PLACENTAL 11-BETA-HYDROXYSTEROID DEHYDROGENASE-ACTIVITY IN NORMOTENSIVE AND PREECLAMPTIC PREGNANCIES

Apparent mineralocorticoid excess and licorice induced hypertension, b oth hypertensive disorders, have been attributed to a defect in the en zyme 11 beta-hydroxysteroid dehydrogenase(11 beta-HSD), which intercon verts cortisol to cortisone. Therefore, we undertook this study to det ermine the role of human placental 11 beta-HSD activity in preeclampsi a, which is a hypertensive disorder in pregnancy. 11 beta-HSD activiti es were determined in placentas of 17 normotensive and 11 preeclamptic patients matched for gestational age at 34-42 weeks. Cortisol levels in umbilical venous and arterial sera were also determined for both gr oups. Statistical analysis was performed using Student's t-test, signi ficance at p < 0.05. 11 beta-dehydrogenase (oxidation activity of 11 b eta-HSD) activity was significantly lower in placentas of preeclamptic compared to normotensive patients (0.19 +/- 0.09 vs. 0.26 +/- 0.08 mm oles/min/placenta, p = 0.02). Cortisol level in umbilical cord blood w as significantly higher in the preeclamptic group (14.99 +/- 14.08 vs. 6.71 +/- 3.69 g/dL, p = 0.02). The decreased 11 beta-HSD activity is accompanied by an expected increase in umbilical cord blood cortisol l evel and decrease in fetal weight. This enzyme may play an important r ole in influencing fetal growth. (Steroids 63:511-515, 1998) (C) 1998 by Elsevier Science Inc.