论文部分内容阅读
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.
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 Mean gestational age of the 44 infants was 26.6 wk (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 assess mortality severity by the Score of Neonatal Acute 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 pre (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 increased corresponded to 17% (-18% to 49%) in ACTH-stimulated cortisol. Furthermore, a1 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.