Abstract
This review article examines the relationship between various etiological factors in the development of mastopathy. Multiple exogenous and endogenous risk factors disrupt the normal ratio of sex hormones, causing hyperestrogenism and hyperproliferation of the epithelium in breast tissue, which leads to the development of mastopathy. In the presence of polymorphism of coding genes (ESR1 and PRG), mastopathy also increases the risk of developing breast cancer. Disturbances in the ESR1 receptor gene (Estrogen Receptor 1) lead to changes in the sensitivity of receptors to hormones and even to its loss. According to the literature, polymorphism in the intronic region of the ESR1 gene is associated with the risk of fibrocystic mastopathy. The presence of polymorphism of the PRG (Progesterone Receptor Genes) gene may cause the occurrence of defective forms of PR (Progesterone Receptor) with disruption of the ligand- and hormone-binding zones, which is confirmed by the effects of progesterone in tissues. Thus, progesterone deficiency makes possible excessive proliferation of not only epithelial cells, but also the connective tissue component of the mammary gland. In this case, the expression of the progesterone receptor gene is regulated by the level of estrogen. The association of various combinations of predisposition genes indicates the presence of a specific combination of genotypes for each clinical and pathogenetic variant. In proliferative forms of mastopathy, foci with an excess content of estrogen receptors in the epithelium and high activity of cell proliferation and apoptosis are formed in the breast tissue; there is an increase in the content of alpha-estrogen receptors, a change in the relative content of alpha- and beta-estrogen receptors, A- and B-progesterone receptors; the sensitivity of the epithelium to estradiol increases; a complex of cyclin-dependent kinases, alpha-transforming and epidermal growth factors is activated; the proliferative activity of the epithelium increases; apoptosis processes are disrupted; vascularization of the parenchyma increases. All these pathological mechanisms that increase the risk of breast cancer have not yet been sufficiently studied both at the experimental and clinical level. In the treatment of mastopathy, diet therapy, psychological correction, hormonal drugs, non-hormonal drugs, such as vitamins, minerals, hepatoprotectors, diuretics, enzyme drugs, immunocorrectors, adaptogens, non-steroidal anti-inflammatory drugs, herbal remedies are used. The general disadvantages of most of the remedies used today are attempts to eliminate the causes of mastopathy rather than conducting pathogenetic treatment.
Publisher
Publishing Center Science and Practice