Adrenal insufficiency in preterm newborns and to a lesser extent in late preterm and term newborns is due to a:
Transient adrenocortical insufficiency of prematurity (TAP): an “immature” hypothalamic-pituitary-adrenal (HPA) axis with reduced capability of the adrenal glands to produce cortisol secondary to intermediate enzyme deficiency in the steroidogenesis pathway, but with rapid recovery of the hormonal axis in early (∼14 days) postnatal life
Relative adrenal insufficiency: failure to produce adequate quantity of stress hormone resulting in inappropriately low-circulating cortisol concentration for the degree of stress or illness experienced (a condition similar to that observed in critically ill adults with seemingly normal adrenal function)
Adrenal insufficiency due to congenital adrenal hyperplasia (CAH) is a different condition and not covered in this chapter.
The exact incidence of TAP and adrenocortical insufficiency in late preterm or term newborns is not known. This is because the normal range of serum cortisol concentration in this age group is difficult to define, and the level that constitutes clinical adrenal impairment has not been ascertained (see Diagnosis).
The earlier the gestation (primarily in those born <30 weeks), the higher is the chance of developing this condition.
It is fallacious to assume that all preterm infants with improvement of blood pressure after receiving systemic corticosteroids are due to TAP, because corticosteroids per se can also elevate the blood pressure in adrenal competent subjects.
Those infants with genuine cortisol deficiency will respond promptly and dramatically to a “replacement” or “stress” dose of corticosteroids.
TAP is most likely due to delay in maturation of the HPA axis, resulting in decreased ability of the adrenal glands to produce adequate amount of cortisol.
Adrenocortical insufficiency is likely related to ineffective adrenal steroidogenesis secondary to immature intermediate enzymes, eg, 11β-hydroxylase and 3β-hydroxysteroid dehydrogenase activity of the glucocorticoid pathway and manifests as increased cortisol precursors/cortisol ratios.
This may be associated with normal fetal development of the adrenal glands that generally do not synthesize cortisol de novo until 30 weeks' gestation, and utilize placental progesterone for production of cortisol, thereby bypassing the intermediate enzymes during the process.
Although the use of antenatal corticosteroids has been shown to suppress the adrenal glands in preterm infants, no significant association has been reported between antenatal corticosteroids usage and TAP. However, prolonged use of steroids during the neonatal period may contribute to the relative adrenal insufficiency seen in infants following their NICU course.
Inadequate circulating cortisol can have two major clinical consequences in preterm infants.
Chronic lung disease: Reduced ability to suppress inflammation can lead to exaggeration of inflammatory responses in the lungs, giving rise to increased risks of developing chronic lung disease.
Cardiovascular instability: Decreased ability to maintain hemodynamic stability resulting in refractory hypotension and cardiovascular collapse.
Transient adrenocortical insufficiency in late preterm or term infants may be related to the above described mechanism, and in addition, transitional changes of hormone production from intrauterine to extrauterine life in the HPA axis.
During intrauterine life, CRH produced by the placenta plays ...
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