11beta-Hydroxysteroid dehydrogenase activity in pregnancies complicated by hydatidiform mole

11beta-Hydroxysteroid dehydrogenase (11beta-HSD) plays an important role in regulating active glucocorticoid reaching the fetus. In normal pregnancy, placental 11beta-HSD functions primarily in oxidative direction. Placental tissue of patients with pregnancies complicated by pre-eclampsia exhibit significantly lower type 1 and 2 11beta-HSD activities and significantly high cortisol level in cord blood suggesting fetal exposure to higher level of active glucocorticoids. The activity of 11beta-HSD in gestational trophoblastic disease has not been determined. The objective of this study was to assess 11beta-HSD activity in tissue from normal second trimester and pregnancies complicated by hydatidiform mole.

Normal placental tissues were obtained from patients undergoing termination of pregnancy, and from patients undergoing uterine evacuation for hydatidiform mole. Both nicotinamide adenine dinucleotide (NAD)- and nicotinamide adenine dinucleotide phosphate (NADP)-dependent activities were assayed in central villous tissue. Comparison of groups was performed using Student's t-test. A P-value of 0.05 was considered significant. Data are presented as mean +/- S.D.

Tissue obtained from five patients with pathology-proven hydatidiform mole demonstrated significantly lower 11beta-HSD activities compared with placental tissue obtained from normal pregnancies. The mean NAD-dependent 11beta-HSD activity in normal placentas was 386 +/- 109 pmol/min/g placenta and in hydatidiform mole was 74 +/- 54 pmol/min/g placenta (P < 0.01). The mean NADP-dependent 11beta-HSD activity in normal placentas was 370 +/- 120 pmol/min/g placenta and in trophoblastic disease was 68 +/- 69 pmol/min/g placenta (P < 0.01).

Our data indicate significant impairment in the ability of hydatidiform mole tissue to inactivate glucocorticoids.