Endometriosis and Infertility A Review of the Pathogenesis and Treatment of Endometriosis-associated Infertility
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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ABSTRACT: Endometriosis is a complex and challenging disease that involves aberrant adhesion, growth, and progression of endometrial tissues outside of the uterine cavity, and there is evidence to suggest that estrogen plays a key role in its development and progression. Numerous in vivo clinical studies have described the ectopic expression and regulation of estrogen receptor (ER) and progesterone receptor (PR) in the different types of endometriosis compared to normal or eutopic endometrium. However, we have noticed that conflicting and contradictory results have been presented in terms of ER subtype (ERα and ERβ) and PR isoform (PRA and PRB) expression. Both ER and PR are transcription factors and ER/PR-mediated responses depend on the coordinated, opposing, and compensatory functions of ER subtypes and PR isoforms. Moreover, analysis of the uterine phenotypes of ERα/ERβ and PRA/PRB knockout mice indicates that different ER subtypes and PR isoforms mediate distinct responses to steroid hormones and play different roles in uterine function. In this review, we outline studies that have elucidated the molecules and signaling pathways that are linked to ER and/or PR signaling pathways in the development and progression of endometriosis.American Journal of Translational Research 01/2014; 6(2):104-113. · 3.23 Impact Factor
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ABSTRACT: This retrospective cohort study was aimed to investigate the impact of endometriosis on the IVF/ICSI outcomes. A total of 1027 cycles of patients undergoing IVF/ICSI treatment in a reproductive medicine unit of academic hospital were enrolled. In the present study, 431 cycles of patients with endometriosis constituted the study group, including 152 cycles of patients with stage I-II endometriosis and 279 cycles of patients with stage III-IV endometriosis, while 596 cycles of patients with tubal factors infertility were considered as the control group. Ovarian stimulation parameters and IVF/ICSI outcomes were compared. Patients with stage I-II and stage III-IV endometriosis required higher dosage and longer duration of gonadotropins, but had lower day 3 high-quality embryos rate, when compared to patients with tubal infertility. In addition, the number of oocytes retrieved, the number of obtained embryos, the number of day 3 high-quality embryos, serum E2 level on the day of hCG, fertilization rate were lower in patients with stage III-IV endometriosis than those in tubal factors group. Except reduced implantation rate in stage III-IV endometriosis group, no differences were found in other pregnancy parameters. This study suggests that IVF/ICSI yielded similar pregnancy outcomes in patients with different stages of endometriosis and patients with tubal infertility. Therefore, IVF/ICSI can be considered as an effective approach for managing endometriosis-associated infertility.International journal of clinical and experimental pathology 01/2013; 6(9):1911-8. · 1.78 Impact Factor
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ABSTRACT: In this month's issue of Biology of Reproduction, Afshar et al. report on the effects of endometriosis on gene expression in the baboon endometrium.Biology of Reproduction 01/2013; 88(2). DOI:10.1095/biolreprod.113.107722 · 3.45 Impact Factor