Rv. Hingre et al., ADRENAL STEROIDOGENESIS IN VERY-LOW-BIRTH-WEIGHT PRETERM INFANTS, The Journal of clinical endocrinology and metabolism, 78(2), 1994, pp. 266-270
Adrenal steroidogenesis was evaluated in 25 sick premature infants wit
h a gestational age of less than 30 weeks. ACTH stimulation tests were
performed on the fourth day of life using synthetic ACTH (36 mu g/ kg
). Considering the stress and degree of illness, preterm newborns had
low basal cortisol levels (mean +/- SEM, 207.4 +/- 23.5 nmol/L), and t
heir levels were similar to basal levels reported for healthy full-ter
m newborns (170.7 +/- 26.8 nmol/L; P = 0.31; reference data from Endoc
rine Sciences, Inc., Calabasas Hills, CA). However, compared to term n
eonates, preterm infants had markedly elevated basal levels of 17-hydr
oxypregnenolone (54.3 +/- 11.2 nmol/L), 17-hydroxyprogesterone (19.7 /- 4.0 nmol/L), and 11-deoxycortisol (19.1 +/- 3.3 nmol/L), which were
7-, 18-, and 8-fold higher, respectively, than values for term infant
s. The activity of 3 beta-hydroxysteroid dehydrogenase was not signifi
cantly reduced in extremely premature neonates (mean basal ratio of 17
hydroxypregnenolone/17-hydroxyprogesterone 2.9 +/- 0.2; ACTH-stimulate
d ratio, 6.5 +/- 0.4). In contrast, the mean basal substrate/product r
atio of 11-deoxycortisol was markedly elevated in the preterm infants
(11.9 +/- 2.2, ratio x 10(-2)) compared to that in the full-term infan
ts (2.1 +/- 0.4, ratio x 10(-2); P < 0.001). These findings are consis
tent with decreased activity of 11 beta-hydroxylase (11 beta OH) in pr
eterm infants born at less than 30 weeks gestation. Decreased 11 beta
OH activity appears to be more prominent than the deficiency of 3 beta
-hydroxysteroid dehydrogenase that has been found in infants with less
er degrees of prematurity, suggesting that 11 beta OH activity may be
regulated during fetal development to increase during the latter part
of gestation.