Article

Endometriosis and Infertility A Review of the Pathogenesis and Treatment of Endometriosis-associated Infertility

Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, 333 Cedar Street, PO Box 208063, New Haven, CT 06520-8063, USA.
Obstetrics and Gynecology Clinics of North America (Impact Factor: 1.38). 12/2012; 39(4):535-49. DOI: 10.1016/j.ogc.2012.10.002
Source: PubMed

ABSTRACT

Endometriois has been associated with infertility; however, the mechanisms by which it affects fertility are still not fully understood. This article reviews the proposed mechanisms of endometriosis pathogenesis, its effects on fertility, and treatments of endometriosis-associated infertility. Theories on the cause of the disease include retrograde menstruation, coelomic metaplasia, altered immunity, stem cells, and genetics. Endometriosis affects gametes and embryos, the fallopian tubes and embryo transport, and the eutopic endometrium; these abnormalities likely all impact fertility. Current treatment options of endometriosis-associated infertility include surgery, superovulation with intrauterine insemination, and in vitro fertilization. We also discuss potential future treatments for endometriosis-related infertility.

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    • "It has been suggested that endometriosis is a heterogeneous disease characterized by the presence of endometrial-type cells outside the uterine cavity (Vercellini et al. 2013). The pathogenesis of endometriosis is still unclear, but retrograde menstruation (Giudice & Kao, 2004), altered immunity (Steele et al., 1984), coelomic metaplasia, metastatic spread (Macer & Taylor, 2012), stem cell and genetic origins have been listed as possible causes (Chan et al., 2004;Du & Taylor, 2007;Zanatta et al., 2010). Endometriosis patients may be asymptomatic or present a wide variety of symptoms, ranging from pelvic pain to infertility (Burns & Schenken, 1999). "

    Full-text · Article · Sep 2015
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    • "It has been suggested that endometriosis is a heterogeneous disease characterized by the presence of endometrial-type cells outside the uterine cavity (Vercellini et al. 2013). The pathogenesis of endometriosis is still unclear, but retrograde menstruation (Giudice & Kao, 2004), altered immunity (Steele et al., 1984), coelomic metaplasia, metastatic spread (Macer & Taylor, 2012), stem cell and genetic origins have been listed as possible causes (Chan et al., 2004;Du & Taylor, 2007;Zanatta et al., 2010). Endometriosis patients may be asymptomatic or present a wide variety of symptoms, ranging from pelvic pain to infertility (Burns & Schenken, 1999). "
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    ABSTRACT: Objective: To identify associations between presence of endometriosis and oocyte defects, embryo developmental potential, and cycle outcomes. Methods: This study looked into the impact of endometriosis on oocyte and embryo quality, and blastocyst formation probability. Endometriosis was also correlated with cycle characteristics. In order to avoid age-related bias, in the first analysis only patients aged 36 years or younger were included, and the cycles were split into endometriosis infertility cycles (n=431; 3172 oocytes) and other cycles (n = 2510; 24480 oocytes). Results: The number of retrieved oocytes (10.6±21.2 vs. 14.6±21.1, P<0.001), oocyte yield (68.1±20.0% vs. 70.6±19.6%, P=0.015), and embryos obtained (6.1±4.43 vs. 7.8±5.12, P<0.001) were lower among patients with endometriosis. Implantation rates (28.1%±38.9% vs. 33.9±42.7, P<0.001) were lower among patients with endometriosis, but fertilization, pregnancy, miscarriage and cycle cancelation rates were not different. There was a significant increase in the incidence of extra-cytoplasmic, but not intra-cytoplasmic, oocyte defects among patients with endometriosis. The quality of embryos (45.3% vs. 47.3%, P=0.037) collected from patients with endometriosis was lower, but blastocyst formation rates were unaltered. Conclusions: A possible explanation for the lower implantation rates seen in patients with endometriosis is the poorer quality of the oocytes and embryos observed in this group of patients. © 2015, Sociedade Brasileira de Reproducao Assistida. All rights reserved.
    Full-text · Article · Jan 2015
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    • "Despite considerable investigation, the precise etiology and pathogenesis of endometriosis is unknown. To date, the leading theories are retrograde menstruation, coelomic metaplasia, embryonic cell rest, and lymphovascular metastasis [2]. However, none of them can annotate the pathogenesis to a point for all types of endometriosis. "
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    ABSTRACT: Background The precise etiology of endometriosis is not fully understood; the involvement of stem cells theory is a new hypothesis. Related studies mainly focus on stemness-related genes, and pluripotency markers may play a role in the etiology of endometriosis. We aimed to analyze the transcription pluripotency factors sex-determining region Y-box 2 (SOX2), Nanog homeobox (NANOG), and octamer-binding protein 4 (OCT4) in the endometrium of reproductive-age women with and without ovarian endometriosis. Methods We recruited 26 women with laparoscopy-diagnosed ovarian endometriosis (endometriosis group) and 16 disease-free women (control group) to the study. Endometrial and endometriotic samples were collected. SOX2, NANOG, and OCT4 expression were analyzed with quantitative real-time polymerase chain reaction, western blotting, and immunohistochemistry. Results Compared to the control group, SOX2 mRNA and protein expression was significantly higher in the eutopic endometrium of participants in the endometriosis group. In the endometriosis group, SOX2 and NANOG mRNA and protein expression were significantly increased in ectopic endometrium compared with eutopic endometrium; there was a trend towards lower OCT4 mRNA expression and higher OCT4 protein expression in ectopic endometrium. Conclusions The transcription pluripotency factors SOX2 and NANOG were overexpression in ovarian endometriosis, their role in pathogenesis of endometriosis should be further studied.
    Full-text · Article · May 2014 · Reproductive Biology and Endocrinology
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