Mifepristone (RU-486) is used in medical abortion. What is its mechanism of action and the physiological consequence of progesterone receptor blockade in early pregnancy?
- A Mifepristone inhibits aromatase in the placenta, reducing estradiol and causing placental detachment
- B Mifepristone competitively antagonizes progesterone receptors in decidua, causing decidual necrosis; withdrawal of progesterone support increases prostaglandin sensitivity, promotes cervical softening, and increases uterine contractility ✓
- C Mifepristone blocks beta-hCG receptors, preventing corpus luteum stimulation and causing luteal regression
- D Mifepristone acts as a GnRH antagonist, suppressing LH and progesterone synthesis from the corpus luteum
Explanation
Mifepristone (RU-486) is a synthetic 19-norsteroid that competitively binds progesterone receptors (and glucocorticoid receptors) with high affinity without agonist activity. In early pregnancy, progesterone maintains the decidua, suppresses myometrial contractility, and inhibits prostaglandin synthesis. Mifepristone blocks progesterone receptors in the decidua, causing decidual necrosis and detachment of the gestational sac. It also upregulates prostaglandin receptors, increasing uterine sensitivity to prostaglandins; promotes cervical ripening (by blocking progesterone-mediated inhibition of collagenase); and sensitizes the myometrium to contractile stimuli. The addition of misoprostol (PGE1 analogue) 24–48 hours later exploits this sensitization to cause uterine contractions and complete the abortion.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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Written and medically reviewed by the StethoPrep medical team.