Endometrium Receptivity in Patients with Repeated Implant Failures

Study Objective: To broaden the understanding of the pathogenesis of impaired receptivity in patients with repeated implant failures (RIF) in in vitro fertilisation programs.

Study Design: Open perspective comparative study.

Materials and Methods. 57 women aged 27 to 42 years old (mean age: 36 ± 6.2 years old) with clinically verified RIF. A morphological control group included 30 fertile women. The subject of the study was endometrium biopsy material obtained on day 5–7 of menstruation, following the peak blood concentration of luteinizing hormone (implantation window).

Study Results. During the implantation window, patients with RIF have statistically significant (р < 0.05) changes: 1.5- and 1.4-fold increase in gland and stromal expression of estrogen α receptors, respectively; 2.3-fold increase in expression of progesterone A and B receptors with simultaneous reduction in stromal expression by 1.6 times; focal reduction in MUC1 expression in apical surface of endometrium; 1.3-fold increase in pinopods density in apical surface of endometrium and 2.3-fold increase in stromal expression of CD56+ NK-cells; 2-fold reduction in CD4+ cell expression, and 2.2-fold increase in CD8+ expression vs morphological controls. During the implantation window, von Willebrand factor and CD34+ levels in endometrial stroma did not demonstrate statistically significant differences when expressed in blood-vessel endothelium.

Conclusion. Pathogenesis of impaired receptivity in patients with RIF can be explained with impaired expression of sex hormone receptors in stroma and glandular component and reduced MUC1 expression, increased density and reduced amount of mature and maturating pinopods in apical surface of endometrium. An increased number of expressed CD56+ NK-cells during the implantation window in patients in both groups (in patients with RIF, CD56+ expression is significantly higher) in combination with the found imbalance between Т-lymphocytes can be a cause of the immunological component of impaired implantation pathogenesis.

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