In necrotizing enterocolitis (NEC) the small (most often distal) and/or large bowel becomes injured, develops intramural air, and may progress to frank necrosis with perforation. Even with early, aggressive treatment, the progression of necrosis, which is highly characteristic of NEC, can lead to sepsis and death. This article reviews the current scientific knowledge related to the etiology and pathogenesis of NEC and discusses some possible preventive measures.

Necrotizing enterocolitis (NEC) afflicts extremely low birth weight neonates, and probiotics reduces its incidence and severity. NO is involved in the pathogenesis of NEC, and caveolin-1 regulates NO signaling. We tested the hypothesis that intestinal caveolin-1 and NOS are deficient in formula-fed neonatal rats and that supplementation with "Florastar Kids" and/or galactooligosaccharides and fructo-oligosaccharides preserves caveolin-1 and NOS. At birth (P0), neonatal rat pups were maternally fed or hand-gavaged with or without supplemented formula. Samples from the terminal ileum were analyzed for total NO metabolites, growth factors, and gene expression of caveolin-1, NOS isoforms, and antioxidants. Our data showed that formula feeding with and without supplementation resulted in significant growth restriction. Despite suboptimal nutrition, growth factors involved in intestinal repair and regeneration were increased in the neonatal rat ileum. Caveolin-1, endothelial NOS, and neuronal NOS were simultaneously downregulated with formula feeding while inducible NOS was upregulated. Superoxide dismutase and glutathione peroxidase were up-regulated with supplementation. These data provide a probable mechanism for the benefits of supplemented formula for decreasing the severity of NEC by preserving the antioxidant systems. (Pediatr Res 67: 526-531, 2010)

No abstract