Features of the species composition and functional activity of mast cells in the decidual tissue of patients with undeveloped pregnancy and polycystic ovary syndrome
Background: Infertility, miscarriage, birth of full-term healthy children take dominant positions among the problems of obstetrics and gynecology. Рolycystic ovary syndrome is a disease one of the clinical manifestations of which is infertility, severe complications of gestation оf spontaneous pregnancy in metabolically uncompensated patients, which makes a significant contribution to the structure of perinatal morbidity, and sometimes mortality. The aim of the study: The aim of the study was to study the species composition and functional activity of mast cells in decidual tissue of patients with рolycystic ovary syndrome and missed abortion, to compare the data obtained with those from patients with missed abortion without metabolic disorders and during the physiological course of pregnancy. Materials and methods: A total of 60 patients were examined. Immunohistochemical identification of mast cell tryptase and chymase in decidual tissue samples of patients was performed using mouse monoclonal antibodies to tryptase and chymase. Secondary antibodies for tryptase (Goat Anti-Rabbit Ig H&L conjugated with Alexa Fluor-488) and chemase (Goat-Anti-Mouse Ig H&L conjugated with Cy3) were used to visualize proteases in multiple immunomarking. Results: The number of mast cells in the decidual tissue of patients with missed abortion and POS is 4,4 times higher than in physiological pregnancy and 1,38 times higher in undeveloped pregnancy and the absence of metabolic disorders. The protease profile of mast cells is shifted towards chemase expression. The comparable functional activity of the studied cells in missed abortion in both groups indicates the absence of the influence of рolycystic ovary syndrome on the degree of mast cell degranulation. Conclusion: The changes in the quantitative and qualitative composition of mast cells confirms their participation in the pathogenetic mechanisms of the formation of missed abortion on a background оf metabolic disorders typical for рolycystic ovary syndrome.