Spontaneous miscarriage in the first trimester.
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Biomedical subjects
Publications and source records attributed to Kristina Gemzell Danielsson.
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At the development of receptivity the endometrium undergoes specific changes. Several factors have been suggested as markers of endometrial receptivity. A common feature for most of these factors is that they are directly, or indirectly, regulated by progesterone. The effect of various doses and regimens of mifepristone on endometrial development and markers of receptivity has been studied. Timed endometrial biopsies were assessed by immunhistochemistry, reverse transcriptase polymerase chain reaction (RT-PCR) and electron microscopy. In addition the contraceptive efficacy of these regimens was investigated. Administration of 200 mg of mifepristone immediately post ovulation has a pronounced effect on endometrial development and on suggested markers of receptivity. This regimen has been shown to be an effective contraceptive method. When 10 mg is given pre or post ovulation, only minor effects on the endometrium are observed. Our studies show that mifepristone, when administered in low doses that do not affect ovulation, significantly affects some of the studied markers of endometrial receptivity and reduces pregnancy rates; however, these activities are more pronounced with the higher dose, which is more effective. Our findings provide insight into the regulation of progesterone receptors of various suggested markers of endometrial receptivity and the possibility of using mifepristone for endometrial contraception.
OBJECTIVE: To study the effect of mifepristone and levonorgestrel on ovarian function and endometrial development in doses effective as emergency contraception. METHODS: Twelve fertile women were treated with either 10 mg of mifepristone as a single dose (n = 6) or two doses of 0.75 mg of levonorgestrel, 12 hours apart (n = 6) before and after ovulation. An endometrial biopsy performed during the implantation period was analyzed for endometrial maturation and expression of markers of endometrial receptivity. The markers tested for were integrin alpha4 and beta3, cyclooxygenase-1 and -2, progesterone receptors, Dolichos biflorus agglutinin lectin binding, and pinopodes. Urinary excretion of luteinizing hormone, estrone, and pregnanediol were also determined. RESULTS: Treatment with mifepristone and levonorgestrel before ovulation inhibited the luteinizing hormone surge showing no significant differences between the means of luteinizing hormone measurements. When mifepristone was administered in the early luteal phase, downregulation of progesterone receptors was inhibited in five of six women. No significant alteration was found in any of the remaining markers of endometrial receptivity. CONCLUSION: The mode of action of emergency contraception with mifepristone or levonorgestrel is primarily due to inhibition of ovulation rather than inhibition of implantation.
Emergency contraception (EC), which prevents pregnancy after unprotected sexual intercourse, has the potential to significantly reduce the incidence of unintended pregnancy and thus the need for abortion. EC is, however, frequently confused with induced abortion, making the method unavailable for millions of women for religious and/or political reasons. In this paper we discuss available data on the mechanism of action and efficacy of the current accessible methods. The main mechanism of action, of emergency contraceptive pills, is to postpone or inhibit ovulation, while the insertion of a copper IUD prevents implantation.
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