Endometriosis is a pathology of the female reproductive system in which the tissue of the uterine lining (endometrium) begins to penetrate the underlying structures (myometrium). The ailment also affects neighboring organs (fallopian tubes) and even far away areas of the body (lungs, liver). At the same time, foci of the endometrium outside the uterus are just as susceptible to the menstrual cycle, periodically contributing to the development of bleeding. The initial manifestations of the pathology protrude with painful, profuse, and prolonged menstruation.
Hereditary factors, disorders in the immune and neuroendocrine system are of importance in the emergence and development of the disease. The spread of endometriosis is often explained by the skidding and engraftment of endometrial particles in other organs and parts of the reproductive system. Cervical endometriosis is characterized by the appearance of small reddish spyholes on its vaginal part. Before menstruation, these foci change color and increase in size.
The emergence of cervical endometriosis is facilitated by the treatment of erosion by diathermocoagulation, cervix injury after childbirth, abortion, and diagnostic curettage. Ovarian endometriosis manifests itself as foci of endometrioid tissue in the thickness or on the surface of the ovaries. The disease manifests itself as infertility with a slight severity. Endometrioid cysts occur with a higher prevalence of the process.
Clinical and anatomical classification of endometriosis of the uterus, endometrioid ovarian cysts, and retrocervical endometriosis describes the four stages of the pathological process spread. Researchers note that the pathological process is limited to the submucous membrane of the uterus at stage I (Fan et al., 2018). The spread of the disease passes to the muscle layers in stage II. Stage III begins with the range of the pathological process throughout the entire thickness of the uterus muscular membrane to its serous cover. Stage IV is characterized by the involvement of the parietal peritoneum of the pelvis and neighboring organs, besides the uterus, in the pathological process.
Endometriosis can be considered as a chronic gynecological disease, the main clinical manifestations of which are persistent pain and infertility. Pathology is a benign growth outside the uterine cavity of the tissue in morphological and functional properties similar to the endometrium. In some cases, after successful surgical removal of the endometriosis focus (ovary or peritoneum) in women with infertility, the symptoms of the disease disappear independently, and pregnancy occurs in the natural cycle.
There are three clinically different forms of the disease, namely, endometriotic foci on the surface of the peritoneum of the pelvis and ovaries (peritoneal endometriosis), ovarian cysts (endometriomas), and stable formations of complex structure. The latter, along with endometrioid tissue, includes adipose and muscle-fibrous. Each of the three forms may or may not tend to infiltrative growth. The kinds of endometriosis can be variants of the same pathological process or as a result of various evolutionary mechanisms. However, the presence of endometrial stromal and epithelial cells, persistent hemorrhages in focus, and signs of inflammation are their common histological characteristics.
The most common theory of the pathogenesis of endometriosis is presented by J.A. Sampson’s hypothesis about the implantation of viable endometrial cells in the pelvic area during retrograde menstruation (Schjenken et al., 2019). Researchers note that this process is physiological and is diagnosed in 70-90% of women, and the disease develops only in 10% of cases (Hanacek et al., 2019). Two interconnected pathogenetic links play a crucial role in the successful implantation, survival, and further development of endometrioid implants in the peritoneum of the pelvis.
On the one hand, pathological cascades of the synthesis of estrogens, cytokines, prostaglandins, and metalloproteinases are characteristic of molecular genetic defects of the eutopic endometrium, which lead to a decrease in the processes of spontaneous apoptosis. Thus, an endometrioid is only similar to the tissue of normal endometrium. On the other hand, immune disorders at different levels modulate cell proliferation and localization, apoptosis processes, and mechanisms of neoangiogenesis, which generally disrupt the physiological processes of endometrioid cell elimination.
The key pathogenetic links of endometriosis are closely interrelated and, in addition to retrograde menstruation, include excessive local production of estrogen, progesterone resistance, inflammation, and neoangiogenesis. The functions do not allow inhibiting the pathological process in the initial stages and explain the infiltrative growth, invasion of the surrounding tissues with their subsequent destruction, and the spread of lesions.
There is also the hypothesis of coelomic metaplasia, that is, the conversion of the coelomic epithelium into glands similar to the endometrium. Microscopically, endometrioid implants compose glands and stroma which are identical to the endometrium. The tissues mentioned above contain estrogen and progesterone receptors and therefore grow, differentiate, and bleed in response to hormonal changes during the menstrual cycle. Implants can become self-sustaining or regress, as it happens during pregnancy. Ultimately, implants cause inflammation and the production of pro-inflammatory cytokines.
Specialists have long drawn attention to the fact that many women have a significant improvement in the regular use of vegetables from the cabbage family. The greens contain a large amount of indole-3-carbinol and help to normalize estrogen metabolism. Researchers note that supplementation with polyunsaturated fatty acids (omega-3,6), multivitamins, B vitamins, zinc, selenium, vitamin E, and magnesium also conduces the alleviation of endometriosis symptoms (Arthur, Kirsh, and Rohan, 2019).
Prevention of endometriosis also consists of the contraceptives use to avoid abortion. It is necessary to control the appointment of intrauterine manipulations with a decrease to a minimum. It should be borne in mind that preventive measures do not exclude the possibility of developing the disease but only reduce its manifestation.
Many factors determine the difficulties that a physician faces when choosing a method of treating patients with endometriosis. Firstly, the etiology and mechanisms of pain formation have not been thoroughly studied. Secondly, the variety of clinical manifestations of pathology should be relevant to the criteria for an objective assessment of pain intensity. Thirdly, the lack of evidence regarding the evaluation of the drug treatment effectiveness compared with placebo and other treatment methods takes place.
Treatment should be prolonged, taking into consideration the chronic course of endometriosis and the high risk of relapse after surgery or discontinuation of drug therapy. The operation was and remained the only method of genital endometriosis treatment, which allows excision or destruction of the morphological substrate of endometriosis using energies of various types. However, during surgery, especially with common endometriosis, only visible and accessible foci are removed. Microscopic and atypically located lesions can go unnoticed and persist for a long time.
In laparoscopy, deep lesions may seem superficial, which leads to a decrease in the detection of infiltrative forms and an underestimation of the disease severity. Empirical drug therapy is possible with adenomyosis, external genital endometriosis in the absence of cystic processes in the ovaries, and other tumor-like formations in the pelvis. Hormone therapy occupies an essential place among the treatment methods used to relieve symptoms, maintain fertility, and improve working capacity, social activity, and the quality of women’s lives in general.
Arthur, R. S., Kirsh, V. A., & Rohan, T. E. (2019). Dietary B-vitamin intake and risk of breast, endometrial, ovarian and colorectal cancer among Canadians. Nutrition and Cancer, 71(7), 1067-1077.
Fan, Y. Y., Chen, H. Y., Chen, W., Liu, Y. N., Fu, Y., & Wang, L. N. (2018). Expression of inflammatory cytokines in serum and peritoneal fluid from patients with different stages of endometriosis. Gynecological Endocrinology, 34(6), 507-512.
Hanacek, J., Havluj, L., Drahonovsky, J., Urbankova, I., Krepelka, P., & Feyereisl, J. (2019). Interposition of the mesorectal flap as prevention of rectovaginal fistula in patients with endometriosis. International Urogynecology Journal, 30(12), 2195-2198.
Schjenken, J. E., Panir, K., Robertson, S. A., & Hull, M. L. (2019). Exosome-mediated intracellular signalling impacts the development of endometriosis—new avenues for endometriosis research. MHR: Basic science of reproductive medicine, 25(1), 2-4.