Abstract
Introduction. Chronic endometritis is one of the most frequent gynecological diseases which negatively impacts the main pathogenetic links in the morphogenesis of secretory and gestational endometrial transformation. These links determine implantation failure. The study aimed to verify the expression of estrogen receptors (ER) and progesterone receptors (PR), progesterone-induced blocking factor (PIBF) and stromal cell-derived factor-1 (SDF-1) in the endometrium of patients having chronic endometritis with ineffective IVF cycles or undeveloped pregnancies occurred after assisted reproductive technologies in their histories. Materials and methods. We formed 3 study groups: group I included samples of the endometrium of patients with ineffective IVF cycles (n=50); group II contained samples received from patients with a history of undeveloped pregnancy after IVF (n=50); and group III (the control group) included endometrial tissue from healthy patients (n=25). We carried out routine histological evaluation followed by an immunohistochemical assay with ER, PR, PIBF, and SDF-1 in the endometrial glands and stroma in the middle secretion phase. esults. The middle stage of the secretion phase of the menstrual cycle in endometrial samples of groups I and II was detected in only 46% and 42% of cases, respectively. We showed a decrease in the ER and PR expression in more than 92% of cases. Statistically significant decrease was detected in PIBF and SDF-1 expression in the endometrial glands and stroma within the implantation window in patients with a history of reproductive loss. Conclusion. Violation of implantation viability with an imbalance of chemokines, cytokines, cellular factors, and structural and functional characteristics of the endometrium was found in patients with revealed chronic endometritis and history of ineffective IVF cycles and miscarriage after ART. Keywords: endometrium,IVF, missed abortion after IVF, estrogen receptor, progesterone receptor, progesterone-induced blocking factor, stromal cell-derived factor-1
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