{"paper_id":"513eaee9-e0e0-4a9b-a719-e9ac3cb3790f","body_text":"The prevalence of infertility in patients with endometriosis varies depending on the\nauthor. Some have reported that 25-50% of women with infertility have endometriosis,\nand about 30-50% of the women with endometriosis have infertility ( Hickey  et al. , 2014 ). Between\n10 and 15 % of all women seek IVF in the UK due to tubal infertility ( HFEA, 2016 ). In this cases, the cause may be\npelvic inflammatory disease, endometriosis, salpingitis isthmica nodosa, polyps and\nsurgical trauma ( Honoré  et\nal.,  1999 ).  Tanahatoe\n et al.  (2003)  found 10 % of infertility in\nendometriosis. These authors also found that the most important causes of\ninfertility in couples are ovulation disorders, tubal obstruction and semen\nabnormalities (mainly azoospermia, oligozoospermia, teratozoospermia and\nastenozoospermia). This causes account for approximately 75% of infertility in\ncouples. The remaining is so far unknown ( Tanahatoe\n et al.,  2003 ). Mild or moderate endometriosis is\nrelated to subfertility with pregnancy rates of 17.7% at nine months of follow-up.\nEndometriosis is a net factor of subfertility, mainly in stages III and IV. In a\nseries of cases, a fertility rate of 3% has been reported after 12 months in cases\nof stage IV endometriosis ( Marcoux  et\nal.,  1997 ).\nIt is a disease that can affect several organs, such as the pelvic peritoneum,\nfallopian tubes, ovaries, subcutaneous tissue, umbilicus, urinary tract, bladder,\nheart, kidney, lung, liver, pancreas, muscles, central nervous system, among others,\nwhich makes it a multi-systemic disease ( Goldberg\n& Bedaiwy, 2007 ;  Lee  et\nal.,  2008 ). Endometriotic lesions are more frequent in the\nperitoneum and pelvic organs, especially in the ovaries, followed by the\nrecto-vaginal septum. It is found less frequently in extra-pelvic regions, such as\ngastrointestinal (sigmoid, rectum, ileocecal and appendix) and urinary tract,\nextremities, subcutaneous tissue and abdominal wall ( Lee  et al.,  2008 ). The mechanism of impaired fertility\nin endometriosis may involve anatomical distortions in the pelvis, adhesions,\nendometriomas or the production of substances (prostaglandins, cytokines, and growth\nfactors) that are harmful to normal ovarian function, ovulation, fertilization and\nimplantation. The really valid mechanisms are tubal obstruction, pelvic adhesions\nand ovarian endometriomas that distort anatomical relationships, limit the access of\noocytes and spermatozoa and alter fimbriae mobility, mainly in stages III and IV\n( Mahutte & Arici, 2002 ). Phenomena\nsuch as anovulation, endocrine dysfunction, luteinized unruptured follicle syndrome,\ninadequate luteal phase, autoimmune dysfunction, abnormalities of the ovule quality\nand sperm alterations are theoretical mechanisms, still unproven, used to explain\ninfertility in endometriosis in stages I and II ( Toya  et al.,  2000 ). However, the two most probable\nmechanisms to explain the infertility in these stages are maturing on the late\nfollicular phase and the antispermatic effect impairing folliculogenesis with oocyte\nalterations.\nThere are very few publications about the effect of endometriosis on tubal\npermeability. Some time ago  Bowman & Cooke\n(1994)  found that there was a strong correlation between the degree of\nintratubal damage and the extent of pelvic adhesions when the etiology was a\nprevious pelvic inflammatory disease (PID), but not when the underlying etiology was\nendometriosis. However, in the endometriosis subgroup, intraluminal ampullary\npathology was noted in 3 of 11 tubes (27%) assessed, and intraluminal fimbrial\npathology was noted in 4 of 11 tubes (36%) assessed.\nOsuga  et al.  (2008)  describe\na case of a patient with endometriosis who sought infertility treatment. During\novarian stimulation, an image of hydrosalpinx without infection appears and changed\ndramatically in size with the menstrual cycle. The patient was 32 years old and had\nhad endometriosis since 24 years of age. She underwent ethanol sclerotherapy of a\nbilateral ovarian endometrioma at age 26 and laparoscopic cystectomy for ovarian\nendometrioma at age 30. Serum  Chlamydia trachomatis  IgA and IgM\nantibodies were negative. During ultrasonography work-up to check follicular growth\nand ovulation, the author noticed a hydrosalpinx-like structure that appeared larger\nat each ultrasound scan. This structure was minimal during the menstrual period. It\nwould reach its maximum size during ovulation, and then shrank again. A later\nlaparoscopy revealed endometriosis and tubal obstruction. Salpingectomy was\nundertaken to improve the IVF-ET outcome. Histologically, they found endometriosis\nat the tubal wall serosa layer.\n\nA case-control study was performed, involving 144 women with and without tubal\nobstruction. We calculated the odds ratio, with a 95% CI, of the patients with\nendometriosis III/IV having tubal obstruction. Calculations were performed using the\nSPSS package v.17.0. The statistical test was the Chi Square, with a\n p  value of 0.05.\n\nThe mean age of the patients was 33.7 years (4.76 SD). The mean infertility duration\ntime was 66.7 months (120.6 SD). The endometriosis prevalence was 20/144 (13%).\nAmong 144 women, the risk group (endometriosis II/IV) with tubal obstruction\ncomprised 7out of 20 (35%), compared with the group without risk that comprised 22\nout of 124 (17%). The X 2  test was 3.19 with a  p -value of\n0.07. The odds ratio (OR) was 2.5 (95% CI: 0.647-9.639) ( Figure 1 ).\nFigure 1 Endometriosis and Tubal Obstruction\nEndometriosis and Tubal Obstruction\n\nDue to diagnostic difficulties and the different types, the literature has few high\nquality publications on endometriosis.  Broeze\n et al.  (2012)  for example, state that this disease\nis a condition that may result in tubal pathology, but information on endometriosis\nwas either not documented in the original databases or not reported in a\nstandardized way, or was in sufficient detail. For these reasons the author could\neven included endometriosis as a clinical variable in a meta-analysis.\nRemoving endometriomas without hydrosalpinx or tubal obstruction remains\ncontroversial. Some authors state that this procedure did not improve the results of\n in vitro  fertilization ( Garcia-Velasco  et al.,  2004 ). Nevertheless assisted\nreproductive technology is better than surgery, and should be offered as a\nfirst-line treatment ( Feinberg  et\nal.,  2008 ).\nOsuga  et al.  (2008)  published\na case of hydrosalpinx and endometrioma without apparent infection. Salpingectomy\nwas undertaken to improve the IVF-ET outcome. However most of the hydrosalpinx was\nan infection sequel, mainly Chlamydia. This publication did not find an association\nbetween endometriosis III and IV and tubal obstruction, thought the statistical test\nalmost reached significance. Further studies with larger data sets are needed to\ncheck these results.\n\nAlthough the OR was 2.5 ( p =0.07) there was no significant difference\nbetween the groups with and without endometriosis III/IV. Further studies with\nlarger samples are needed.","source_license":"CC-BY-4.0","license_restricted":false}