-75%ile]. (*=p<0.05, CLD vs no-CLD) Conclusions: (1) Infants develo** CLD had decreased basal and stimulated cortisols, but higher concentrations of cortisol precursors, leading to elevated precursor:product ratios. (2) This pattern is consistent with decreased activity of both 11β and 21 hydroxylase enzymes. (3) Immaturity of the glucocorticoid synthetic pathway may increase susceptibility of preterm infants to inflammatory stress, leading to CLD.

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