gynecology and obstetrics
Endometriosis
Etiology and Pathophysiology of Endometriosis
The most widely accepted hypothesis for the pathophysiology of endometriosis is that endometrial cells are transported from the uterine cavity during menstruation and subsequently become implanted at ectopic sites. Retrograde flow of menstrual tissue through the fallopian tubes is common and could transport endometrial cells intra-abdominally; the lymphatic or circulatory system could transport endometrial cells to distant sites (eg, the pleural cavity). Another hypothesis is coelomic metaplasia: Coelomic epithelium is transformed into endometrium-like glands. Microscopically, endometriotic implants consist of glands and stroma histologically identical to intrauterine endometrium. These tissues containestrogenandprogesteronereceptors and thus usually grow, differentiate, and bleed in response to changes in hormone levels during the menstrual cycle; also, some endometriotic implants produceestrogenand prostaglandins. Implants may become self-sustaining or regress, as may occur during pregnancy (probably becauseprogesteronelevels are high). Ultimately, the implants cause inflammation and increase the number of activated macrophages and the production of proinflammatory cytokines. The increased incidence in 1st-degree relatives of women with endometriosis and in large twin studies ( Etiology and pathophysiology reference ) suggests that heredity is a factor. In patients with severe endometriosis and distorted pelvic anatomy, the infertility rate is high, possibly because the distorted anatomy and inflammation interfere with mechanisms of ovum pickup, oocyte fertilization, and tubal transport. Some patients with minimal endometriosis and normal pelvic anatomy are also infertile; reasons for impaired fertility are unclear but may include the following: Increased incidence of luteinized unruptured ovarian follicle syndrome (trapped oocyte) Increased peritoneal prostaglandin production or peritoneal macrophage activity that may affect fertilization, sperm, and oocyte function Nonreceptive endometrium (because of luteal phase dysfunction or other abnormalities) Potential risk factors for endometriosis are Family history of 1st-degree relatives with endometriosis Delayed childbearing or nulliparity Early menarche Late Menopause None Shortened menstrual cycles (< 27 days) with menses that are heavy and prolonged (> 8 days) Müllerian duct defects (eg, noncommunicating uterine horn remnant, cervical hypoplasia with obstruction of the uterine outflow tract) Exposure to diethylstilbestrol in utero Potential protective factors seem to be Multiple births Prolonged lactation Late menarche Long-term use of low-dose oral contraceptives (continuous or cyclic) Regular exercise (especially if begun before age 15, if done for > 4 hours/week, or both) 1.Saha R, Pettersson HJ, Svedberg P, et al: Heritability of endometriosis.Fertil Steril104 (4):947–952, 2015. doi: 10.1016/j.fertnstert.2015.06.035 Epub 2015 Jul 22. 