dead fetus, the ability of antiprogestins to shorten the therapeutic process is attractive. The use of antiprogestins given 36 to 48 hours before either a surgical procedure or prostaglandin installation appears to be well tolerated without the addition of significant clinical complications.
Studies in ewes and monkeys have indicated that, at term, antiprogestins induce uterine contractions and enhance the myometrial sensitivity to oxytocin, a drug used to induce labor. An initial study in humans with promising results compared mifepristone to a placebo for labor induction in term or post-term pregnancies. In this study, a significantly higher percentage of women receiving mifepristone experienced a spontaneous onset of labor, and the time to onset of labor was about 24 hours earlier than in the placebo control group. Mifepristone also reduced the amount of oxytocin required to induce labor in the patients who did not have a spontaneous onset of labor.
Research should include physiologic studies to assess the effects of antiprogestins on maternal lactation and on primate neonates to evaluate the pulmonary, cardiac and adrenal status of neonates as well as their later development and fertility potential.
Recommendation No. 12. The committee recommends studies to determine the minimal dose of antiprogestins necessary to induce labor. Studies in animal models (most likely the primates) should assess possible adverse outcomes on infants. Research is also needed to determine the effect of antiprogestins on maternal lactation.
Endometriosis is a disease caused by the presence of endometrial tissue in ectopic (outside the endometrium of the uterus) locations, most commonly within the pelvic cavity. During the menstrual cycle this tissue undergoes changes similar to those in the endometrium. Endometriosis is a common disease (some have estimated that 5 to 15 percent of reproductive-age women and 30 to 40 percent of infertile women have this disorder), and it can be painful.
The etiology of endometriosis is uncertain, but there is little question about the hormonal responsiveness of the ectopic endometrial tissue. Current therapeutic approaches are designed to interrupt cyclic hor-