PREGNANCY AND UNDIFFERENTIATED CONNECTIVE TISSUE DYSPLASIA
DOI:
https://doi.org/10.11603/24116-4944.2024.2.15084Keywords:
undifferentiated connective tissue dysplasia, fetal growth retardation, placental dysfunction, uterine scar defect, isthmic-cervical insufficiency, magnesiumAbstract
The aim of the study – to establish the frequency of markers of undifferentiated connective tissue dysplasia (uCTD) in obstetric and perinatal complications and to assess the pathogenetic role of magnesium deficiency as a factor in the dysregulation of connective tissue metabolism.
Materials and Methods. The analysis of the history of childbirth was conducted in 240 women aged (32.6±2.4) years, who were divided into two groups: 160 patients with the uCTD phenotype (main group), and 80 patients of the control group with a physiological course of pregnancy without uCTD markers.
Results and Discussion. Assessment of the «perinatal portrait» allowed us to reveal a complex of numerous symptoms, including a woman's body weight deficit at birth (24.4 %), premature birth (19.4 %), an increased burden of cardiovascular, cerebrovascular pathological conditions and reproductive losses in the family history of such women (21.3 %). uCTD markers were characterized by pronounced variability and represented the most common phenotypic features. The spectrum of pregnancy and childbirth pathology allowed us to indicate a high percentage of premature rupture of the amniotic membranes (25.6 %), rapid labor or labor abnormalities (19.4 %), prematurity (16.9 %), pathological placentation (24.4 %), maternal trauma resistant to therapy, hypotonic uterine dysfunction (13.1 %), which can be attributed to the so-called «obstetric» markers of uCTD. Hypomagnesemia was detected in the case of uCTD.
Conclusions. Thus, it can be stated that the programmed predictors of connective tissue disorders in uCTD initiate insufficient capacity to fully support gestational transformations (trophoblast invasion, spiral artery modification, vascular adaptation), which is accompanied by miscarriage and the development of gestational and perinatal pathology. The results of the study demonstrate convincing evidence that connective tissue weakness is associated with uteroplacental apoplexy (OR – 5.68; p<0.004), isthmic-cervical insufficiency (OR – 17.49, p<0.001), uterine scar defect (OR – 8.73; p<0.04), and obstetric trauma (OR – 6.55; p<0.04). A reduced level of microcollagen-specific bioelement was found, such as a deficiency in magnesium concentration, which contributes to the severity and implementation of hereditary and acquired connective tissue defects in uCTD.
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