Disease relevance of Enterocolitis, Necrotizing

• More indomethacin-exposed infants had necrotizing enterocolitis (29 percent vs. 8 percent, P = 0.005), intracranial hemorrhage grade II to IV (28 percent vs. 9 percent, P = 0.02), and patent ductus arteriosus (62 percent, vs. 44 percent, P = 0.05) [1].
• BACKGROUND & AIMS: Platelet-activating factor (PAF) is a potent inflammatory mediator implicated in the pathogenesis of inflammatory bowel disease and necrotizing enterocolitis [2].
• CONCLUSIONS: Luminal perfusion of 1-day-old piglet jejunoileum with predigested and bile acid-solubilized preterm infant formula, in combination with ischemia/reperfusion, produces an animal model of necrotizing enterocolitis, but only if the lipid fraction of the formula is present [3].
• Prednisone therapy was instituted, but her disease was further complicated by the development of necrotizing enterocolitis [4].
• In the setting of intestinal vasculitis due to SLE or polyarteritis nodosa, these characteristic radiologic features indicate necrotizing enterocolitis [5].

High impact information on Enterocolitis, Necrotizing

• Tumor necrosis factor alpha in the pathophysiology of necrotizing enterocolitis [6].
• Prevention of necrotizing enterocolitis in the rat with prenatal cortisone [7].
• We have previously shown that injection of platelet-activating factor causes necrotizing enterocolitis in the rat and that platelet-activating factor is an endogenous mediator in lipopolysaccharide-induced bowel necrosis [8].
• Moreover, plasma TNF levels are elevated in patients with necrotizing enterocolitis [9].
• A novel urease-negative Helicobacter species associated with colitis and typhlitis in IL-10-deficient mice [10].

Chemical compound and disease context of Enterocolitis, Necrotizing

• PAF-acether in necrotizing enterocolitis [11].
• Urine from another 13 neonates without necrotizing enterocolitis who did not receive iohexol was collected [12].
• In pathogenicity tests in 1-day-old chicks and 14-month-old hens, chicken spirochete 91-1207/C1 produced pale-yellow, watery cecal contents and mild lymphocytic typhlitis [13].
• Changes in the gastrointestinal microflora were noted in 22 infants during combined topical and parenteral antimicrobial therapy for necrotizing enterocolitis (NEC) [14].
• These changes may limit the normal adaptation to vasoconstriction, thus exacerbating the already insufficient compensatory mechanisms for responding to ischemic injury, and thus may be one of the important factors predisposing cocaine-exposed infants to necrotizing enterocolitis [15].

Biological context of Enterocolitis, Necrotizing

• Cellular localization of tumor necrosis factor (TNF)-alpha transcripts in normal bowel and in necrotizing enterocolitis. TNF gene expression by Paneth cells, intestinal eosinophils, and macrophages [9].
• OBJECTIVES: To determine whether supplementation with L -arginine reduces the incidence of all stages of necrotizing enterocolitis (NEC) in premature infants with birth weight < or =1250 g and gestational age < or =32 weeks [16].
• Genetic polymorphisms of CD14, toll-like receptor 4, and caspase-recruitment domain 15 are not associated with necrotizing enterocolitis in very low birth weight infants [17].
• The oral absorption of neomycin was studied in 2 premature infants (32 weeks of gestation) with suspected necrotizing enterocolitis [18].
• In the present study we examined the effect of recombinant human erythropoietin (rhEPO) on intestinal malondialdehyde (MDA) as an index of lipid peroxidation, related to iron-catalysed free radical reaction and platelet-activating factor (PAF) synthesis in the experimental model of necrotizing enterocolitis (NEC) [19].

Anatomical context of Enterocolitis, Necrotizing

• Since vitamin A is involved in the promotion of mucous-secreting cells, the premature neonate may be at greater risk than the term infant for diseases involving the mucosal epithelium, including necrotizing enterocolitis [20].
• Overproduction/accumulation of short chain fatty acids, but not lactic acid, in the proximal colon and/or distal ileum may play a role in the pathogenesis of necrotizing enterocolitis in premature infants [21].
• The use of indomethacin to treat patent ductus arteriosus in preterm infants may either decrease the incidence of necrotizing enterocolitis by stabilizing or closing the ductus arteriosus or increase its incidence by a direct constricting effect on mesenteric blood vessels [22].
• BACKGROUND/PURPOSE: Because epidermal growth factor (EGF) is trophic to the intestinal mucosa, and neonatal necrotizing enterocolitis (NEC) is associated with a disrupted intestinal mucosal barrier, the authors sought to determine whether diminished levels of EGF were present in infants with NEC [23].
• Does maternal nicotine exposure during gestation increase the injury severity of small intestine in the newborn rats subjected to experimental necrotizing enterocolitis [24].

Gene context of Enterocolitis, Necrotizing

• Intestinal and hepatic expression of BNIP3 in necrotizing enterocolitis: regulation by nitric oxide and peroxynitrite [25].
• Matrilysins-1 and -2 (MMP-7 and -26) and metalloelastase (MMP-12), unlike MMP-19, are up-regulated in necrotizing enterocolitis [26].
• Erythropoietin protects against necrotizing enterocolitis of newborn rats by the inhibiting nitric oxide formation [27].
• Epidermal growth factor reduces the development of necrotizing enterocolitis in a neonatal rat model [28].
• OBJECTIVES: To evaluate the relationship between the severity of necrotizing enterocolitis (NEC) and circulating concentrations of proinflammatory cytokines interleukin (IL)-1beta and IL-8 and counterinflammatory cytokines IL-1 receptor antagonist (IL-1ra) and IL-10 [29].

Analytical, diagnostic and therapeutic context of Enterocolitis, Necrotizing

• Since the outbreaks of neonatal necrotizing enterocolitis occurring in maternity hospitals of Paris and suburbs in 1979-1980, it has been possible to examine by light and electron microscopy gut specimens from ten newborns with this illness [30].
• We attribute the low incidence of necrotizing enterocolitis in our experience to delay of enteral feedings and reliance on prolonged peripheral or central total parenteral nutrition, or both, for nutritional maintenance of stressed or low birth weight infants [31].
• The incidence of respiratory distress syndrome, need for surfactant treatment, patent ductus arteriosus, necrotizing enterocolitis, and intraventricular hemorrhage was similar between the indomethacin-exposed group and the control group [32].
• CONCLUSION: Tocolysis with indomethacin as a single agent was not associated with necrotizing enterocolitis in this case-control study [33].
• Two cases of typhlitis have occurred after combined treatment with taxol and doxorubicin, while typhlitis has not been described after treatment with either drug alone [34].

References