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Basal and post-ACTH cortisol levels in preterm infants following treatment with dexamethasone
C M Cronin1, H Dean, N T MacDonald
1Section of Neonatology, St. Boniface General Hospital, Winnipeg, Manitoba.
Insights
Dexamethasone treatment in infants with bronchopulmonary dysplasia can cause low cortisol levels, indicating adrenal suppression. However, their adrenal glands remain responsive to ACTH stimulation, suggesting a potential hypothalamic-pituitary issue.
Area of Science:
- Neonatal Medicine
- Endocrinology
- Pediatric Pulmonology
Background:
- Dexamethasone (DEX) reduces ventilator dependence in bronchopulmonary dysplasia (BPD).
- Abnormal metapyrone tests suggest adrenal suppression in infants after DEX treatment.
- The response of these infants to adrenocorticotrophic hormone (ACTH) stimulation is not fully understood.
Purpose of the Study:
- To investigate adrenal function in premature infants treated with dexamethasone.
- To assess morning cortisol levels and ACTH stimulation test responses in these infants.
- To determine if dexamethasone causes adrenal suppression at the hypothalamic-pituitary level.
Main Methods:
- Measured morning cortisol levels in 14 premature infants treated with dexamethasone.
- Performed ACTH stimulation tests on 12 of these infants.
- Analyzed cortisol levels before and 60 minutes after ACTH administration.
Main Results:
- Low morning cortisol levels were observed in most infants post-dexamethasone treatment.
- All infants showed a three-fold increase in cortisol levels after ACTH stimulation.
- Basal cortisol levels were also low in infants tested.
Conclusions:
- Infants treated with dexamethasone exhibit low cortisol levels, suggesting secondary adrenal suppression.
- The adrenal gland remains responsive to ACTH stimulation, indicating intact adrenal function.
- Dexamethasone may suppress the hypothalamic-pituitary axis, impacting adrenal function in preterm infants.
Abstract:
Dexamethasone (DEX) has been shown to decrease ventilator dependence in bronchopulmonary dysplasia (bronchopulmonary dysplasia). Abnormal metapyrone tests have been reported in 50% of infants who were weaned from a 45-day course of dexamethasone. We postulated that such infants would have adrenal suppression and would not respond to Cosyntropin (ACTH). We examined morning cortisol levels in 14 premature infants who had been treated with dexamethasone for 36 +/- 4 (mean +/- SEM) days, starting at 38 +/- 6 days of life, and performed ACTH stimulation tests in 12 of them. Morning cortisol levels were 87 +/- 36 nmol/L (range undetectable: 543; n = 14). Random basal cortisol levels were 109 +/- 42 nmol/L (range 34-540; n = 12). The mean cortisol level was 568 +/- 63 nmol/L (range 117-934) 60 min after adrenocorticotrophic hormone. In all cases, cortisol level increased three-fold after adrenocorticotrophic hormone. Low cortisol levels are almost universal in infants after treatment with dexamethasone, but the adrenal gland remains responsive to adrenocorticotrophic hormone stimulation. We speculate that dexamethasone causes secondary adrenal suppression at the hypothalamic-pituitary level. Normal adrenal function in the preterm infant needs to be defined.