Risk factors of perinatal and obstetric pathology depending on cytokines and oxidative status of a pregnant.
DOI:
https://doi.org/10.26641/2307-0404.2016.4.90783Keywords:
amniotic fluid, risk factors, inflammation, cytokinesAbstract
The aim of the study was to determine risk factors for perinatal damage in newborns depending on the level of cytokines secretion and nitrate/nitrite amount in the amniotic mileu. A total of 464 patients were examined. The content of IL-1β, IL-2, IL-4, IL-10, IFN-γ, TNF-α in the amniotic fluid were determined by ELISA, evaluation of nitrate and nitrite amount was performed by Griess reaction in Veremey et al. modification. Outcomes of labor, neonatal status and morphological structure of placentas were studied. To determine the risk factors odds ratios (OR) for delivery outcomes, perinatal pathology and damage the placenta were calculated. It was found that the exacerbation of chronic pyelonephritis during pregnancy increases the odds of perinatal pathology of the nervous system by9.6 times ([95% CI 3.8, 17.0], p=0.008) and low birth weight – by13.2 ([95% CI 4.3, 25.3]; p=0.03]). The syndrome of "short" cervix during pregnancy increases the odds of respiratory distress syndrome by 8.0 times ([95% CI 2.2, 16.7], p=0.019), perinatal pathology of the nervous system by11.4 ([95% CI 2.8, 17.3], p=0.005). Acute respiratory infections up to 18 weeks increase the or of respiratory distress syndrome by 27.6 ([95% CI 11.7, 46.2], p=0.021), fetal growth retardation by 11.0 times ([95% CI 2 0, 21.6], p=0.006). Preterm delivery and implementation of intrauterine infection is followed by a decrease of IL-4, IL-10 concentration and enhancement of IL-2, IFN-γ in the amniotic mileu with synergistic increase in the concentration of NO2-/NO3-. Perinatal damage of the nervous system in the presence of acute pyelonephritis, acute respiratory infections in the term of up to 18 weeks, syndrome of "short" cervix, PROM is preceded by reduction of IL-4 and IL-10, decrease of NO2- / NO3- and increased activity of TNF-α in the amniotic mileu.
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