![]() Endometriotic lesions over-express β-estrogen receptor, steroidogenic acute regulatory protein and P450 aromatase. Almost all of the currently available treatment options for endometriosis suppress ovarian function and are not curative.Įndometriotic lesions are associated with hormonal imbalance, including increased estrogen synthesis, and progesterone resistance. To date, none of these theories has been proven beyond doubt.Īlthough the scientific community is trying to find an algorithm of treatment for endometriosis that can be universally applied, to date, there is no ideal drug that can prevent, inhibit, or stop the development of endometriosis ( 9). Other theories as celomic metaplasia, stem cell origin and lymphatic or hematogenous spread were considered. This disorder affects women’s health and quality of life, with consequences for personal, romantic, family and workplace relationships ( 8).Īlthough the exact pathogenesis is still a subject of research, the most prevalent theory is retrograde menstruation, according to which endometrial glands and stroma are attached and implanted in the peritoneal cavity. Infertility in endometriosis has multiple mechanisms, including the production of inflammatory mediators with damage to oocytes and sperm, reducing anti-müllerian hormone with an impact on follicular reserve, underlying adhesions, ovarian cysts and changes in tubal anatomy ( 7). Endometriosis - related pain is attributed to the increase of inflammatory cells and pro-inflammatory cytokines in endometrial lesions, and peripheral sensory neuronal dysfunction mediated by estrogens ( 6). ![]() It is associated with a wide spectrum of pain symptoms (dysmenorrhea, dyspareunia, periovulatory pain, chronic pelvic pain without any relation to menstrual cycle, dyschezia, dysuria, pain due to nerve root compromise) and infertility. Endometriosis is a disease that affects an estimated 5%–10% of women of reproductive age with a prevalence peak between 25 and 35 years of age. More recently, hereditary factors were estimated to account for 50% of endometriosis and familial clustering of endometriosis was demonstrated in humans ( 2).Įndometriosis occurs most commonly in fertile women and occasionally in women without an endometrium ( 3), in men ( 4) and unexpected, even before menarche ( 5). Although a benign proliferative disease, endometriosis shares common characteristics with neoplastic processes (inflammatory state, invasion of adjacent tissues, induction of angiogenesis, and resistance to apoptosis) ( 1).Įndometriosis is an estrogen-dependent chronic multifactorial disease involving mechanical, molecular, genetic, immunological and environmental causes. Endometriosis is a progressive severe gynecological disorder defined as the presence of functional endometrial-type mucosa (endometrium glands and stroma) outside the uterine cavity, in other areas of the pelvis, and sometimes even in the great abdomen cavity.
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