{"paper_id":"ae78de21-1e44-46ea-a7fe-73ad43ad2647","body_text":"Abstract\nEndometriosis is an estrogen-dependent disease. It predominantly affects reproductive-age women and becomes less active or regresses with the onset of the menopause. Nevertheless, some data from case series and case reports demonstrate that this pathology is, in fact, increasingly reported even after the decrease of ovarian hormonal secretion. Is it a persistence or a recurrence of a premenopausal disease or a new lesion? Does the malignant risk increase with advancing age? (16). Therefore, clinicians must take this into account in the case of pelvic pain affecting the quality of life (QOL) (dysmenorrhea, dyspareunia, chronic pelvic pain), heavy bleeding, or urinary symptoms at this period. Endometriosis can be considered as an intraperitoneal benign proliferation with a “malignant proliferation” like, which can metastase to the ovaries, bowel, and even the lungs. Endometriosis is strongly associated with the increased risk of ovarian cancer; this risk is around 2% or 3%.\nAccess this chapter\nTax calculation will be finalised at checkout\nPurchases are for personal use only\nSimilar content being viewed by others\nReferences\nAlio L, et al. Endometriosis: seeking optimal management in women approaching menopause. Climacteric. 2019;22(4):329–38.\nSampson JA. Metastatic or embolic endometriosis due to premenstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol. 1927;3:93–110.\nVercellini P, Vigano P, Somigliana E, Fedele L. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol. 2014;10:261–75.\nBurney RO, Talbi S, Hamilton AE, Vo KC, Nezhat CR, Lessey BA, Giudice LC. Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis. Endocrinology. 2007;148:3814–26.\nSantulli P, Borghese B, Noel JC, Fayt I, Anaf V, de Ziegler D, Batteux F, Vaiman D, Chapron C. Hormonotherapy deregulates prostaglandin-endoperoxidase synthase (PTGS2) expression in endometriotic tissues. J Clin Endocrinol Metab. 2014;99:881–90.\nSantulli P, Chouzenoux S, Fiorese M, Marcellin L, Lemarechal H, Millischer AE, Batteux F, Borderie D, Chapron C. Protein oxidative stress markers in peritoneal fluids of women with deep infiltrating endometriosis are increased. Hum Reprod. 2015;30:49–60.\nLeconte M, Nicco C, Ngo C, Chereau C, Chouzenoux S, Marut W, Guibourdenche J, Arkwright S, Weill B, Chapron C, Dousset B, Batteux F. The mTOR/AKT inhibitor temsirolimus prevents deep infiltrating endometriosis in mice. Am J Pathol. 2011;179:880–9.\nNgo C, Nicco C, Leconte M, Chereau C, Arkwright S, VAcher Lavenu MC, Weill B, Chapron C, Batteux F. Protein kinase inhibitors can control the progression of endometriosis in vitro and in vivo. J Pathol. 2010;222:148–57.\nBorghese B, Tost J, de Surville M, Busato F, Letourneur F, Mondon F, Vaiman D, Chapron C. Identification of susceptibility genes for peritoneal, ovarian, and deep infiltrating endometriosis using a pool sample-based genome-wide association study. Biomed Res Int. 2015;2015:461024.\nNyholt DR, et al. Genome-wide association meta-analysis identifies new endometriosis risk loci. Nat Genet. 2012;44:1355–9.\nPagliardini L, Gentilini D, Vigano P, Panina-Bordignon P, Busacca M, Candiani M, Di Blasio AM. An Italian association study and meta-analysis with previous GWAS confirm WNT4, CDKN2BAS and FN1 as the first identified susceptibility loci for endometriosis. J Med Genet. 2013;50:43–6.\nBorghese B, Barbaux S, Mondon F, Santulli P, Pierre G, Vinci G, Chapron C, Vaiman D. Research resource: genome wide profiling of methylated promoters in endometriosis. Mol Endocrinol. 2010;24:1872–8.\nUmezawa M, Sakata C, Tanaka N, Tabata M, Takeda K, Ihara T, Sugamata M. Pathological study for the effects of in utero and postnatal exposure to diesel exhaust on a rat endometriosis model. J Toxicol Sci. 2011;36:493–8.\nTan DA, Almaria MJ. Postmenopausal endometriosis: drawing a clearer clinical picture. Climateric. 2018;21(3):249–55.\nToki T, et al. Proliferative activity of postmenopausal endometriosis: a histopathologic and immunocytochemical study. Int J Gynecol Pathol. 1996;15(1):45–53.\nBendon CL, Becker CM. Potential mechanisms of postmenopausal endometriosis. Maturitas. 2012;72:214–9.\nBulun SE. Endometriosis. N Engl J Med. 2009;360:268–79.\nBulun SE, Yang S, Fang Z, Gurates B, Tamura M, Sebastian S. Estrogen production and metabolism in endometriosis. Ann N Y Acad Sci. 2002;955:396–40.\nGemmell LC, Webster KE, Kirtley S, Vincent K, Zondervan KT, Becker CM. The management of menopause in women with a history of endometriosis: a systematic review. Hum Reprod Update. 2017;23(4):481–500.\nSoliman NF, Hillard TC. Hormone replacement herapy in women with past history of endometriosis. Climateric. 2006;9:325–35.\nPolyzos NP, Fatemi HM, Zavos A, Papanikolau EG. Aromatase inhibitors in post menopausal endometriosis. Reprod Biol Endocrinol. 2011;9:90.\nZanello M, et al. Hormonal replacement therapy in menopausal women with history of endometriosis: a review of literature. Medicina (Kaunas). 2019;55(8):477.\nWriting Group for the Women’s Health Initiative Investigator. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. Principal results from the women’s health initiative randomized controlled trial. JAMA. 2002;288:321–33.\nFedele L, Bianchi S, Raffaelli R, Zanconato G. Comparison of transdermal estradiol and tibolone for the treatment of oophorectomized women with deep residual endometriosis. Fertil Steril. 1989;51(5):781–5.\nEMAS Position Statement: Managing the Menopause in Women with a Past History of Endometriosis. Moen MH. European menopause and Andropause society. Maturitas. 2010;67(1):94–7.\nStern RC, Dash R, Bentley RC, Snyder MJ, Haney AF, Robboy SJ. Malignancy in endometriosis: frequency and comparison of ovarian and extraovarian types. Int J Gynecol Pathol. 2001;20:133–9.\nMelin A, SParen P, Perrson I, Bergqvist A. Endometriosis and the risk of cancer with special emphasis on ovarian cancer. Hum Reprod. 2006;21:1237–42.\nWiegand KC, et al. ARID1A mutations in endometriosis-associated ovarian carcinomas. N Engl J Med. 2010;363(16):1532–43.\nAudebert A. Women with endometriosis: are they different from others? Gynecol Obstet Fertil. 2005;33(4):239–46.\nChene G. L’endométriose est elle une lesion pré cancéreuse? Perspectives et implications cliniques. Gynécol Obstét Fertil. 2016;44:106–12.\nInceboz U. ENdometriosis after menopause. Womens Health (Lond). 2015;11:711–5.\nStreuli I, Gaitzch H, Wenger JM, Petignat P. Endometriosis after menopause: physiopathology and management of an uncommon condition. Climateric. 2017;20:138–43.\nChapron C, Marcellin L, Borghese B, Santulli P. Rethinking mechanisms, diagnosis and management of endometriosis. Nat Rev Endocrinol. 2019;15:666–82.\nAuthor information\nAuthors and Affiliations\nEditor information\nEditors and Affiliations\nRights and permissions\nCopyright information\n© 2021 International Society of Gynecological Endocrinology\nAbout this chapter\nCite this chapter\nMarie-Scemama, L., Carbonnel, M., Ayoubi, J.M. (2021). Endometriosis and Menopause: Realities and Management. In: Genazzani, A.R., Nisolle, M., Petraglia, F., Taylor, R.N. (eds) Endometriosis Pathogenesis, Clinical Impact and Management. ISGE Series. Springer, Cham. https://doi.org/10.1007/978-3-030-57866-4_15\nDownload citation\nDOI: https://doi.org/10.1007/978-3-030-57866-4_15\nPublished:\nPublisher Name: Springer, Cham\nPrint ISBN: 978-3-030-57865-7\nOnline ISBN: 978-3-030-57866-4\neBook Packages: MedicineMedicine (R0)","source_license":"CC0","license_restricted":false}