Comparative efects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis

Musemeche, Catherine A.; Kosloske, Ann M.; Bartow, Sue A.; Umland, Edith T.

doi:10.1016/s0022-3468(86)80228-7

Cited by 88 publications

(43 citation statements)

References 14 publications

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“…It is speculated that NEC occurs with the coincidence of two of the following three pathologic events: intestinal ischemia, colonization of the intestine by pathologic bacteria, and excess protein substrate in the intestinal lumen [10,11] . Bacterial colonization is necessary for the development of NEC [12,13] . When compared to term infants, VLBW infants at risk of NEC have abnormal fecal colonization, demonstrate a paucity of normal enteric bacterial species, and have delayed onset of bacterial colonization [14,15] .…”

Section: Introductionmentioning

confidence: 99%

Probiotics Reduce the Risk of Necrotizing Enterocolitis in Preterm Infants: A Meta-Analysis

AlFaleh¹,

Anabrees²,

Bassler³

2009

Neonatology

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Background: Necrotizing enterocolitis (NEC) is the most common serious acquired disease of the gastrointestinal tract in preterm infants. Probiotic bacteria are live microbial supplements that colonize the gastrointestinal tract and potentially provide benefit to the host. Objective: To compare the efficacy and safety of prophylactic enteral probiotics administration versus placebo or no treatment in the prevention of severe NEC and other morbidities in preterm infants. Methods: A meta-analysis was performed in accordance with the Cochrane Neonatal Review Group methods. Preterm infants <37 weeks’ gestational age and/or <2,500 g birth weight were included. Literature searches were made of MEDLINE, EMBASE, Cochrane Library Controlled Trials Register (CENTRAL), and abstracts of annual meetings of the Society for Pediatric Research and the European Society of Pediatric Research. Results: Nine eligible trials randomizing 1,425 infants were included. Included trials were highly variable with regard to enrollment criteria, baseline risk of NEC in the control groups, timing, dose, formulation of the probiotics, and feeding regimens. In a meta-analysis, enteral probiotics supplementation significantly reduced the incidence of severe NEC [typical RR 0.32 (95% CI 0.17, 0.60)] and mortality [typical RR 0.43 (95% CI 0.25, 0.75)]. There was no evidence of significant reduction of nosocomial sepsis [typical RR 0.93 (95% CI 0.73, 1.19)] or days on total parenteral nutrition [weighted mean difference –1.9 (95% CI –4.6, 0.77)]. The statistical test of heterogeneity for NEC, mortality and sepsis was insignificant. Data regarding extremely low birth weight infants (ELBW) could not be extrapolated. The included trials reported no systemic infection with the probiotics supplemental organism. Conclusion: Enteral supplementation of probiotics reduces the risk of severe NEC and mortality in preterm infants. A large randomized controlled trial is required to investigate the benefit and safety profile of probiotics supplementation in ELBW infants.

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Section: Introductionmentioning

confidence: 99%

Probiotics Reduce the Risk of Necrotizing Enterocolitis in Preterm Infants: A Meta-Analysis

AlFaleh¹,

Anabrees²,

Bassler³

2009

Neonatology

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“…The precise etiology and pathophysiology of NEC remain unclear. It has been suggested that many factors contribute to the development of NEC, including prematurity, intestinal ischemia, hypoxia, pathogenic bacterial colonization and enteral feeding [4,5,6]. Hypoxia is a common condition in the premature neonates and intestinal mucosa is one of the most sensitive tissue to the hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Effects of omeprazole and gentamicin on the biochemical and histopathological alterations of the hypoxia/ reoxygenation induced intestinal injury in newborn rats

et al. 2005

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We utilized a newborn rat model of hypoxia/reoxygenation (H/R) that resembles human necrotizing enterocolitis (NEC) to investigate the effects of omeprazole and/or gentamicin on the formation of free oxygen radicals (FOR) and bowel histopathology. For H/R, 1-day-old rats were placed into a chamber of 100% CO2 for 5 min, then they were reoxygenized for the next 5 min. The rats (n = 70) were divided into seven groups: group 1 (control), group 2 (H/R), group 3 (omeprazole), group 4 (H/R + omeprazole), group 5 (gentamicin), group 6 (H/R + gentamicin), group 7 (H/R + omeprazole + gentamicin). Gentamicin and/or omeprazole were given orally for 3 days, then all animals were killed; bowel specimens were harvested. Histopathologic injury scores (HIS) and malonyldialdehyde (MDA) and XO/(XO+XDH) rates (XO; xanthine oxidase, XDH; xanthine dehydrogenase) were measured, which reflect the FOR levels. In group 2, the HIS was significantly higher than groups 4 and 6. The mean MDA values in groups 1-7 were as follows: 54.16, 104.2, 56.85, 63.43, 62.31, 76.85, 79.13, respectively. The mean XO/(XO + XDH) levels were 0.306, 0.461, 0.286, 0.335, 0.323, 0.410, 0.375 from groups 1 -7, respectively. Group 2 rats had significantly more MDA and XO/(XO + XDH) rates versus other groups (P < 001). Histopathologic injury and biochemical results were significantly more severe in group 2 than in groups 4 and 6 (P < 001). There was no difference between groups 1 and 4 according to XO/(XO + XDH) rates. In newborn rats, H/R produces FOR, which cause serious intestinal damage. Omeprazole and/or gentamicin reduce biochemical and histopathologic bowel damage. This effect was more obvious in omeprazole treated rats. We think omeprazole may open new insights into the treatment of H/R related bowel injuries like NEC.

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“…In a rodent model of NEC, germ-free mice failed to develop NEC [5]. However, beyond this key finding, the interplay between bacteria and neonatal human host is still incompletely understood, and the precise bacterial triggers for NEC have yet to be found.…”

Section: Environmental Factors Bacteriamentioning

confidence: 99%

Pathogenesis of neonatal necrotizing enterocolitis

2015

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Although necrotizing enterocolitis (NEC) is the most lethal gastrointestinal disease in the neonatal population, its pathogenesis is poorly understood. Risk factors include prematurity, bacterial colonization, and formula feeding. This review examines how mucosal injury permits opportunistic pathogens to breach the gut barrier and incite an inflammatory response that leads to sustained overproduction of mediators such as nitric oxide and its potent adduct, peroxynitrite. These mediators not only exacerbate the initial mucosal injury, but they also suppress the intestinal repair mechanisms, which further compromises the gut barrier and culminates in bacterial translocation, sepsis, and full-blown NEC.

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Comparative efects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis

Cited by 88 publications

References 14 publications

Probiotics Reduce the Risk of Necrotizing Enterocolitis in Preterm Infants: A Meta-Analysis

Probiotics Reduce the Risk of Necrotizing Enterocolitis in Preterm Infants: A Meta-Analysis

Effects of omeprazole and gentamicin on the biochemical and histopathological alterations of the hypoxia/ reoxygenation induced intestinal injury in newborn rats

Pathogenesis of neonatal necrotizing enterocolitis

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