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Comparative Study
Journal Article
Proliferative activity of the endometrium throughout the menstrual cycle in infertile women with and without endometriosis.
Fertility and Sterility 1996 September
OBJECTIVE: To assess whether changes in endometrial proliferation in patients with endometriosis contribute to ectopic endometrial implantation.
DESIGN: Endometrial biopsies from patients with endometriosis were stained immunohistochemically and compared with endometrium of a control group (n = 111). The newly developed monoclonal antibody Ki-S3 was used as a marker of cellular proliferation in surface and glandular epithelia and in stromal cells.
SETTING: Female Infertility Clinic, Research Centre of Obstetrics, Gynecology, and Perinatology, Moscow, Russia, and Institute of Pathology, Christian-Albrechts-University, Kiel, Germany.
PATIENTS: One hundred thirty-nine women with endometriosis and 111 women without endometriosis, all being infertile.
INTERVENTION: Collecting endometrial samples during diagnostic and therapeutic laparoscopy.
MAIN OUTCOME MEASURE: Number of proliferating cells in endometrial stroma, glandular, and surface epithelia.
RESULTS: Endometrial proliferation showed a characteristic cyclic dependency with greatest activity in the follicular phase. Although epithelial proliferation ceased completely during the luteal phase, the number of proliferating cells in the stroma increased again toward the end of the menstrual cycle after its maximum at ovulation. No significant differences could be found between both investigated groups.
CONCLUSIONS: Endometriosis is not due to an altered proliferative activity in eutopic endometrium. Proliferating stromal cells at the end of the menstrual cycle may reflect increasing numbers of immunocompetent cells. Endometrium of patients with endometriosis reveals almost the same cyclical changes as endometrium of patients without endometriosis does. Further attention to cells and cell-mediated reactions in the extrauterine milieu is required to elucidate the pathogenesis of endometriosis.
DESIGN: Endometrial biopsies from patients with endometriosis were stained immunohistochemically and compared with endometrium of a control group (n = 111). The newly developed monoclonal antibody Ki-S3 was used as a marker of cellular proliferation in surface and glandular epithelia and in stromal cells.
SETTING: Female Infertility Clinic, Research Centre of Obstetrics, Gynecology, and Perinatology, Moscow, Russia, and Institute of Pathology, Christian-Albrechts-University, Kiel, Germany.
PATIENTS: One hundred thirty-nine women with endometriosis and 111 women without endometriosis, all being infertile.
INTERVENTION: Collecting endometrial samples during diagnostic and therapeutic laparoscopy.
MAIN OUTCOME MEASURE: Number of proliferating cells in endometrial stroma, glandular, and surface epithelia.
RESULTS: Endometrial proliferation showed a characteristic cyclic dependency with greatest activity in the follicular phase. Although epithelial proliferation ceased completely during the luteal phase, the number of proliferating cells in the stroma increased again toward the end of the menstrual cycle after its maximum at ovulation. No significant differences could be found between both investigated groups.
CONCLUSIONS: Endometriosis is not due to an altered proliferative activity in eutopic endometrium. Proliferating stromal cells at the end of the menstrual cycle may reflect increasing numbers of immunocompetent cells. Endometrium of patients with endometriosis reveals almost the same cyclical changes as endometrium of patients without endometriosis does. Further attention to cells and cell-mediated reactions in the extrauterine milieu is required to elucidate the pathogenesis of endometriosis.
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