DYSMENORRHEA, ADENOMYOSIS, ENDOMETRIOSIS, TUMOR PROCESS: CAUSATION

A. L. Unanyan, Sidorova Is, Н. А. Никитина, Yu.V. Chushkov, Т. Д. Гуриев, А Д Никонец, D.V. Baburin
In: Medical Council · 2017 · pp. 186–188 · doi:10.21518/2079-701x-2017-11-186-188 · W2735484205
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⚙ AI-generated summary by claude@2026-06, 2026-06-18 ⓘ

This paper examines the causal links between dysmenorrhea and endometriosis, adenomyosis, and tumor processes, noting NSAIDs as a therapeutic and preventative measure.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-18 · read from full text ⓘ

The paper discusses causal relationships among dysmenorrhea and endometrioid and tumor processes, describing how dysmenorrhea may be associated with the development of disorders including endometriosis and adenomyosis as well as tumor diseases, with mechanistic emphasis on inflammatory and eicosanoid pathways. It frames the evidence broadly, referencing studies of adenomyosis and endometriosis biology (including junctional zone concepts and eicosanoid changes) alongside literature on cyclooxygenase-2, prostaglandin signaling, and cancer-related inflammation, but the limitation is that it is a narrative/overview article rather than original empirical research presented in a defined study cohort. A central claim is that nonsteroidal anti-inflammatory drugs are positioned as not only symptomatic therapy for dysmenorrhea but also pathogenetically grounded for prevention of distant complications. This paper is centrally about endometriosis and adenomyosis — it specifically links dysmenorrhea as a potential causal factor for endometriosis and adenomyosis and discusses related inflammatory mechanisms alongside tumor processes.

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Abstract

The article focuses on the identification of causal relationships between dysmenorrhea, endometrioid and tumor processes. Studies have shown that dysmenorrhea, apart from a decline in the quality of life, can be the cause of development of a number of serious health disturbances, including endometriosis, adenomyosis and even tumoral diseases. Non-steroidal anti-inflammatory drugs are not only the effective means of therapy for dysmenorrhea patients, but also a pathogenetically reasonable approach to prevent the outbreak of the disease.
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ДИСМЕНОРЕЯ, АДЕНОМИОЗ, ЭНДОМЕТРИОЗ, ОПУХОЛЕВЫЙ ПРОЦЕСС: ПРИЧИННО-СЛЕДСТВЕННЫЕ СВЯЗИ https://doi.org/10.21518/2079-701X-2017-11-186-188 Аннотация Статья посвящена выявлению причинно-следственных связей между дисменореей, эндометриоидным и опухолевым процессами. Как показали исследования, дисменорея, кроме снижения качества жизни, может обуславливать развитие целого ряда серьезных нарушений, включая эндометриоз, аденомиоз и даже опухолевые заболевания. Нестероидные противовоспалительные препараты являются не только эффективным средством терапии больных с дисменореей, но и патогенетически обоснованным подходом к профилактике отдаленных осложнений заболевания. Об авторах А. Л. УнанянРоссия Доктор медицинских наук, профессор И. С. Сидорова Россия Академик РАН, Доктор медицинских наук, профессор Е. А. Соснова Россия Доктор медицинских наук, профессор Ю. В. Чушков Россия Кандидат медицинских наук Т. Д. Гуриев Россия Доктор медицинских наук, профессор А. Д. Никонец Россия Д. В. Бабурин Россия Список литературы 1. Bird CC, McElin TW, Manalo-Estrella P. The elusive adenomyosis of the uterus-revisited. Am J Obstet Gynecol, 1972, 112: 583-593. 2. Lee NC, Dicker RC, Rubin GL, Ory HW. Confirmation of the preoperative diagnoses for hysterectomy. Am J Obstet Gynecol, 1984, 150: 283–287. 3. Barrier BF, Malinowski MJ, Dick EJ Jr, Hubbard GB, Bates GW. Adenomyosis in the baboon is associated with primary infertility. Fertil Steril, 2004, 82: 1091–1094. 4. Ryan GL, Stolpen A, Van Voorhis BJ. An unusual cause of adolescent dysmenorrhea. Obstetrics and gynecology, 2006, 108(4): 1017-1022. 5. Dietrich JE. An update on adenomyosis in the adolescent. Curr Opin Obstet Gynecol, 2010, 22: 388–392. 6. Pontis A, D’Alterio MN, Pirarba S, de Angelis C, Tinelli R, Angioni S. Adenomyosis: a systematic review of medical treatment. Gynecol Endocrinol, 2016 Jul 5: 1-5. 7. Zhou C, Zhang T, Liu F, Zhou J, Ni X, Huo R, Shi Z. 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Zelenay S, Reis E Sousa C. Reducing prostaglandin E2 production to raise cancer immunogenicity. Oncoimmunology, 2016 Jan 4, 5(5): e1123370. 18. Eberhart CE, Coffey RJ, Radhika A, Giardiello FM, Ferrenbach S, DuBois RN.Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology, 1994 Oct, 107(4): 1183-8. 19. Rigas B, Goldman IS, Levine L. Altered eicosanoid levels in human colon cancer. J Lab Clin Med, 1993 Nov, 122(5): 518-23. 20. Pockaj BA, Basu GD, Pathangey LB, Gray RJ, Hernandez JL, Gendler SJ, Mukherjee P. Reduced T-cell and dendritic cell function is related to cyclooxygenase-2overexpression and prostaglandin E2 secretion in patients with breast cancer. Ann Surg Oncol, 2004 Mar, 11(3): 328-39. 21. Wallace AE, Sales KJ, Catalano RD, Anderson RA, Williams AR, Wilson MR, Schwarze J, Wang H, Rossi AG, Jabbour HN. Prostaglandin F2alpha-Fprostanoid receptor signaling promotes neutrophil chemotaxis via chemokine (C-X-C motif) ligand 1 in endometrial adenocarcinoma. Cancer Res, 2009 Jul 15, 69(14): 5726-33. 22. Tong BJ, Tan J, Tajeda L, Das SK, Chapman JA, DuBois RN, Dey SK. Heightened expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor-delta in human endometrial adenocarcinoma. Neoplasia, 2000 NovDec, 2(6): 483-90. 23. Jabbour HN, Milne SA, Williams AR, Anderson RA, Boddy SC. Expression of COX-2 and PGE synthase and synthesis of PGE(2)in endometrialadenocarcinoma: a possible autocrine/paracrine regulation of neoplastic cell function via EP2/EP4 receptors. Br J Cancer, 2001 Sep 28, 85(7): 1023-31. 24. Wallace AE, Gibson DA, Saunders PT, Jabbour HN. Inflammatory events in endometrial adenocarcinoma. J Endocrinol, 2010 Aug, 206(2): 141-57 25. Babic A, Cramer DW, Titus LJ, Tworoger SS, Terry KL. Menstrual pain and epithelial ovarian cancer risk. Cancer Causes Control, 2014 Dec, 25(12): 1725-31. 26. Kvaskoff M, Mu F, Terry KL, Harris HR, Poole EM, Farland L, Missmer SA. / Endometriosis: a highrisk population for major chronic diseases? Hum Reprod Update, 2015 Jul-Aug, 21(4): 500-16. doi: 10.1093/humupd/dmv013. Epub 2015 Mar 11. 27. Collaborative Group on Epidemiological Studies on Endometrial Cancer. Endometrial cancer and oral contraceptives: an individual participant meta-analysis of 27 276 women with endometrial cancer from 36 epidemiological studies. Lancet Oncol, 2015 Sep, 16(9): 1061-70. Epub 2015 Aug 4. 28. Beral V, Doll R, Hermon C, Peto R, Reeves G. Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23,257 women with ovarian cancer and 87,303 controls. Collaborative Group on Epidemiological Studies of Ovarian Cancer. Lancet, 2008 Jan 26, 371(9609): 303-14. 29. McLaughlin JR, Risch HA, Lubinski J, Moller P, Ghadirian P, Lynch H, Karlan B, Fishman D, Rosen B,Neuhausen SL, Offit K, Kauff N, Domchek S, Tung N, Friedman E, Foulkes W, Sun P, Narod SA, Hereditary Ovarian Cancer Clinical Study Group. Reproductive risk factors for ovarian cancer in carriers of BRCA1 or BRCA2 mutations: a casecontrol study. Lancet Oncol, 2007 Jan, 8(1): 26-34. 30. Bosetti C, Bravi F, Negri E, La Vecchia C. Oral contraceptives and colorectal cancer risk: a systematic review and meta-analysis. Hum Reprod Update, 2009 Sep-Oct, 15(5): 489-98. 31. Инструкция к применению препарата Амелотекс http: //www.sotex.ru/production/catalog/detail.php?ELEMENT_ID=4268. Рецензия Для цитирования: Унанян АЛ, Сидорова ИС, Соснова ЕА, Чушков ЮВ, Гуриев ТД, Никонец АД, Бабурин ДВ. ДИСМЕНОРЕЯ, АДЕНОМИОЗ, ЭНДОМЕТРИОЗ, ОПУХОЛЕВЫЙ ПРОЦЕСС: ПРИЧИННО-СЛЕДСТВЕННЫЕ СВЯЗИ. Медицинский Совет. 2017;(11):186-188. https://doi.org/10.21518/2079-701X-2017-11-186-188 For citation: Unanyan AL, Sidorova IS, Nikitina NA, Chushkov YV, Guriev TD, Nikonets AD, Baburin DV. DYSMENORRHEA, ADENOMYOSIS, ENDOMETRIOSIS, TUMOR PROCESS: CAUSATION. Meditsinskiy sovet = Medical Council. 2017;(11):186-188. (In Russ.) https://doi.org/10.21518/2079-701X-2017-11-186-188 JATS XML

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