Path ogenetic relationship of endometrial hyperplasia with aseptic nonspecific inflammatory process

The aim is to reveal pathogenetic relationship of endometrial hyperplasia with inflammatory process and to show intercellular mechanisms of its realization on the basis of complex morphological analysis. The leading factor in the pathogenesis of simple endometrial hyperplasia is absolute or relative hyperplasia in combination with a defect in the action of progestins. The absence of a direct relationship between the quantitative indicators of serum estradiol, morphology of proliferation and the degree of endometrial atypia, indicates the existence of other mechanisms underlying this pathology. The study of the relationship of local changes with a variety of molecular biological mechanisms involved in the development of endometrial hyperplasia is relevant for improving approaches to treatment, for example, a combination of
hormonal and anti-inflammatory therapy, as well as some new forms of anti-oncogenic drugs. Material and methods. A morphological study was carried out on the endometrium in women aged 35-55 years in the following groups: control, simple endometrial hyperplasia without atypia, complex hyperplasia without atypia, adenocarcinoma. Reviewing stains of paraffin sections helped to clarify the diagnosis, and immunohistochemical research revealed the expression of markers of cellular renewal and inflammation.
Results. Our studies have shown an increase in the expression of the total leukocyte antigen CD45+, that is, an increase in the activity and severity of inflammation depending on the nature of the hyperplastic process. In all samples of the tissue with endometrial hyperplasia there were cells with CD45 + expression, their number increased during the transition from a simple form of hyperplasia to a complex one. Among other factors, reflecting the degree of severity and nature of inflammatory changes in the endometrium, it included the presence of various subpopulations of lymphocytes, decrease in the intensity of apoptosis of epithelial cells in the glands of the endometrium (unlike stroma) and activation of vascular growth factor. At the same time, it is important to note the mechanism of inflammation as a vascular-stromal, mesenchymal reaction involving connective tissue cells, including various inflammatory cells. Conclusion. The progression of the hyperplastic process led to more severe inflammatory changes in the endometrium. In case of simple endometrial hyperplasia, the more important progressive factor was hormonal imbalance, but in case of complex and atypical hyperplasia, the role of the inflamatory process increased. The formation of
inflammation in endometrial hyperplasia can be considered a factor in the development and progression of the pathology, as well as a risk factor for malignancy in hyperplastic processes.