Abstract
Necrotizing enterocolitis (NEC) is one of the most severe and unpredictable complications of prematurity. There are two possible mechanisms involved in the pathogenesis of NEC: individual inflammatory response and impaired blood flow in mesenteric vessels with secondary ischemia of the intestine. The aim of this study was to evaluate the possible relationship between polymorphisms: Il-1β 3953C>T, Il-6 −174G>C and −596G>A, TNFα −308G>A, and 86 bp variable number tandem repeat polymorphism of interleukin-1 receptor antagonist (Il-1RN VNTR 86 bp) and three polymorphisms that may participate in arteries tension regulation and in consequence in intestine blood flow impairment: eNOS (894G>T and −786T>C) and END-1 (5665G>T) and NEC in 100 infants born from singleton pregnancy, before 32 + 0 weeks of gestation, exposed to antenatal steroids therapy, and without congenital abnormalities. In study population, 22 (22%) newborns developed NEC. Surgery-requiring NEC was present in 7 children. Statistical analysis showed 20-fold higher prevalence of NEC in infants with the genotype TT [OR 20 (3.71–208.7); p = 0.0004] of eNOS 894G>T gene polymorphism. There was a higher prevalence of allele C carriers of eNOS 786T>C in patients with surgery-requiring NEC [OR 4.881 (1.33–21.99); p = 0.013]. Our investigation did not confirm any significant prevalence for NEC development in another studied genotypes/alleles. This study confirms the significant role of polymorphisms that play role in intestine blood flow. Identifying gene variants that increase the risk for NEC development may be useful in screening infants with inherent vulnerability and creating strategies for individualized care.
Highlights
Necrotizing enterocolitis (NEC) is one of the most severe and unpredictable complications of prematurity
The aim of this study was to evaluate the possible relationship between polymorphisms: interleukin 1b (Il-1b) 3953C[T, interleukin 6 (Il-6) -174G[C and -596G[A, TNFa -308G[A, and 86 bp variable number tandem repeat polymorphism of interleukin-1 receptor antagonist (Il-1RN VNTR 86 bp) and three polymorphisms that may participate in arteries tension regulation and in consequence in intestine blood flow impairment: eNOS (894G[T and -786T[C) and endothelin 1 (END-1) (5665G[T) and NEC in 100 infants born from singleton pregnancy, before 32 ? 0 weeks of gestation, exposed to antenatal steroids therapy, and without congenital abnormalities
Identifying gene variants that increase the risk for NEC development may be useful in screening infants with inherent vulnerability and creating strategies for individualized care
Summary
Necrotizing enterocolitis (NEC) is one of the most severe and unpredictable complications of prematurity. There are two possible mechanisms involved in the pathogenesis of NEC: individual inflammatory response and impaired blood flow in mesenteric vessels with secondary ischemia of the intestine. A baseline increased reactivity of the premature intestinal mucosa to microbial ligands leads to increased and flawed inflammatory response [5, 6] The proof of this theory seems to be the fact that plasma concentrations and tissue expression of the proinflammatory cytokines interleukin 1b (Il-1b) and interleukin 6 (Il-6), as well as tumor necrosis factor alpha (TNF-a) [7], are elevated in neonates with NEC [8, 9]. Nitric oxide synthase is crucial for intestinal microcirculation and it may play a key role in the pathogenesis of NEC [16]. Endothelin 1 (END-1) is the strongest known vasoconstrictor and plays a major role in maintaining hemodynamic homeostasis by changing the distribution of blood in the system [17]
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