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Adrenal function in premature infants during inhaled beclomethasone therapy
1Department of Pediatrics, Division of Newborn Medicine, The Floating Hospital for Children at New England Medical Center, Boston, Massachusetts 02111, USA.
Insights
Inhaled beclomethasone therapy for premature infants did not cause adrenal suppression. While basal cortisol levels slightly decreased, stimulated cortisol responses remained normal, indicating safety for preventing bronchopulmonary dysplasia.
Area of Science:
- Neonatal Medicine
- Pediatric Pulmonology
- Endocrinology
Background:
- Bronchopulmonary dysplasia (BPD) is a significant complication in premature infants.
- Corticosteroids are used to prevent BPD, but concerns exist regarding adrenal suppression.
- Evaluating the safety of inhaled beclomethasone is crucial for its clinical application.
Purpose of the Study:
- To test the hypothesis that inhaled beclomethasone therapy for BPD prevention does not cause adrenal suppression.
- To assess adrenal function in premature infants receiving beclomethasone versus placebo.
Main Methods:
- Multicenter randomized trial involving infants with birth weights <=1250 g and gestational age <33 weeks.
- Adrenal function assessed on study day 21 via basal and stimulated plasma cortisol levels.
- Initial assessment used insulin-induced hypoglycemia test (IIHT), later switching to cosyntropin stimulation due to insufficient response.
Main Results:
- Beclomethasone therapy showed a statistically significant but small decrease in median basal cortisol levels (P=.04).
- Insulin-induced hypoglycemia test revealed insignificant cortisol response changes within groups.
- Cortisol response to cosyntropin stimulation was similar between beclomethasone and placebo groups (P=.86).
Conclusions:
- Inhaled beclomethasone therapy is associated with a minor reduction in basal cortisol levels.
- No evidence of adrenal suppression was found in response to cosyntropin stimulation.
- The blunted response to hypoglycemia may be related to the premature infants' developing hypothalamic-pituitary-adrenal axis.
Objective:
We tested the hypothesis that inhaled beclomethasone therapy for prevention of bronchopulmonary dysplasia does not cause adrenal suppression.
Study Design:
Infants receiving ventilatory support with birth weights =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 bronchopulmonary dysplasia. Adrenal function was assessed on study day 21 (+/- 2 days) by determination of basal and stimulated plasma cortisol levels. Initially, cortisol response was assessed with insulin-induced hypoglycemia test (IIHT) (n = 63) until an interim analysis revealed insignificant cortisol response in both study groups. Thereafter, cosyntropin stimulation was used (n = 85).
Results:
Beclomethasone therapy was associated with lower median basal cortisol levels (5 microg/dL beclomethasone, 6 microg/dL placebo, P =.04). IIHT revealed insignificant change in cortisol response within each group. Cortisol response to cosyntropin stimulation was similar for each group (17 microg/dL beclomethasone, 18 microg/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 response to cosyntropin stimulation during beclomethasone therapy. Lack of cortisol response to hypoglycemia may reflect missed timing and/or decreased response of the premature infants' hypothalamic-pituitary-adrenal axis to hypoglycemia.