The placental enzyme 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) transforms maternal cortisol to inactive cortisone. Fetal glucocorticoid excess due to reduced 11β-HSD2 activity could make small preterm infants susceptible to early adrenal insufficiency when the maternal cortisol source is no longer sustained. We assessed whether placental 11β-HSD2 activity is related to early adrenal insufficiency and postnatal clinical course in extremely low birth weight (<1000 g) infants. Mean gestational age of the 44 infants was 26.6wk (range,23.7-32.0),birth weight was 747 g (440-981),and relative birth weight was -1.9 SD (-4.9 to 1.0). We determined placental 11β-HSD2 activity,baseline,and ACTH-stimulated cortisol and assessed illness severity by the Score of Neonatal Acute Physiology (SNAP). One standard deviation decrease in placental 11β-HSD2 activity corresponded to a 1.85 (95%CI 0.55 to 3.14; p = 0.006) unit increase in SNAP score and 2.9 mm Hg decrease in minimum mean arterial pressure (95%CI 0.3 to 5.6 mm Hg; p=0.03). Placental 11β-HSD2 activity was not associated with cortisol concentrations,although the confidence interval of the ACTH-stimulated cortisol was close to zero:1 SD increase corresponded to 17%(-18%to 49%) increase in ACTH-stimulated cortisol. Moreover,a 1 SD decrease in enzyme activity was associated with a hazard ratio for postnatal glucocorticoid treatment of 1.63 (95%CI 1.00 to 2.65); p = 0.05. In ELBW infants,lower placental 11β-HSD2 activity is associated with more severe early postnatal illness and hypotension. Although an association with baseline or ACTH-stimulated cortisol was not seen,possible relationships with other components of the hypothalamic-pituitary-adrenal axis remain to be determined.
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