INTERRELATIONSHIP BETWEEN INDICATORS OF LOCAL AND SYSTEMIC INFLAMMATORY REACTION IN NEWBORNS WITH NEONATAL ENCEPHALOPATHY
Authors: Popov Serhiy , Profatylo Anastasiia 
Published: October 2024

Introduction. Neonatal encephalopathy is one of the most common diseases in newborns. Several factors influence the development of neonatal encephalopathy including adverse obstetric history, fetal distress, meconium-containing amniotic fluid and cesarean section. In moderate and severe neonatal encephalopathy, damage to internal organs, local and systemic inflammation may occur. Cytokines, which are activated in the central nervous system and released in response to its damage, play an important role in brain inflammation caused by neonatal encephalopathy. C-reactive protein is also a possible biomarker of neonatal encephalopathy severity, being considered a protein of the innate immune system with anti-inflammatory properties. The state of the inflammatory response can be influenced by a local inflammatory reaction, as a result of which children with neonatal encephalopathy have been shown to have increased levels of fecal calprotectin in the first weeks of life. Also, one of the results of the transferred inflammatory reaction is a change in the composition of the neonatal intestinal microbiome.
Objective. To study risk factors for neonatal encephalopathy in newborns, the features of the relationship between local and systemic inflammatory response parameters in asphyxia of varying degrees, and the features of severity and control of inflammatory response parameters.
Materials and methods. The study was conducted in 119 full-term newborns, of which 87 children had neonatal encephalopathy and 32 healthy children. To determine the features of severity and control of inflammatory response parameters, group A was identified, which included 60 newborns, 46 of them with moderate neonatal encephalopathy, 14 with severe neonatal encephalopathy. The study was conducted using a culture method to determine the composition of the intestinal microbiome in feces. Using a semi-automated Thermo Scientific Multiskan FC enzyme immunoassay analyzer, the level of fecal calprotectin in feces and C-reactive protein and interleukins 1β and 10 in the blood serum were estimated by the enzyme immunoassay. The results were analyzed using SPSS version 28.0. The correlation between the parameters was analyzed using the Pearson correlation coefficient. The odds ratio was used to quantitatively describe the closeness of the relationship between the features in the statistical population. Binary logistic regression was used to determine the dependencies of the severity of the inflammatory reaction and create a model for calculating its severity.
Results. Risk factors for neonatal encephalopathy included mother’s acute respiratory infections and fetal distress. Bifidobacterium levels were positively correlated throughout the study, and there was also a relationship with lactobacilli in the control and non-probiotic treated neonatal encephalopathy groups. E. coli values were positively associated with opportunistic pathogens in the control and probiotic treated groups. Fecal calprotectin was negatively correlated with birth weight and height, Apgar scores, and gestational age. Fecal calprotectin levels were positively correlated with E. coli and opportunistic pathogens in healthy neonates. In children with neonatal encephalopathy interleukin 1β and 10 values were positively associated with fecal calprotectin, interleukin 1β were positively correlated with interleukin 10 and C-reactive protein.
Conclusions. The most significant risk factors for the development of neonatal encephalopathy are mother’s acute infectious diseases and fetal distress. The severity of hypoxia/asphyxia at birth correlated with the levels of interleukin 1β and 10 at 2 and 5 weeks of life, and Bifidobacterium at 2 weeks of life. The severity of the inflammatory response in the study population was characterized by a change in the level of interleukin 1β and Bifidobacterium at 2 weeks and a change in the level of interleukin 10 at 5 weeks