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Hum. Reprod. Advance Access originally published online on November 25, 2005
Human Reproduction 2006 21(3):798-809; doi:10.1093/humrep/dei383
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© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Effects of mifepristone on proliferation and apoptosis of human endometrium in new users of medroxyprogesterone acetate

John K. Jain1,4, Aimin Li1, Wangrong Yang1, Parviz Minoo2 and Juan C. Felix1,3

Department of 1 Obstetrics and Gynecology, 2 Pathology and 3 Pediatrics, The Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA

4 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, The Keck School of Medicine of the University of Southern California, 1240 Mission Street, Room 8K9, Los Angeles, CA 90033, USA. E-mail: jjain{at}usc.edu

BACKGROUND: Mifepristone has been demonstrated to decrease breakthrough bleeding (BTB) in users of progestin-only contraceptives. METHODS: Endometrial biopsies were collected from 50 normal cycling women who were new users of depot medroxyprogesterone acetate (DMPA) randomized to receive either mifepristone or placebo before, during and after treatment. Proliferation, apoptosis and sex steroid receptors were evaluated by either immunohistochemistry or TUNEL assay. RESULTS: Administration of mifepristone to DMPA-exposed endometrium for 1 week significantly increased endometrial expression of Ki-67 (MKI67), estrogen receptor (ER){alpha} and progesterone receptors A and B (PRAB) and decreased the number of TUNEL-positive and caspase-3 (CASP3)-active cells in the endometrial stroma. However, after 10 weeks of mifepristone treatment, no significant difference in proliferation, apoptosis and the expression of ER{alpha} or PRAB could be detected between the endometrium treated with DMPA alone and endometrium treated with mifepristone and DMPA. CONCLUSIONS: Administration of mifepristone to DMPA users significantly increases endometrial proliferation and decreases endometrial stromal apoptosis in the short term. Prolonged exposure to mifepristone does not counteract the inhibitory effects of progestin therapy on endometrial proliferation. Estrogen and progesterone receptors may play an important role in these effects.

Key words: apoptosis/breakthrough bleeding/endometrium/mifepristone/proliferation


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Stimulation of epithelial repair is a likely mechanism for the action of mifepristone in reducing duration of bleeding in users of progestogen-only contraceptives
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