HEALTH OF WOMAN. 2019.2(138): 74–79; doi 10.15574/HW.2019.138.74

Grek L. P. , Dubossarskaya Z. M.
SI «Dnipropetrovsk Medical Academy», Ministry of Health of Ukraine, Dnipro

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.

REFERENCES

1. Kuznetsova IV. 2017. Chronic pelvic pain as a female problem. Gynecology 19 (3): 62–67. https://doi.org/10.26442/2079-5696_19.3.62-67

2. Stenyaeva NN, Apolihina IA. 2012. Сhronic pelvic pain: psychosomatic aspects. Consilium Medicum 6:19-20.

3. Orazov MR, Chayka AV, Nosenko EN. 2015. Some mechanisms that predispose stimulation of vascular and nervous growth in patients with adenomyosis. Materials of the International Scientific and Practical Conf. «Priorities of Modern Medicine: Theory and Practice». Odessa, International Humanitarian University: 79-82. https://doi.org/10.18370/2309-4117.2014.20.79-84

4. Chernuha GE. 2011. Endometriosis and chronic pelvic pain: causes and effects. Reproduction problems 5:83-86. 

5. Yarotskaya EL. 2016. Pelvic pain in women: diagnosis and treatment issues. Consilium Medicum 18(6): 82–86. https://doi.org/10.26442/2075-1753_2016.6.82-86

6. A classification of chronic pain for International Classification of Diseases (ICD-11) Pain. 156(6):1003–1007. 2015, Jun.  https://doi.org/10.1097/j.pain.0000000000000160; PMid:25844555 PMCid:PMC4450869

7. Cheong Y, William Stones R. 2006. Chronic pelvic pain: aetiology and therapy. Best Pract. Res. Clin. Obstet. Gynaecol. 20: 695–711. https://doi.org/10.1016/j.bpobgyn.2006.04.004; PMid:16765092

8. Jabbour HN, Milne SA, Williams AR et al. 2001.Expression of COX-2 and PGE synthase and synthesis of PGE(2) in endometrial adenocarcinoma: a possible autocrine/paracrine regulation of neoplastic cell function via EP2/EP4 receptors. Br J Cancer. 85(7): 1023–31. https://doi.org/10.1054/bjoc.2001.2033; PMid:11592775

9. Ferenczy A. 1998. Pathophysiology of adenomyosis .Hum Reprod Update 4(4):312–22. https://doi.org/10.1093/humupd/4.4.312; PMid:9825847

10. 232. Garcia-Manero M, Alcazar JL, Toledo G. 2007. Vascular endothelial growth factor (VEGF) and ovarian endometriosis: correlation between VEGF serum levels, VEGF cellular expression, and pelvic pain. 88(2): 777 – 782. https://doi.org/10.1016/j.fertnstert.2006.11.117; PMid:17296185

11. Merskey H and Bogduk N. 1994. Classification of Chronic Pain. 2nd Edition, IASP Task Force on Taxonomy. IASP Press, Seattle. http://www.iasp-pain.org/Education/content.aspx?ItemNumber=1698276]

12. Pockaj BA, Basu GD, Pathangey LB et al.  2004. Reduced T-cell and dendritic cell function is related to cyclooxygenase-2 overexpression and prostaglandin E2 secretion in patients with breast cancer. Ann Surg Oncol. 11(3):328–39. https://doi.org/10.1245/ASO.2004.05.027; PMid:14993030

13. Brosens I, Derwig I, Brosens J et al. 2010 The enigmatic uterine junctional zone: the missing link between reproductive disorders and major obstetrical disorders? Hum Reprod. 25(3):569–74. https://doi.org/10.1093/humrep/dep474; PMid:20085913

14. Eberhart CE, Coffey RJ, Radhika A et al. 1994.Up-regulation of cyclooxygenase-2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology 107(4): 1183–8. https://doi.org/10.1016/0016-5085(94)90246-1