Objective: We tested the hypothesis that inhaled beclomethasone therapy for
prevention of bronchopulmonary dysplasia does not cause adrenal suppressio
n.
Study design: Infants receiving ventilatory support with birth weights less
than or equal to 1250 g and born at <33 weeks' gestation, age 3 to 14 days
, were enrolled in a multicenter randomized trial to study the efficacy and
safety of beclomethasone therapy Versus placebo for prevention of bronchop
ulmonary dysplasia. Adrenal function was assessed on study day 21 (+/- 2 da
ys) by determination of basal and stimulated plasma cortisol levels. Initia
lly, cortisol response was assessed with insulin-induced hypoglycemia test
(IIHT) (n = 63) until an interim analysis revealed insignificant cortisol r
esponse in both study groups. Thereafter cosyntropin stimulation was used (
n = 85).
Results: Beclomethasone therapy was associated with lower median basal cort
isol levels (5 mu g/dL beclomethasone, 6 mu g/dL placebo, P = .04). IIHT re
vealed insignificant change in cortisol response within each group. Cortiso
l response to cosyntropin stimulation was similar for each group (17 mu g/d
L beclomethasone, 18 mu g/dL placebo, P = .86).
Conclusion: Beclomethasone therapy was associated with a small decrease in
basal cortisol levels. There was no evidence of adrenal suppression in resp
onse to cosyntropin stimulation during beclomethasone therapy Lack of corti
sol response to hypoglycemia may reflect missed timing and/or decreased res
ponse of the premature infants' hypothalamic-pituitary-adrenal axis to hypo
glycemia.