Maturity of the Adrenal Cortex in Very Preterm Infants Is Related to Gestational Age

Abstract

To study the maturity of the adrenal cortex in preterms born before 33 wk of gestation, basal levels of cortisol and cortisone and the cortisol and 17-hydroxyprogesterone (17-OHP) response to 1 g/kg adrenocorticotropic hormone stimulation were measured in 24 appropriate-for-gestational age preterm infants (26-33 wk; 690-1985 g). Gestational age influenced the response of cortisol, 17-OHP, and the ratio between cortisol/17-OHP in the studied infants. In preterms born Ͻ30 wk of gestation, levels of cortisol, and the ratio between cortisol/17-OHP were lower compared with preterms born between 30 and 33 wk. Levels of cortisone were higher in preterms born Ͻ30 wk, suggesting a lower activity of 11␤-hydroxysteroid dehydrogenase that may be related to maturity as well. The adrenal gland plays an important role during gestation. Steroid hormones produced by the fetal adrenal cortex are involved in the maturation of organ systems necessary for intrauterine and extrauterine life. For example, secretion of cortisol in late gestation is essential for lung maturation in sheep, rats, monkeys, and possibly humans (1, 2). It has been suggested that the adrenal cortex function may be more closely related to gestational age rather than to birth (3, 4), which implicates that in very preterm infants the adrenal activity may still be immature. Immaturity of the hypothalamic-pituitaryadrenal (HPA)-axis in preterm infants has been suggested to be associated with the occurrence of respiratory distress syndrome, chronic lung disease of prematurity, or even cardiovascular instability (5-7). Therefore, the ability of the HPA-axis to regulate, synthesize, and secrete cortisol in response to stress may be critical for survival and pulmonary development in very preterm infants.To evaluate the adrenal function the plasma cortisol response to i.v. administered ACTH is a common screening test. In general, 250 g synthetic ACTH is given as a bolus dose to stimulate cortisol release from the adrenal cortex, in adults as well as children as described by Wood et al. in 1965 (8). This supra-physiologic dose is much higher than required to produce a maximal adrenal response and could elicit an appropriate response despite of adrenal insufficiency (9, 10). Therefore, a lower dose of ACTH has been proposed to study the adrenal function.We hypothesize that differences in the maturity of the HPAaxis related to gestational age can be observed in the levels of hormones produced by the adrenal cortex and the adrenal response to ACTH in preterm infants of different gestational ages. The objective was to study basal levels of glucocorticoids and to establish the effect of stimulation of the adrenal cortex with ACTH in very preterm infants at the end of the 1st week of life. PATIENTS AND METHODS Patients.The study group consisted of 24 preterm infants with gestational ages ranging from 26 to 33 wk and birth weights ranging from 690 to 1985 g. Patients admitted to our July 11, 2001; January 10, 2002

Contingency Learning and Reactivity in Preterm and Full‐Term Infants at 3 Months

“…Instead, we found that preterm infants showed lower cortisol levels than full-term infants. Clinical studies have found that preterm neonates, while hospitalized in intensive medical care, may be at risk of adrenal insufficiency (e.g., Bolt et al, 2002). Accordingly, our findings suggest that a hyposecretion pattern of cortisol may persist in preterm infants up to 3 months of age (adjusted for gestation) especially those most exposed to neonatal pain (Granau et al, 2005).…”

Lack of Adult-Type Salivary Cortisol Circadian Rhythm in Hospitalized Preterm Infants

“…The larger (compared to fetal) placental contribution to F inactivation, however, is removed at birth. While plasma E levels do remain higher than at other times in life in both preterm and term infants [32,33,34], functional deactivation of F does not appear to occur after birth in infants born <30 weeks’ gestation, resulting in F levels higher than E [35, 36]. …”

Cortisol production in preterm infants with or without late-onset adrenal insufficiency of prematurity: A prospective observational study

“…The ratios of cortisol/17-OH-progesterone and cortisol/cortisone were calculated to estimate the activities of 21a-hydroxylase and/or 11b-hydroxylase, and 11b-hydroxysteroid dehydrogenase (11b-HSD), respectively. 17…”

“…The maturity of adrenocortical function is related to the duration of gestation, 17 but the timing of fetal adrenal involution in preterm infants is uncertain. 18,19 Thus, we hypothesized that maturity of the adrenal cortex in preterm infants is related to postmenstrual age, and that those with late-onset AOP have limited function to produce cortisol until the corresponding age of late gestation, 32e36 weeks postmenstrual age.…”