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      Endometrial polyps: Pathogenesis, sequelae and treatment

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          Abstract

          Endometrial polyps are overgrowths of endometrial glands that typically protrude into the uterine cavity. Endometrial polyps are benign in nature and affect both reproductive age and postmenopausal women. Although endometrial polyps are relatively common and may be accompanied by abnormally heavy bleeding at menstruation. In asymptomatic women, endometrial polyps may regress spontaneously, in symptomatic women endometrial polyps can be treated safely and efficiently with hysteroscopic excision.

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          FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age.

          Malcolm G Munro, Hilary O. D. Critchley, Michael Broder … (2011)
          There is general inconsistency in the nomenclature used to describe abnormal uterine bleeding (AUB), in addition to a plethora of potential causes-several of which may coexist in a given individual. It seems clear that the development of consistent and universally accepted nomenclature is a step toward rectifying this unsatisfactory circumstance. Another requirement is the development of a classification system, on several levels, for the causes of AUB, which can be used by clinicians, investigators, and even patients to facilitate communication, clinical care, and research. This manuscript describes an ongoing process designed to achieve these goals, and presents for consideration the PALM-COEIN (polyp; adenomyosis; leiomyoma; malignancy and hyperplasia; coagulopathy; ovulatory dysfunction; endometrial; iatrogenic; and not yet classified) classification system for AUB, which has been approved by the International Federation of Gynecology and Obstetrics (FIGO) Executive Board as a FIGO classification system. Copyright © 2011. Published by Elsevier Ireland Ltd.
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            Mast cells and angiogenesis.

            Klas Norrby (2002)
            Angiogenesis is tightly regulated by pro- and anti-angiogenic factors. Secreting mast cells are able to induce and enhance angiogenesis via multiple in part interacting pathways. They include mast cell-derived (i) potent pro-angiogenic factors such as VEGF, bFGF, TGF-beta, TNF-alpha and IL-8, (ii) proteinases and heparin, that release heparin-binding pro-angiogenic factors lodged on cell surfaces and in the extracellular matrix (ECM), (iii) histamine, VEGF, and certain lipid-derived mediators that induce microvascular hyperpermeability having pro-angiogenic effects, (iv) chemotactic recruitment of monocytes/macrophages and lymphocytes that are able to contribute with angiogenesis-modulating molecules, (v) activation of platelets that release pro-angiogenic factors, (vi) activation of neighboring stationary non-mast cells, which secrete pro-angiogenic factors, ECM-degrading proteinases and stem cell factor which attracts, mitogenically stimulates and activates mast cells, (vii) auto- and paracrine stimulation of mast cells by stem cell factor, (viii) recruitment of mast cells by pro-angiogenic factors such as VEGF, bFGF and TGF-beta. As a result of ECM-degradation and changes in the microenvironment following initial mast cell secretion, the mast cell populations may change significantly in number, phenotype and function. In tumor models, mast cells have been shown to play a decisive role in inducing the angiogenic switch which precedes malignant transformation. There is, moreover, strong evidence that mast cells significantly influence angiogenesis and thus growth and progression in human cancers.
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              Mast cells in the promotion and limitation of chronic inflammation.

              Michele Grimbaldeston, Mindy Tsai, Susumu Nakae … (2007)
              Observations of increased numbers of mast cells at sites of chronic inflammation have been reported for over a hundred years. Light and electron microscopic evidence of mast cell activation at such sites, taken together with the known functions of the diverse mediators, cytokines, and growth factors that can be secreted by appropriately activated mast cells, have suggested a wide range of possible functions for mast cells in promoting (or suppressing) many features of chronic inflammation. Similarly, these and other lines of evidence have implicated mast cells in a variety of adaptive or pathological responses that are associated with persistent inflammation at the affected sites. Definitively characterizing the importance of mast cells in chronic inflammation in humans is difficult. However, mice that genetically lack mast cells, especially those which can undergo engraftment with wildtype or genetically altered mast cells, provide a means to investigate the importance of mast cells and specific mast cell functions or products in diverse models of chronic inflammation. Such work has confirmed that mast cells can significantly influence multiple features of chronic inflammatory responses, through diverse effects that can either promote or, perhaps more surprisingly, suppress aspects of these responses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): SAGE Open Med
                Journal ID (iso-abbrev): SAGE Open Med
                Journal ID (publisher-id): SMO
                Journal ID (hwp): spsmo
                Title: SAGE Open Medicine
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Electronic): 2050-3121
                Publication date (Electronic): 02 May 2019
                Publication date Collection: 2019
                Volume: 7
                Electronic Location Identifier: 2050312119848247
                Affiliations
                [1 ]Discipline of Obstetrics, Gynaecology and Neonatology, The University of Sydney, Sydney, NSW, Australia
                [2 ]Sydney Medical School, The University of Sydney, Sydney, NSW, Australia
                [3 ]Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
                Author notes
                [*]Frank Manconi, Discipline of Obstetrics, Gynaecology and Neonatology, The University of Sydney, Medical Foundation Building, Sydney, NSW 2006, Australia. Email: frank.manconi@ 123456sydney.edu.au
                Author information
                https://orcid.org/0000-0002-4980-1656
                Article
                Publisher ID: 10.1177_2050312119848247
                DOI: 10.1177/2050312119848247
                PMC ID: 6501471
                PubMed ID: 31105939
                SO-VID: ff32008c-5f0d-44bc-99fd-c904d05485f5
                Copyright © © The Author(s) 2019
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 6 June 2018
                Date accepted : 10 April 2019
                Categories
                Subject: Review Paper
                Custom metadata
                cover-date January-December 2019

                Keywords: polyps,endometrial,uterine
                Data availability:
                Keywords: polyps, endometrial, uterine

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