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Response to ACTH in the newborn
Insights
Newborn infants, especially preterm and ill ones, show altered adrenal steroid levels. Adrenocorticotrophic hormone (ACTH) stimulation reveals appropriate adrenal responses, even in stressed infants with low cortisol.
Area of Science:
- Neonatal endocrinology
- Pediatric endocrinology
- Adrenocortical physiology
Background:
- Adrenocortical function is critical in newborns, particularly in preterm and ill infants.
- Maternal glucocorticoid use during pregnancy can influence fetal adrenal development.
- Understanding basal and stimulated steroidogenesis is essential for neonatal care.
Purpose of the Study:
- To assess basal and adrenocorticotrophic hormone (ACTH)-stimulated adrenocortical function in different newborn groups.
- To establish reference data for adrenal steroid levels in infants, considering maternal glucocorticoid exposure.
- To investigate adrenal response in highly stressed newborns with initially undetectable cortisol.
Main Methods:
- Studied 52 newborn infants categorized into preterm well, preterm ill, and term ill groups.
- Measured basal plasma 17-hydroxyprogesterone and cortisol concentrations.
- Administered intramuscular ACTH (36 mcg/kg) and measured steroid responses.
Main Results:
- Significantly increased basal 17-hydroxyprogesterone in preterm infants (well and ill).
- No significant difference in basal cortisol, but highest in preterm ill infants.
- All infants showed a 2-3 fold increase in steroids post-ACTH stimulation; preterm ill infants had a higher peak 17-hydroxyprogesterone response.
- Stressed infants with undetectable basal cortisol responded appropriately to ACTH.
Conclusions:
- Provides reference data for assessing infant adrenal function, especially with maternal glucocorticoid exposure.
- Highlights a shift in fetal adrenal steroidogenesis post-birth, influenced by exogenous ACTH.
- Suggests potential need for temporary glucocorticoid replacement in ~10% of stressed newborns with basal cortisol deficiency.
Abstract:
Adrenocortical function was studied in 52 newborn infants who had been divided into three groups: preterm well, preterm ill, and term ill. Basal plasma 17-hydroxyprogesterone concentrations were significantly increased in both groups of preterm infants. There was no significant difference in basal plasma cortisol concentrations, although they were highest in preterm ill infants. All infants responded to adrenocorticotrophic hormone (ACTH) stimulation (36 micrograms/kg intramuscularly) with a two to three fold increase in the concentration of both steroids. The peak plasma 17-hydroxyprogesterone response was significantly higher in preterm ill infants. A subgroup of five infants, who were highly stressed but had undetectable basal plasma cortisol concentrations, also showed an appropriate response to ACTH. The results provide useful reference data to assess adrenal function in the infant of a mother given glucocorticoids during pregnancy. There is also a change from the pattern of fetal adrenal steroidogenesis soon after birth, which may be affected by exogenous ACTH stimulation. Roughly 10% of stressed newborns failed to synthesise cortisol basally; temporary glucocorticoid replacement for such infants may be appropriate.