UTERINE SCAR FORMATION AND EXPRESSION OF SPECIFIC CONNECTIVE TISSUE PROTEINS
DOI:
https://doi.org/10.11603/24116-4944.2020.1.11498Keywords:
uterine scar, diagnosis, prognosis, pathomorphologyAbstract
The aim of the study – to evaluate the role of expression of specific connective tissue proteins in the formation of the scar on the uterus.
Materials and Methods. The study was performed on the basis of the regional perinatal center and KU PB No. 5 during 2017–2019. 426 women with a scar on the uterus were examined, including 115 (27.0 %) with two or more scars. The mean age of the subjects was (33.4±1.1) years. The results of sonographic studies were analyzed. For pathomorphological examination, three cases of intranatal rupture of the uterine wall along the “old” scar after cesarean section from middle-aged women with a gestational age of 33 to 40 weeks are presented. The expression of collagen types 1 and 3 and the protein of the intermediate filaments of the muscle tissue of desmin was determined using a semi-quantitative method with the calculation of H-score.
Results and Discussion. Analysis of ultrasound data showed that the average assessment of the degree of insolvency of the scar on the uterus was in the examined women X=(1.3±0.2) points, a high level of insolvency was found in 114 (26.8 %) pregnant women. At the same time, 225 (52.8 %) pregnant women showed no signs of scar failure at all. In 87 (20.4 %) one sign of uterine scar failure was found, in 76 (17.8 %) – two signs, in 20 (4.7 %) – three signs, and in 18 (4.2 %) – four signs. Subsequently, 44 (10.3 %) women were born operatively, the rest gave birth per via naturales. Local myometrial defect after ultrasound delivery was detected in 25 of 182 (13.7 %) women who gave birth independently.
Conclusions. A high level of scar failure risk is found in 26.8 % of pregnant women. H-score valuesfor collagen types 1 and 3 averaged (212±24) and (188±22), for desmin – (193±17). Thus, reparative processes at the site of previous surgery on the uterine wall are by incomplete regeneration (substitution) and compensatory hyperplasia of structural tissue elements.
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