Experimentally induced endometriosis in rats: effect on fertility and the effects of pregnancy and lactation on the ectopic endometrial tissue
Fertility and SterilityPublished 1 December 1992
Juan C. Barragán, Jaime Brotons, José Antonio Palacios Ruíz, Pedro Acién
Citations44
SJR quartileQ1
SJR score2.03
SNIP2.05
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TL;DR
It is not pregnancy, but the anestrus condition created by lactation that exerts a beneficial effect on experimentally induced endometriosis in rats, and this condition diminishes pregnancy rate in rats.
Abstract
Experimentally induced endometriosis diminishes pregnancy rate in rats. It is not pregnancy, but the anestrus condition created by lactation that exerts a beneficial effect on experimentally induced endometriosis in rats.
Keywords
Immunology and MicrobiologyPsychologyMedicine
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The successful growth and development of surgically transplanted endometrial tissue in the rat offers a research model that can be used to study those aspects of endometriosis that cannot be adequately investigated in women.
American Journal of Obstetrics and GynecologyThe use of newer progestins in the treatment of endometriosis
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It was suggested that estrogens might be eliminated in treatment of endometriosis since a decidua may be produced with progestins.
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The increased PGF in peritoneal fluid may alter follicular rupture, ovum transport, corpus luteum function, or implantation, thus representing a mechanism by which endometriosis may cause infertility.
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Pregnancy is suggested as the optimal prophylactic treatment for endometriosis since the symptoms and signs regress during gestation and for varying periods thereafter.
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The results encourage the belief that a 1-month release parenteral preparation of leuprolide acetate may be potentially useful in the therapy of endometriosis in human beings.
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The results suggest a cell-mediated immune response in the presence of endometriosis, and an increased number of T and B cells in peritoneal fluid and peripheral blood from patients with endometRIosis as compared with controls.
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It is concluded that endometrial cells may survive at the implanted site even after apparent complete morphological regression, which has the potential to grow into an implant.
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The observed activity of steroidal and non-steroidal compounds in this study demonstrates the usefulness of a rat model in the study of endometriosis and suggests that inhibiting or eliminating ovarian steroid production alone will not produce a permanent regression of the endometrial explant.
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It is suggested that pregnancy commonly results in complete resolution of minimal or mild disease and endometriosis in nonpregnant monkeys tended to progress.
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This animal model represents an excellent method for quantitative evaluation of potential therapeutic agents for endometriosis and shows that ovariectomy, histrelin, or danazol treatment reduced the number of endometrial glands and atrophied the stroma.
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In the adhesion-free rabbit model, peritoneal implants of endometriosis do not have an effect on fertility, which supports the contention that therapies focused toward the implants are unlikely to change the pregnancy outcomes.
RECIMUNDOEndometriosis como causa de infertilidad
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