Plasma Cortisol, Cortisone and Urinary Glucocorticoid Metabolites in Preterm Infants

Abstract

Objective and Methods: In the fetal circulation, there is a low cortisol:cortisone (F:E) ratio (∼0.3) suggesting high activity of 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2). The circulating F:E ratio rises after birth in term infants, but little is known about infants born prematurely. Our hypothesis was that the low fetal plasma F:E ratio would persist in infants born prematurely, due to persistently high tissue 11βHSD2 activity. To test this hypothesis, a longitudinal observational study of plasma F, E levels and urinary F and E metabolites was performed in 22 preterm infants of 24–31 weeks gestation. Results: Median plasma F was 234–380 nmol l^–1, median 124–177 nmol l^–1 from 1 to 14 days age. Plasma F fell with increasing postnatal and postconceptional age. The F:E ratio was 3 in the first week of life, and thereafter was 1–2, falling with postnatal age. Urinary glucocorticoid metabolites were low in quantity (∼48–120 µg kg^–1 day^–1), consisted of E metabolites until term, and did not reflect the plasma F:E ratio. Conclusions: The fetal plasma F:E ratio did not persist in these preterm infants, due to tenfold higher levels of F. The F:E ratios were similar to those reported in term infants. These data suggest that the low F:E ratio in utero is due to low fetal production of cortisol, and effective placental inactivation of maternal F by 11βHSD2.