Экспрессия ноцицептивных генов в патогенезе тазовой боли, обусловленной овариальным эндометриозом

Pathogenetic mechanisms of the pain syndrome, with ovarian endometriosis remain controversial and require further study. The aim of the study was to expand understanding of the pathogenesis of pelvic pain caused by ovarian endometriosis. Material and methods: the study included 64 (n=64), patients of reproductive age (mean age 35±5 years) applied for surgical treatment with a diagnosis of endometrioid ovarian cysts. The patients were stratified: group I - basic capsules biopsies of endometrioid ovarian cysts from the operated patients (n=51),with pelvic pain of severe intensity due to ovarian endometriosis; group II - morphological control capsules biopsies of endometrioid ovarian cysts from operated patients with infertility on the background of ovarian endometriosis without pelvic pain (n=13). Quantitative analysis of the level of gene expression was performed using the method of polymerase chain reaction in real time, when comparing the indicator cycles ( ∆∆Cq ). The results of the study. Expression analysis of genes TAC1 nociceptors, TRPV1, SCN9A, SCN11 a samples of endometriotic cysts in the group with pain syndrome ovarian endometriosis, significantly exceeded the threshold in the group of morphological control. At the same time, the expression ofTRPA1 and P2RX3 differed slightly compared to the control. Conclusion. The pathogenesis of chronic pelvic pain due to ovarian endometriosis, compared to the silent shape, lies significantly increased expression of candidate genes responsible for nociceptive sensitivity in ectopic endometrium in contrast to such in eutopic, which together is one of the key triggers the generation of pain.