open access

Vol 91, No 4 (2020)
Research paper
Published online: 2020-04-29
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Increased risk of endometriosis in patients with endometritis — a nationwide cohort study involving 84,150 individuals

Kent Yu-Hsien Lin1, Cherry Yin-Yi Chang23, Wu-Chou Lin34, Lei Wan345
·
Pubmed: 32374019
·
Ginekol Pol 2020;91(4):193-200.
Affiliations
  1. Department of Obstetrics and Gynecology, Women and Children’s Health, Royal North Shore Hospital, Sydney, NSW, Australia
  2. School of Medicine, China Medical University, Taichung, Taiwan
  3. Department of Obstetrics and Gynecology, China Medical University Hospital, Taichung, Taiwan
  4. School of Chinese Medicine, China Medical University, Taichung, Taiwan
  5. Department of Biotechnology, Asia University, Taichung, Taiwan

open access

Vol 91, No 4 (2020)
ORIGINAL PAPERS Gynecology
Published online: 2020-04-29

Abstract

Objectives: To evaluate the incidence of endometriosis among endometritis patients and its association with confounding
comorbidities.
Material and methods: A population-based, retrospective cohort study of women aged between 20 to 55 years, who were
newly diagnosed with endometritis between 2000 to 2013. A total of 16,830 endometritis patients and 67,230 non-endometritis
individuals were enrolled by accessing data from the National Health Insurance Research Database of Taiwan.
The comorbidities accessed were uterine leiomyoma, rheumatoid arthritis, ovarian cancer, infertility and allergic diseases.
Results: The mean follow-up period was 9.15 years for the non-endometritis cohort and 9.13 years for the endometritis
cohort. There were significantly higher percentages of uterine leiomyoma, rheumatoid arthritis, infertility, ovarian cancer
and allergic diseases in the endometritis cohort than in the non-endometritis cohort. Patients with endometritis had
a 1.5-fold increased risk of their condition advancing to endometriosis (HR 1.58, 95% CI 1.48–1.68).
Conclusions: Our results suggest that patients with endometritis exhibited a positive correlation in developing endometriosis.

Abstract

Objectives: To evaluate the incidence of endometriosis among endometritis patients and its association with confounding
comorbidities.
Material and methods: A population-based, retrospective cohort study of women aged between 20 to 55 years, who were
newly diagnosed with endometritis between 2000 to 2013. A total of 16,830 endometritis patients and 67,230 non-endometritis
individuals were enrolled by accessing data from the National Health Insurance Research Database of Taiwan.
The comorbidities accessed were uterine leiomyoma, rheumatoid arthritis, ovarian cancer, infertility and allergic diseases.
Results: The mean follow-up period was 9.15 years for the non-endometritis cohort and 9.13 years for the endometritis
cohort. There were significantly higher percentages of uterine leiomyoma, rheumatoid arthritis, infertility, ovarian cancer
and allergic diseases in the endometritis cohort than in the non-endometritis cohort. Patients with endometritis had
a 1.5-fold increased risk of their condition advancing to endometriosis (HR 1.58, 95% CI 1.48–1.68).
Conclusions: Our results suggest that patients with endometritis exhibited a positive correlation in developing endometriosis.

Get Citation

Keywords

endometritis; inflammation; microbial infection; endometriosis

About this article
Title

Increased risk of endometriosis in patients with endometritis — a nationwide cohort study involving 84,150 individuals

Journal

Ginekologia Polska

Issue

Vol 91, No 4 (2020)

Article type

Research paper

Pages

193-200

Published online

2020-04-29

Page views

1504

Article views/downloads

1183

DOI

10.5603/GP.2020.0040

Pubmed

32374019

Bibliographic record

Ginekol Pol 2020;91(4):193-200.

Keywords

endometritis
inflammation
microbial infection
endometriosis

Authors

Kent Yu-Hsien Lin
Cherry Yin-Yi Chang
Wu-Chou Lin
Lei Wan

References (34)
  1. Laux-Biehlmann A, d'Hooghe T, Zollner TM. Menstruation pulls the trigger for inflammation and pain in endometriosis. Trends Pharmacol Sci. 2015; 36(5): 270–276.
  2. De Graaff AA, D'Hooghe TM, Dunselman GAJ, et al. WERF EndoCost Consortium. The significant effect of endometriosis on physical, mental and social wellbeing: results from an international cross-sectional survey. Hum Reprod. 2013; 28(10): 2677–2685.
  3. McCunn R, Aus der Fünten K, Whalan M, et al. Metastatic or Embolic Endometriosis, due to the Menstrual Dissemination of Endometrial Tissue into the Venous Circulation. Am J Pathol. 1927; 3(2): 93–110.43.
  4. D'Hooghe TM, Debrock S. Endometriosis, retrograde menstruation and peritoneal inflammation in women and in baboons. Hum Reprod Update. 2002; 8(1): 84–88.
  5. Khoufache K, Michaud N, Harir N, et al. Anomalies in the inflammatory response in endometriosis and possible consequences: a review. Minerva Endocrinol. 2012; 37(1): 75–92.
  6. Kajihara H, Yamada Y, Kanayama S, et al. New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal. Gynecol Endocrinol. 2011; 27(2): 73–79.
  7. Bertschi D, McKinnon BD, Evers J, et al. Enhanced inflammatory activity of endometriotic lesions from the rectovaginal septum. Mediators Inflamm. 2013; 2013: 450950.
  8. Wu Y, Kajdacsy-Balla A, Strawn E, et al. Transcriptional characterizations of differences between eutopic and ectopic endometrium. Endocrinology. 2006; 147(1): 232–246.
  9. Kao LC, Germeyer A, Tulac S, et al. Expression profiling of endometrium from women with endometriosis reveals candidate genes for disease-based implantation failure and infertility. Endocrinology. 2003; 144(7): 2870–2881.
  10. Tao Yu, Zhang Q, Huang W, et al. The peritoneal leptin, MCP-1 and TNF-α in the pathogenesis of endometriosis-associated infertility. Am J Reprod Immunol. 2011; 65(4): 403–406.
  11. Lebovic DI, Mueller MD, Taylor RN. Immunobiology of endometriosis. Fertil Steril. 2001; 75(1): 1–10.
  12. Bedaiwy MA, Falcone T. Peritoneal fluid environment in endometriosis. Clinicopathological implications. Minerva Ginecol. 2003; 55(4): 333–345.
  13. Missmer SA, Cramer DW, Cramer DW, et al. The epidemiology of endometriosis. Ann N Y Acad Sci. 2002; 955(1): 11–22; discussion 34.
  14. Moreno I, Franasiak JM. Endometrial microbiota-new player in town. Fertil Steril. 2017; 108(1): 32–39.
  15. Lin WC, Chang CYY, Hsu YA, et al. Increased Risk of Endometriosis in Patients With Lower Genital Tract Infection: A Nationwide Cohort Study. Medicine (Baltimore). 2016; 95(10): e2773.
  16. Tai FW, Chang CYY, Chiang JH, et al. Association of Pelvic Inflammatory Disease with Risk of Endometriosis: A Nationwide Cohort Study Involving 141,460 Individuals. J Clin Med. 2018; 7(11).
  17. Cicinelli E, De Ziegler D, Nicoletti R, et al. Poor reliability of vaginal and endocervical cultures for evaluating microbiology of endometrial cavity in women with chronic endometritis. Gynecol Obstet Invest. 2009; 68(2): 108–115.
  18. Kitaya K, Matsubayashi H, Takaya Y, et al. Live birth rate following oral antibiotic treatment for chronic endometritis in infertile women with repeated implantation failure. Am J Reprod Immunol. 2017; 78(5).
  19. Moreno I, Codoñer FM, Vilella F, et al. Evidence that the endometrial microbiota has an effect on implantation success or failure. Am J Obstet Gynecol. 2016; 215(6): 684–703.
  20. Miles SM, Hardy BL, Merrell DS. Investigation of the microbiota of the reproductive tract in women undergoing a total hysterectomy and bilateral salpingo-oopherectomy. Fertil Steril. 2017; 107(3): 813–820.e1.
  21. Bailey MT, Coe CL. Endometriosis is associated with an altered profile of intestinal microflora in female rhesus monkeys. Hum Reprod. 2002; 17(7): 1704–1708.
  22. Khan KN, Kitajima M, Hiraki K, et al. Escherichia coli contamination of menstrual blood and effect of bacterial endotoxin on endometriosis. Fertil Steril. 2010; 94(7): 2860–3.e1.
  23. Khan KN, Kitajima M, Hiraki K, et al. Toll-like receptors in innate immunity: role of bacterial endotoxin and toll-like receptor 4 in endometrium and endometriosis. Gynecol Obstet Invest. 2009; 68(1): 40–52.
  24. Khan KN, Fujishita A, Hiraki K, et al. Bacterial contamination hypothesis: a new concept in endometriosis. Reprod Med Biol. 2018; 17(2): 125–133.
  25. Khan KN, Fujishita A, Masumoto H, et al. Molecular detection of intrauterine microbial colonization in women with endometriosis. Eur J Obstet Gynecol Reprod Biol. 2016; 199: 69–75.
  26. Mitchell CM, Haick A, Nkwopara E, et al. Colonization of the upper genital tract by vaginal bacterial species in nonpregnant women. Am J Obstet Gynecol. 2015; 212(5): 611.e1–611.e9.
  27. Herath S, Fischer DP, Werling D, et al. Expression and function of Toll-like receptor 4 in the endometrial cells of the uterus. Endocrinology. 2006; 147(1): 562–570.
  28. Beagley KW, Gockel CM. Regulation of innate and adaptive immunity by the female sex hormones oestradiol and progesterone. FEMS Immunol Med Microbiol. 2003; 38(1): 13–22.
  29. Khan KN, Kitajima M, Inoue T, et al. Additive effects of inflammation and stress reaction on Toll-like receptor 4-mediated growth of endometriotic stromal cells. Hum Reprod. 2013; 28(10): 2794–2803.
  30. Imamura T, Khan KN, Fujishita A, et al. Toll-like receptor 4-mediated growth of endometriosis by human heat-shock protein 70. Hum Reprod. 2008; 23(10): 2210–2219.
  31. Bourlev V, Volkov N, Pavlovitch S, et al. The relationship between microvessel density, proliferative activity and expression of vascular endothelial growth factor-A and its receptors in eutopic endometrium and endometriotic lesions. Reproduction. 2006; 132(3): 501–509.
  32. Takehara M, Ueda M, Yamashita Y, et al. Vascular endothelial growth factor A and C gene expression in endometriosis. Hum Pathol. 2004; 35(11): 1369–1375.
  33. Khan KN, Kitajima M, Inoue T, et al. 17β-estradiol and lipopolysaccharide additively promote pelvic inflammation and growth of endometriosis. Reprod Sci. 2015; 22(5): 585–594.
  34. Montagna P, Capellino S, Villaggio B, et al. Peritoneal fluid macrophages in endometriosis: correlation between the expression of estrogen receptors and inflammation. Fertil Steril. 2008; 90(1): 156–164.

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