P-370 Impaired endometrial decidualization with a hyperinflammation environment is involved in poor reproductive outcomes in adenomyosis patients

Abstract Study question Do patients with adenomyosis have an impaired inflammatory state of the endometrium that could affect implantation and pregnancy? Summary answer Adenomyosis show increased proinflammatory cytokines expression deregulated decidualization markers in eutopic which lead to altered endometrial receptivity implantation. What is known already estrogen-dependent chronic condition, characterized by presence glands stroma within myometrium. present defective embryo-endometrium communication, resulting failure, miscarriage, other fertility-related disorders. Although underlying mechanisms this infertility remain unknown, it a favorable immune uterine environment necessary for developmental pregnancy. It has been proposed hyperinflammatory be involved adenomyosis-related infertility. For reason, we aim evaluate status during from patients. design, size, duration Sixteen samples were collected infertile without undergoing hormonal replacement therapy before vitro fertilization (IVF) at IVIRMA Valencia between January December 2022. Participants/materials, setting, methods Eutopic obtained secretory phase (LH + 7) diagnosed (n = 8) ultrasound or hysteroscopy gynecological diseases (control, n 8). Total RNA extraction was performed later determine gene decidualization-related genes Prolactin (PRL), SPP1 PAEP qRT-PCR. In addition, proteins extracted using lysis buffer relative levels human measured Human Cytokine Array (Raybiotech). Main results role chance Gene evaluation compared control showed significant downregulation key marker PRL (fold change [fc] 0.56, p 0.0047) upregulation (fc 1.75, 0.009) 1.56, 0.0192), both regulation. Regarding expression, array different interleukins (IL) mediation response previously described adenomyosis. Specifically, IL1ß (12±19.63 vs. 1.37±2.77, regulates several responses, including cell proliferation, differentiation, apoptosis; IL6 (584.7±121.8 488.4±57.44, 0.06) acts on inflammation maturation B cells, contributing development autoimmune diseases. Similarly, related promotion cellular proliferation endometriosis, IL17a (173.6±44.75 102.10±71.85, 0.04) TNFβ (430.9±139.6 315.3±37.09, 0.04), also upregulated control. There diverse functions like anti-inflammation response, growth factors modulation: IL5 (308.1±88.77 202.6±45.72, 0.01), IL2 (341.4±60.38 270.8±35.13, 0.014), TGFα (215.3±27.04 117.8±36.67, 0.002), IL31 (77.74±40.57 14±15.96, 0.0012), IL7 (739.1±147.1 511.8±103.7, 0.003) IL15 (301.9±95.73 209.8±50.62, 0.03). Limitations, reasons caution Our findings are limited relatively small sample size inherent biological variability samples. Wider implications affecting consequently, embryo These open insight further investigations study mechanism exaggerated affects fertility context define new management approaches. Trial registration number Not applicable