Endometriosis (endometrioid disease) is a disease characterized by proliferation of tissue similar to endometrium, outside the normally located mucous membrane of the uterus.
Endometriosis is capable of infiltrative growth with penetration into the surrounding tissues and their destruction, can grow into any tissue or organ: the wall of the intestine, bladder, ureter, peritoneum, skin, can metastasize by lymphogenous or hematogenous. Foci of endometriosis are found in the lymph nodes, subcutaneous tissue of the anterior abdominal wall or in the postoperative scar, as well as in remote areas of the body, such as the navel and conjunctiva of the eye. Endometriosis differs from a true tumor in the absence of pronounced cell atypia and the dependence of clinical manifestations on menstrual function.
Classification. Depending on the location, genital and extragenital endometriosis are distinguished. Genital endometriosis is divided into internal (uterine body, isthmus, interstitial departments of the fallopian tubes) and external (external genitalia, vagina and vaginal part of the cervix, retrocervical region; ovaries, fallopian tubes, lining the pelvic organs). When extragenital endometriosis, endometrial implants are detected in other organs and tissues of the woman’s body (lungs, intestines, navel, postoperative wounds, etc.).
EpidbMiology. Endometriosis is one of the most common diseases of the reproductive system in women 20-40 years of age, the frequency of its detection is sharply reduced in postmenopausal women. Endometriosis is diagnosed in 6-8% of patients with gynecological clinics, and in patients with infertility, its detection increases to 35-44%. The main part is genital endometriosis (92–94%), extragenital endometriosis (6–8%) is much less common.
Etiology and pathogenesis. To date, the etiology of endometriosis has not been established. Of the numerous hypotheses proposed, not one has become conclusively and generally accepted.
Theory of Endometriosis
The translocation theory (implant ionic) considers the possibility of the development of endometrioid heterotopies from the elements of the endometrium that were transferred retrograde with menstrual secretions into the abdominal cavity and spread to various organs and tissues. Implantation of endometrial cells and its further development can be carried out only under additional conditions: when endometrial cells have an increased ability to adhere and implant, and when there is a violation of the hormonal and immune systems.
The theory of trial-derived origin considers the development of endometrioid heterotopies from endometrial elements displaced in the thickness of the uterus wall. It has been proven that intrauterine medical manipulations (abortion, diagnostic curettage of the uterine mucosa, manual examination of its cavity after delivery, caesarean section, enucleation of myomatous nodes, etc.) contribute to the direct germination of the endometrium into the uterine wall, leading to the development of internal endometriosis of the uterus. During gynecological operations, elements of the endometrium can also spread through the blood and lymph to other organs and tissues. Lymphogenous and hematogenous pathways of spread lead to the development of endometriosis of the lungs, skin, muscles.
Embryonic and dilontohemethy theories consider the development of endometriosis from displaced areas of embryonic material, from which the female genital organs and, in particular, the endometrium are formed during embryogenesis. The discovery of clinically active endometriosis at a young age and its frequent combination with abnormalities of the genital organs, organs of the urinary system and the gastrointestinal tract confirm the validity of the embryonic or dystontogenetic concept of the origin of endometriosis.
Mshshasticheskaya concept. According to this hypothesis, endometriosis develops as a result of metaplasia of the embryonic peritoneum or coelomic epithelium. The possibility of the transformation into the endometrium-like tissue of the endothelium of the lymphatic vessels, the mesothelium of the peritoneum and pleura, the epithelium of the tubules of the kidneys and other tissues is allowed.
Of the many factors contributing to the development and spread of endometriosis, hormonal disorders and immune system dysfunction should be distinguished.
Hormonal disorders are not the direct cause of the formation of endometriotic foci, but only are predisposing conditions for the occurrence of the pathological process. In patients with endometriosis, the presence of non-systematic peaks of FSH and LC, as well as a decrease in the basal level of progesterone secretion, were noted; development of a follicle syndrome is noted. However, 40% of patients with endometriosis maintain a normal two-phase menstrual cycle. In these patients, the mechanism of cytoplasmic binding of progesterone is impaired, which leads to a perversion of the biological action of hormones.
The excretion of estrogen in patients with endometriosis does not have a classic cycle, it is erratic and forms hyperestrogenic background. When studying the excretion of estradiol, estrone and estriol, a high level of estrone is established. In patients with endometriosis, estrone is converted into a powerful estrogen, 17-p-estradiol, with increased enzymatic activity (hydroxysteroid cehydrogenase). Estrogens stimulate the growth of the endometrium, their excess leads to the growth of foci of endometriosis.
In patients with endometriosis, hyperprolactinemia and impaired androgenic function of the adrenal cortex are often detected.
An important role in the pathogenesis of endometriosis belongs to autoimmune reactions. When the hormonal status is disturbed, the immune system dysfunction is expressed in suppressing the activity of natural killer cells, as well as in increasing the concentration of vascular endothelial growth factor, which causes excessive angiogenesis. Inhibition of apoptosis and an increase in the aromatase content in the foci of endometriosis are revealed, which is one of the reasons for the development of relative hyperestrogenism.