Cervical ripening after treatment with prostaglandin E2 or antiprogestin (RU486). Possible mechanisms in relation to gonadal steroids

Ylva Vladic Stjernholm; Lena Sahlin; Håkan A. Eriksson; Birgitta Byström; Per-Mårten Stenlund; Gunvor Ekman

doi:10.1016/s0301-2115(98)00329-7

Cervical ripening after treatment with prostaglandin E2 or antiprogestin (RU486). Possible mechanisms in relation to gonadal steroids

Ylva Vladic Stjernholm, Lena Sahlin, Håkan A. Eriksson, Birgitta Byström, Per-Mårten Stenlund, Gunvor Ekman

In: European Journal of Obstetrics & Gynecology and Reproductive Biology · 1999 · vol. 84(1) , pp. 83–88 · doi:10.1016/s0301-2115(98)00329-7 · PMID:10413233 · W2108324067

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Abstract

ObjectiveTo compare the mechanisms for cervical ripening after treatment with prostaglandin E2 or antiprogestin (RU486) to spontaneous cervical ripening, with focus on gonadal steroid receptors.Study designCervical biopsies were obtained from postpartal women after treatment with prostaglandin E2 (n=10), or antiprogestin (n=5). Postpartal women after spontaneous cervical ripening (n=10) served as controls. Levels of estrogen and progesterone receptors, their mRNAs, insulin-like growth factor I mRNA and serum estradiol and progesterone were quantitated. The collagen concentration and solubility by pepsin were determined. Statistical tests used were Kruskal-Wallis and Mann-Whitney U test.ResultsAfter prostaglandin E2 treatment the collagen concentration was higher (P<0.05) as compared to spontaneous ripening. After antiprogestin treatment the estrogen receptor concentration was higher (P<0.05) in comparison to spontaneous ripening.ConclusionThe elevated estrogen receptor concentration after antiprogestin treatment, in contrast to spontaneous ripening, and prostaglandin E2 treatment, indicates a that a receptor-mediated progesterone withdrawal does not explain the events behind spontaneous cervical ripening at parturition.

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[1] Differential expression of cyclooxygenase-1 and -2 proteins in rat uterus and cervix during the estrous cycle, pregnancy, labor and in myometrial cells 1996

[2] Potential Roles for Gonadal Steroids and Insulin-like Growth Factor I During Final Cervical Ripening 1997