Neonatal Necrotizing Enterocolitis

Brown, Edwin G.; Sweet, Avron Y.

doi:10.1016/s0031-3955(16)34252-3

Cited by 93 publications

(34 citation statements)

References 39 publications

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“…Neonatal rat intestine will peroxidize HM, supporting the presence of reactive oxygen species in the gut (20). The release of oxygen radicals by the intestine has been implicated in the pathology of necrotizing enterocolitis (21). Early feeding of HM reduces the incidence of necrotizing enterocolitis in the premature infant (22).…”

Section: Discussionmentioning

confidence: 98%

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

et al. 2002

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Section: Discussionmentioning

confidence: 98%

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

et al. 2002

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“…Clustering suggested nosocomial infection with a remarkable variation in incidence between hospitals [22] . An impressive list of etiologic proposals has been published, some of which are shown chronologically in table 1 .…”

Section: Putative Causes and Pathogenesismentioning

confidence: 99%

Necrotizing Enterocolitis – 150 Years of Fruitless Search for the Cause

Obladen¹

2009

Neonatology

126

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Necrotizing enterocolitis (NEC) is not a new disease but one that has been reported since special care units began to house preterm infants. It was observed in foundling hospitals in Paris [Billard, 1828] and Vienna [Bednar, 1850] and, as it occurred in clusters, was regarded as a nosocomial infection in the infant hospitals of Zurich [Willi, 1944] and Berlin [Ylppö, 1931]. Clinical and patho-anatomic characterization was achieved by Schmidt and Quaiser in 1952. The unproven hypothesis of mesenteric hypoperfusion as a major etiological factor arose from animal models and analogous perforating disorders in term infants. Despite similarities between NEC and clostridial infections, few studies employed anaerobic culture techniques. The pathogenesis remains unclear and its distinction from related disorders uncertain. It is unlikely that strategies to prevent NEC will be successful unless the disease is better understood.

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“…Reperfusion of the intestine is often associated with increases in vascular [1] and mucosal [2] permeability. The etiology of necrotizing enterocolitis (NEC) is probably multifactorial, involving intestinal ischemia, intraluminal substrate, and bacterial infection to varying degrees in individual patients [3]. The pathogenic mechanisms involved have been the focus of recent investigations.…”

Section: Introductionmentioning

confidence: 99%

Effect of N<sup>G</sup>-Nitro-<i>L</i>-Arginine Methyl Ester on Intestinal Permeability following Intestinal Ischemia-Reperfusion Injury in a Rat Model

et al. 2001

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Subclinical intestinal ischemia-reperfusion injury (IRI) causes an increase in mucosal permeability and may represent an early event in the pathogenesis of necrotizing enterocolitis in premature infants. Previous studies suggested that continuous, endogenous formation of nitric oxide (NO) maintains the mucosal integrity of the intestine, thus protecting the gut from injuries from blood-borne toxins and tissue-destructive mediators. This study was undertaken to assess whether the inhibition of NO production causes an increase in intestinal permeability in rats following IRI. Sprague-Dawley rats weighing 200–300 g were divided into 4 groups: (1) untreated group (normal control); (2) ischemia-reperfusion group; (3) early N^G-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of NO production, treatment group, and (4) late L-NAME treatment group. Transient IRI was induced by 30-min occlusion, followed by reperfusion of the isolated ileal loop. The L-NAME was administered 15 min before and after mesenteric ischemia as a 25-mg/kg bolus. Fluorescein isothiocyanate-dextran (FITC-D) was used to quantitatively assess the alteration in mucosal permeability of the intestine. There was no significant increase in the portal vein FITC-D level among normal controls, ischemia-reperfusion group and late L-NAME-treated group, but there was an approximately 6-fold increase in the early L-NAME treatment group. The pathological features of the intestine following IRI include denudation of the villus epithelium and reduction of villus height, associated with marked inflammatory cell infiltration over the lamina propria. These results suggest that endogenous NO may play a role in the protecting intestinal integrity after IRI.

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Neonatal Necrotizing Enterocolitis

Cited by 93 publications

References 39 publications

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

Necrotizing Enterocolitis – 150 Years of Fruitless Search for the Cause

Effect of N<sup>G</sup>-Nitro-<i>L</i>-Arginine Methyl Ester on Intestinal Permeability following Intestinal Ischemia-Reperfusion Injury in a Rat Model

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