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      Peritoneal fluid progesterone and progesterone resistance in superficial endometriosis lesions

      1 , 2 , 3 , 4 , 5 , 4 , 6 , 7 , 8 , 9 , 10
      Human Reproduction
      Oxford University Press (OUP)

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          Abstract

          Peritoneal fluid in ovulatory women is an ovarian exudate with higher estrogen and progesterone concentrations than in plasma. In the follicular phase, progesterone concentrations are as high as plasma concentrations in the luteal phase. After ovulation, estrogen and progesterone concentrations in the peritoneal fluid are 5–10 times higher than in plasma, both in women with and without endometriosis. The histologically proliferative aspect without secretory changes of most superficial subtle lesions is not compatible with the progesterone concentrations in the peritoneal fluid. Therefore, we have to postulate a strong progesterone resistance in these lesions. The mechanism is unclear and might be a peritoneal fluid effect in women with predisposing defects in the endometrium, or isolated endometrial glands with progesterone resistance, or subtle lesions originating from the basal endometrium: the latter hypothesis is attractive since in basal endometrium progesterone does not induce secretory changes while progesterone withdrawal, not occurring in peritoneal fluid, is required to resume mitotic activity and proliferation. Hormone concentrations in the peritoneal fluid are an important factor in understanding the medical therapy of endometriosis. The effect of oestro-progestin therapy on superficial endometriosis lesions seems to be a consequence of the decreased estrogen concentrations rather than a direct progestin effect. In conclusion, the peritoneal fluid, being a secretion product of the ovarian follicule, deserves more attention in the pathophysiology and treatment of endometriosis.

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          Clinical practice. Endometriosis.

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            Endometriosis

            Pelvic endometriosis is a complex syndrome characterized by an estrogen-dependent chronic inflammatory process that affects primarily pelvic tissues, including the ovaries. It is caused when shed endometrial tissue travels retrograde into the lower abdominal cavity. Endometriosis is the most common cause of chronic pelvic pain in women and is associated with infertility. The underlying pathologic mechanisms in the intracavitary endometrium and extrauterine endometriotic tissue involve defectively programmed endometrial mesenchymal progenitor/stem cells. Although endometriotic stromal cells, which compose the bulk of endometriotic lesions, do not carry somatic mutations, they demonstrate specific epigenetic abnormalities that alter expression of key transcription factors. For example, GATA-binding factor-6 overexpression transforms an endometrial stromal cell to an endometriotic phenotype, and steroidogenic factor-1 overexpression causes excessive production of estrogen, which drives inflammation via pathologically high levels of estrogen receptor-β. Progesterone receptor deficiency causes progesterone resistance. Populations of endometrial and endometriotic epithelial cells also harbor multiple cancer driver mutations, such as KRAS, which may be associated with the establishment of pelvic endometriosis or ovarian cancer. It is not known how interactions between epigenomically defective stromal cells and the mutated genes in epithelial cells contribute to the pathogenesis of endometriosis. Endometriosis-associated pelvic pain is managed by suppression of ovulatory menses and estrogen production, cyclooxygenase inhibitors, and surgical removal of pelvic lesions, and in vitro fertilization is frequently used to overcome infertility. Although novel targeted treatments are becoming available, as endometriosis pathophysiology is better understood, preventive approaches such as long-term ovulation suppression may play a critical role in the future.
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              Endometriosis is a chronic systemic disease: clinical challenges and novel innovations

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                Author and article information

                Contributors
                (View ORCID Profile)
                (View ORCID Profile)
                Journal
                Human Reproduction
                Oxford University Press (OUP)
                0268-1161
                1460-2350
                November 29 2021
                November 29 2021
                Affiliations
                [1 ]Obstetrics and Gynecology, Latifa Hospital, Dubai, United Arab Emirates
                [2 ]Prof Emeritus OBGYN, KULeuven, Leuven, Belgium
                [3 ]University of Oxford-Hon Consultant, Obstetrics and Gynaecology, Oxford, UK
                [4 ]Gemelli hospitals, Obstetrics and Gynecology, University Cattolica, Roma, Italy
                [5 ]Moscow State University, Obstetrics and gynecology, Moscow, Russia
                [6 ]Gruppo Italo Belga, Obstetrics and Gynecology, Villa Del Rosario Rome, Rome, Italy
                [7 ]Department of Operative Gynecology, Federal State Budget Institution V. I. Kulakov Research Centre for Obstetrics, Gynecology, and Perinatology, Ministry of Health of the Russian Federation, Moscow, Russia; Department of Reproductive Medicine and Surgery, Moscow State University of Medicine and Dentistry, Moscow, Russia
                [8 ]Department of Obstetrics and Gynecology, University of British Columbia, Women's Hospital, Vancouver, British Columbia, Canada
                [9 ]Professor Emeritus, University of Tennessee Health Science Centre, Memphis, TN, USA
                [10 ]Institutional Review Board, Virginia Commonwealth University, Richmond, VA, USA
                Article
                10.1093/humrep/deab258
                34849906
                7c176984-267c-4959-adc7-74b625effcee
                © 2021

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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