Clinical and morphological characteristics of chronic pelvic pain in patients with hyperproliferative diseases of the genitals

In: HEALTH OF WOMAN · 2019 · pp. 74–79 · doi:10.15574/hw.2019.138.74 · W4232324623
article OA: diamond CC0 ⤵ 1 in-corpus citation
AI-generated summary by claude@2026-06, 2026-06-13

This study investigated proliferative and inflammatory markers in the endometrium of women with chronic pelvic pain from combined gynecological conditions, finding correlations between pain levels and expression of ER, PGR, Ki-67, and COX-2.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-13 · read from full text

This study investigated mechanisms of chronic pelvic pain (CPP) in 85 women with chronic pelvic pain attributed to genital hyperproliferative conditions (genital endometriosis, uterine leiomyoma, endometrial hyperplasia, and chronic salpingitis/oophoritis in various combinations), compared with 35 women with similar gynecologic pathology without CPP. Using VAS for pain severity and immunohistochemistry on eutopic endometrium, the authors measured expression of ER, PGR, Ki-67, VEGF, COX-2, and NF and reported direct rank correlations between VAS pain scores and ER (ρ=0.58), PGR (p=0.42), Ki-67 (ρ=0.55), and COX-2 (p=0.42). They concluded CPP in this context is associated with high ER/PGR/Ki-67/COX-2 and moderate VEGF expression, and note that the “combined” pathology context limits isolation of a single disease mechanism. This paper is centrally about endometriosis — it directly studies eutopic endometrium markers and their association with chronic pelvic pain in women with genital endometriosis, often in combination with other hormone-dependent proliferative diseases.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

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.
Full text 5,943 characters · extracted from oa-html · 2 sections · click to expand

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

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Outcome instruments

VAS-pain

Condition tags

endometriosischronic_pelvic_pain

Citation neighborhood (sparse)

Too few in-corpus citations on either side for a chart; here are the lists.

Cited by (1)

Cited by (1)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK