Objective: To examine RU486 action on decidua at the level of cellular estrogen receptor (ER) and P receptor (PR).
Design: Controlled basic study for contragestion mechanism of mifepristone.
Setting: Normal human volunteers in an academic research environment.
Patients: Sixty women with 6 to 7 weeks of gestation who voluntarily requested termination of pregnancy were recruited and randomly divided into three groups.
Intervention: A single dose of 200 mg RU486 was orally administered to the two treatment groups 12 and 24 hours, respectively, before surgical interruption of pregnancies. Placebo was used for control group. Decidual tissues were collected right after operation.
Main outcome measure: Immunocytochemical reactions of PR and ER in decidua after RU486 treatment were compared with the control subjects. The differences of the reaction in decidual area with or without trophoblast invasion were noted.
Results: RU486 treatment increased PR and ER staining in vessel and stroma of decidua without trophoblast invasion (decidua parietalis) but not in decidua with trophoblast invasion (decidua capsularis or basalis). Chi-squared analysis indicated a significant increase in the number of ER-positive samples after RU486 treatment.
Conclusion: The decidua parietalis was the primary target site of RU486. The lack of RU486 effect on decidua capsularis implied that trophoblast invasion prevented against antiprogestin impact.
PIP: In China, physicians randomly placed 60 pregnant women of 6-7 weeks gestational age into a group receiving one oral dose of RU-486 12 or 24 hours before undergoing vacuum aspiration or into a group receiving a placebo. Aspirate samples were submitted to a laboratory to determine the effect of Ru-486 on progesterone (P) and estrogen (E) receptors in human decidua. RU-486 multiplied P and E receptor staining in vessel and stoma cells of decidua (decidua parietalis) without fetal trophoblast invasion (89% for 12-hour group and 84% in 24-hour group vs. 26%; p M .005). This did not occur, however, in decidua with fetal trophoblast invasion (decidual capsularis or basalis). These findings confirmed the hypothesis that the P antagonist, RU-486, increases P and E receptor levels in decidual tissue. Further, the findings indicated that the contragestive mechanisms of RU-486 is directed at the maternal endometrium and not at the developing embryo or those interfacing cells which anchor it to the endometrium. In fact, the cytological barrier inhibits antiprogestin effects and may even play a role in protecting against spontaneous abortion.