Necrotizing enterocolitis (NEC) is a life-threatening disease that predominantly affects very low birth weight preterm infants. Development of NEC in preterm infants is accompanied by high mortality. Surgical treatment of NEC can be complicated by short bowel syndrome, intestinal failure, parenteral nutrition-associated liver disease, and neurodevelopmental delay. Issues surrounding pathogenesis, prevention, and treatment of NEC remain unclear. This review summarizes data on prenatal risk factors for NEC, the role of pre-eclampsia, and intrauterine growth retardation in the pathogenesis of NEC. The role of hypoxia in NEC is discussed. Recent data on the role of the intestinal microbiome in the development of NEC, and features of the metabolome that can serve as potential biomarkers, are presented. The Pseudomonadota phylum is known to be associated with NEC in preterm neonates, and the role of other bacteria and their metabolites in NEC pathogenesis is also discussed. The most promising approaches for preventing and treating NEC are summarized.
BACKGROUND Necrotizing enterocolitis (NEC) is a multifactorial disease that predominantly affects premature neonates. Intestinal dysbiosis plays a critical role in NEC pathogenesis in premature neonates. The main risk factor for NEC in term infants is mesenteric hypoperfusion associated with ductal-dependent congenital heart disease (CHD) that eventually leads to intestinal ischemia. The incidence of NEC in neonates with critical CHD is 6.8%-13%. However, the role of the intestinal microbiome in NEC pathogenesis in infants with ductal-dependent CHD remains unclear. CASE SUMMARY A male term neonate with right atrial isomerism underwent modified Blalock-Taussig shunt placement on the 14 th day of life and had persistent mesenteric hypoperfusion after surgery. The patient had episodes of NEC stage IIA on the 1 st and 28 th days after cardiac surgery. Fecal microbial composition was analyzed before and after cardiac surgery by sequencing region V4 of the 16S rRNA gene. Before surgery, species belonging to genera Veillonella and Clostridia and class Gammaproteobacteria were detected, Bifidobacteriaceae showed a low abundance. The first NEC episode was associated with postoperative hemodynamic instability, intestinal ischemia-reperfusion injury during cardiopulmonary bypass, and a high abundance of Clostridium paraputrificum (Clostridium sensu stricto I ) (56.1%). Antibacterial therapy after the first NEC episode resulted in increased abundance of Gammaproteobacteria, decreased abundance of Firmicutes, and low alpha diversity. These changes in the microbial composition promoted the growth of Clostridium sensu stricto I (72.0%) before the second NEC episode. CONCLUSION A high abundance of Clostridium sensu stricto I and mesenteric hypoperfusion may have contributed to NEC in the present case.
Relevance of the research. Intrauterine growth restriction in children is associated with an increased risk of insulin resistance and non-insulin-dependent diabetes mellitus later in life. The influence of type of intrauterine growth restriction and the mechanisms of insulin resistance are still unknown; the role of catch-up growth in this process is controversial. The aim of the study was to identify insulin resistance in children with different types of intrauterine growth restriction and to analyze the role of catch-up growth in this process. Materials and methods. The research involved 95 newborns, which were divided into groups based on birth weight and length: 60 newborns with intrauterine growth restriction (group I – 31 with asymmetrical intrauterine growth restriction; group II – 29 with symmetrical intrauterine growth restriction) and control group (group III) – 35 newborns without intrauterine growth restriction. Children also were divided into groups according to the presence of catch-up growth to 3 months old. The levels of insulin, insulin-like growth factor-1, growth hormone were measured in cord blood at birth and in blood serum at 3 months old. Glucose levels were measured in serum and insulin resistance index “the homeostasis model assessment of insulin resistance” (HOMA-IR) was calculated in children at 3 months. Results. The children with intrauterine growth restrictioncompared to control group had significantly lower levels of insulin-like growth factor-1 in cord blood. The differences between types of intrauterine growth restrictionhave been observed: children with symmetrical intrauterine growth restriction had higher levels of growth hormone, insulin and HOMA-IR then in asymmetrical one. Correlations between insulin and glucose in children with symmetrical intrauterine growth restriction were absent unlike to asymmetrical intrauterine growth restriction (+0.61). The negative role of catch-up growth in insulin resistance development has been defined: it was related to hyperinsulinemia and increased the frequency of insulin resistance in children either in asymmetrical or in symmetrical intrauterine growth restriction, but more in symmetrical one. Conclusion. Children with symmetrical intrauterine growth restriction especially with catch-up growth are at the highest risk of metabolic syndrome development in later life and require increased monitoring by pediatricians and endocrinologists.
Necrotizing enterocolitis (NEC) is a serious complication in newborns with critical congenital heart disease (CHD), prolonging hospital stay, worsening neurological prognosis, and increasing mortality. The leading role in the pathogenesis of NEC in these infants is the violation of mesenteric perfusion. A decrease in arterial blood oxygenation may be an additional risk factor for intestinal hypoxia. Objective. To assess the incidence and risk factors for NEC in full-term newborns with CHD born in 2019–2021 at the Perinatal Center of Almazov National Research Medical Center. Patients and methods. The article presents an analysis of the frequency and risk factors of NEC in children with CHD born at the Almazov National Medical Research Centre in 2019–2021. In the group of critical and duct-dependent CHD (n = 264), the overall incidence of NEC was 15.9% (42 cases). The frequency of surgical stages of NEC (IIIA) was 1.1% (3 cases). In the preoperative period, there was a trend towards a higher frequency of inotropic therapy in a subgroup of children who subsequently developed NEC. NEC in newborns with duct-dependent CHD developed mainly in the early postoperative period after cardiac surgery. In children with duct-dependent pulmonary blood flow, a higher incidence of NEC after surgery was noted compared to children with duct-dependent systemic blood flow. Conclusion. Risk factors for NEC in the postoperative period were arterial hypotension and hemodynamically significant cardiac arrhythmias. Dysbiosis of the gut microbiota and changes in microbial metabolism may be additional risk factors for NEC in children with CHD. Key words: necrotizing enterocolitis, risk factors, congenital heart disease, cardiopulmonary bypass, intestinal microbiome, metabolomics
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