This lecture addresses the etiopathogenesis of endometriosis, as defined by the presence of endometrial glands and stroma out of the uterine cavity. Endometriosis is present in 6-10% of women worldwide, 50-70% of women with pelvic pain and 30-50% of women with infertility. The main risk factors are early menarche, nulliparity and family history. Diagnosis frequently takes a long time from the onset of the first symptoms and constitutes a major healthcare problem in the United States. The most popular theory is retrograde menstruation, but other explanations are coelomic metaplasia, genetic predisposition, immune system dysfunction and environmental factors, which by means of inflammation, prostaglandin production and nerve regeneration could lead to pain and infertility. Endometriosis lesions have a known dependence with ovarian estrogens, but local conversion of androstenedione to estradiol inside the implants has been demonstrated, leading to proliferation of nerve fibers even after oophorectomy. Medical treatment aims to decrease inflammation, estrogen synthesis and local conversion of androgens to estrogens for a limited period of time. Surgical treatment aims to remove lesions and disrupt nerve production in the tissue, but there is a high percentage of symptom recurrence. Regarding infertility, endometriosis can cause adhesions affecting the ovary and the tube, but can also affect spermatozoa motility, migration of the embryo and prevent implantation, accounting for poor pregnancy outcomes in women with endometriosis.
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