Background: Systemic steroid therapy for neonatal chronic lung disease may cause variable adrenal suppression in preterm infants. However, it is not known whether inhaled steroid therapy results in adrenal suppression. Our objective was to determine whether inhaled beclomethasone therapy for prevention of neonatal chronic lung disease results in adrenal suppression in premature infants (BW <1251 gms/GA <33 wks). Methods: This was a multicenter, double-blind, randomized, placebo-controlled trial designed to evaluate pulmonary outcome and systemic side effects, including adrenal suppression, in premature infants treated with beclomethasone v. placebo. Adrenal evaluation was conducted on study day 21±2d. Insulin induced hypoglycemia test (IIHT) was used for the first 22 months of the study until an interim analysis revealed no cortisol response to hypoglycemia in either study group (Ped Res 1996;39:202a). For the remainder of the study, adrenal function was assessed by measuring cortisol response to 1-24ACTH stimulation (3.5 μg/kg IV). Baseline and 1 hour post infusion plasma cortisol levels were obtained. This report provides full information for the entire study population regarding the effect of beclomethasone therapy on basal cortisol levels and beclomethasone's effect on cortisol response as assessed by 1-24ACTH stimulation. Results: 147 of 253 enrolled infants had adrenal assessment by IIHT or 1-24ACTH (63 IIHT, 84 1-24ACTH). There was no difference between the study groups in mean± SD basal cortisol levels (210 ± 265 nmol/L beclomethasone vs. 231 ± 172 nmol/L placebo). Cortisol response (mean ± SD) to1-24 ACTH stimulation test was appropriate and similar between study groups (462 ± 341 nmol/L beclomethasone vs. 519 ± 243 SD nmol/L placebo). Conclusion: Neither basal cortisol levels nor cortisol responses to 1-24ACTH stimulation suggests a differential suppression of cortisol response using this regimen of inhaled beclomethasone.