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

Problem: 11 β-Hydroxysteroid dehydrogenase (11 β-HSD) plays an important role in regulating active glucocorticoid reaching the fetus. In normal pregnancy, placental 11β-HSD functions primarily in oxidative direction. Placental tissue of patients with pregnancies complicated by pre-eclampsia exhibit significantly lower type 1 and 2 11β-HSD activities and significantly high cortisol level in cord blood suggesting fetal exposure to higher level of active glucocorticoids. The activity of 11β-HSD in gestational trophoblastic disease has not been determined. The objective of this study was to assess 11 β-HSD activity in tissue from normal second trimester and pregnancies complicated by hydatidiform mole. Method of study: 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. Results: Tissue obtained from five patients with pathology-proven hydatidiform mole demonstrated significantly lower 11 β-HSD activities compared with placental tissue obtained from normal pregnancies. The mean NAD-dependent 11 β-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 11 β-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). Conclusion: Our data indicate significant impairment in the ability of hydatidiform mole tissue to inactivate glucocorticoids.