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

Abstract

BackgroundImmature adrenocortical function in preterm infants may cause inadequate production of cortisol under stress, resulting in adrenal insufficiency of prematurity (AOP). The objective of this study is to compare cortisol production in preterm infants with and without late-onset AOP.MethodsOf 27 preterm infants born at less than 32 weeks gestation, cortisol production was analyzed in those who did (patients, group P) and did not (controls, group C) eventually develop late-onset AOP. Blood samples were prospectively collected every two weeks after birth, and steroid hormone concentrations in the pathway to cortisol production were measured retrospectively.ResultsWe restricted the initial subjects to infants with gestation less than 29 weeks to adjust for confounding factors, culminating in matched infants in groups P (n = 8) and C (n = 11). The cortisol concentrations did not differ between the groups before AOP onset (P = 0.20), but the total concentrations of precursors for cortisol were higher in group P (P < 0.0001). The total concentrations of precursors in group C were inversely correlated with postmenstrual age (ρ = −0.38, P < 0.01). The pattern of changes in total concentrations of precursors differed between the groups (P < 0.05).ConclusionAdrenal cortex maturity in preterm infants develops in parallel with postmenstrual age. Infants with late-onset AOP have undeveloped maturation of adrenocortical function after birth.Clinical trial registrationUMIN000022453. Immature adrenocortical function in preterm infants may cause inadequate production of cortisol under stress, resulting in adrenal insufficiency of prematurity (AOP). The objective of this study is to compare cortisol production in preterm infants with and without late-onset AOP. Of 27 preterm infants born at less than 32 weeks gestation, cortisol production was analyzed in those who did (patients, group P) and did not (controls, group C) eventually develop late-onset AOP. Blood samples were prospectively collected every two weeks after birth, and steroid hormone concentrations in the pathway to cortisol production were measured retrospectively. We restricted the initial subjects to infants with gestation less than 29 weeks to adjust for confounding factors, culminating in matched infants in groups P (n = 8) and C (n = 11). The cortisol concentrations did not differ between the groups before AOP onset (P = 0.20), but the total concentrations of precursors for cortisol were higher in group P (P < 0.0001). The total concentrations of precursors in group C were inversely correlated with postmenstrual age (ρ = −0.38, P < 0.01). The pattern of changes in total concentrations of precursors differed between the groups (P < 0.05). Adrenal cortex maturity in preterm infants develops in parallel with postmenstrual age. Infants with late-onset AOP have undeveloped maturation of adrenocortical function after birth.