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  • Title: Effect of two antiprogestins (mifepristone and onapristone) on endometrial factors of potential importance for implantation.
    Author: Cameron ST, Critchley HO, Buckley CH, Kelly RW, Baird DT.
    Journal: Fertil Steril; 1997 Jun; 67(6):1046-53. PubMed ID: 9176442.
    Abstract:
    OBJECTIVE: To investigate the effects of postovulatory administration of antiprogestins on endometrial factors that may be of importance for successful implantation. DESIGN: Ten women were given 200 mg mifepristone and an additional 10 women 400 mg of onapristone 48 hours after the LH surge in urine (LH + 2). MAIN OUTCOME MEASURE(S): Biopsies were assessed for histologic dating and the immunolocalization of [1] leukemia inhibitory factor, [2] 15-hydroxyprostaglandin dehydrogenase, and [3] the cell proliferation marker Ki 67. Hormonal measurements in blood and urine were used to monitor the effects on the ovarian cycle. Glycodelin (placental protein 14) concentrations were measured in blood taken on LH + 12. RESULT(S): Treatment with antiprogestins retarded the development of secretory changes without affecting the length of the luteal phase. In addition, there was reduced immunostaining for 15-hydroxyprostaglandin dehydrogenase within glands and a significant reduction in serum levels of glycodelin. Reduced immunostaining for leukemia inhibitory factor also was apparent within glands in biopsies taken on LH + 6 of the treatment cycle. Increased Ki 67 immunostaining was observed on both cycle days after treatment, consistent with P antagonism. CONCLUSION(S): Administration of mifepristone and onapristone adversely affects uterine receptivity. This adds further evidence to support their potential as a method of postovulatory fertility control. Further support for the use of mifepristone and onapristone as postovulatory fertility control agents was provided by a clinical study of 15 healthy volunteers with regular menstrual cycles. Of interest were the effects of these antiprogestins on endometrial factors that may affect implantation. Subjects were studied over control, treatment, and follow-up cycles. In the treatment cycle, women received either 200 mg of mifepristone or 400 mg of onapristone by mouth 48 hours after the onset of the luteinizing hormone surge in the urine. Five subjects agreed to undertake treatment with each antiprogestin, yielding a total of 20 treatment cycles. Treatment with either antiprogestin did not affect the length of the luteal phase between cycles or the follicular phase. The histologic appearance and immunohistochemistry of the endometrial biopsies taken 4 and 6 days post-ovulation after treatment with the antiprogestins indicated an adverse effect on uterine receptivity. After treatment with either agent, the endometrium was retarded and secretory changes were absent or poorly developed. These agents further inhibited the appearance of 15-hydroxyprostaglandin dehydrogenase and prevented the down-regulation of estrogen and progesterone receptors in the glands in the midluteal phase of the cycle. Both antiprogestins produced a significant suppression in serum levels of the endometrial protein glycodelin. Reduced immunostaining for leukemia inhibitory factor also was apparent. Neither agent exerted a significant effect on the pituitary-adrenal axis in the doses used in this study.
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