Abstract

Chronic pelvic pain is one of the most significant medical and social problems. The high prevalence of concomitant benign genital diseases in women of reproductive age are genial endometriosis, uterine fibroids, endometrial hyperplasia with common clinical manifestations, namely chronic pelvic pain, abnormal uterine bleeding, impaired reproductive function, and a high frequency of cancer pathology of the reproductive organs in young age that require a holistic approach to patient management and comprehensive problem solving. The objective: to investigate the proliferative and inflammatory activity of the glandular and stromal components of the eutopic endometrium (EE), the presence of nerve fibers in it as mechanisms for the formation of СРР in genital endometriosis in combination with other benign hormonedependent diseases of the genitals Materials and methods. The study involved 85 women with chronic pelvic pain due to genial endometriosis, uterine leiomyoma, endometrial hyperplasia, chronic salpingitis and oophoritis in various combinations, and 35 women by the comparison group with similar gynecological pathology without CPP. In order to objectify pain syndrome, a 10-point visual analogue scale (VAS) was used. Echography of the pelvic organs, the thyroid gland (if necessary) was performed by the Toshiba, Nemio17-pro apparatus. In order to study the molecular mechanisms of the development of CPP, the expression of ER, PGR, KI-67, VEGF, COX-2, NF in the eutopic endometrium was determined by immunohistochemistry. Results. The leading painful role in combined gynecological pathology was assigned to diseases in clinical group 1, which had the most pronounced algogenic anatomical and structural features. Formation of CРР is confirmed by the presence of rank correlations between the level of pain syndrome in VAS and immunohistochemistry characteristics with reliable direct connections of average strength with the ER (Spearman’s coefficient of correlation ρ =0.58; p<0.001), with PGR (p=0.42; p=0.021), with Ki-67 (ρ =0.55; p=0.004) and with COX-2 (ρ =0.42; p=0.021). Conclusions. The concept of the pathogenesis of СРР in proliferative genital diseases has been expanded. It is characterized by moderate expression of VEGF, high expression of ER and PGR, Ki-67 and COX-2, with NF in EE; which determines the development of СРР by the criteria being studied, both individually and in combination. Key words: chronic pelvic pain, proliferative diseases of the genitals, morphogenesis markers.

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