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enterocolitis/carbohydrate
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Carbohydrate malabsorption in necrotizing enterocolitis.
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A prospective investigation was conducted to determine if infants with necrotizing enterocolitis had evidence of carbohydrate intolerance prior to the onset of clinical symptoms of advanced disease. Stool specimens were examined for fecal reducing substances with Clintest tablets from well,
Carbohydrate maldigestion induces necrotizing enterocolitis in preterm pigs.
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Necrotizing enterocolitis (NEC) remains the most severe gastrointestinal disorder in preterm infants. It is associated with the initiation of enteral nutrition and may be related to immature carbohydrate digestive capacity. We tested the hypothesis that a formula containing maltodextrin vs. a
[Absorption of carbohydrates in children with chronic enterocolitis].
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Absorption of carbohydrates was studied over time (according to the D-xylose test in 140 patients. Excretion of D-xylose with urine was found to be lowered in the overwhelming majority of the patients both during exacerbation and remission. Absorption of D-xylose was established to depend on the
Colonic fermentation of carbohydrate in the premature infant: possible relevance to necrotizing enterocolitis.
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[Comparative data on disorders of carbohydrate metabolism in acute and chronic enterocolitis].
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Necrotising enterocolitis: the state of the science.
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Necrotizing enterocolitis is the most common gastrointestinal emergency of the neonate, affecting 5-10% of infants, yet the pathogenesis remains unclear. Widely accepted risk factors include prematurity, enteral feeds, bacterial colonization and mucosal injury. How these or other yet identified
[Pathogenetic concepts of neonatal necrotizing enterocolitis].
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The pathogenesis of neonatal necrotizing enterocolitis is still unknown today. Only prematurity has been confirmed as a primary risk factor. Previous studies demonstrated the special pathophysiological conditions in prematurity. Differences in intestinal permeability, blood flow in anemia and
Endemic necrotizing enterocolitis: lack of association with a specific infectious agent.
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We conducted a comprehensive analysis of bacterial, parasitic and viral agents present in stool samples of 23 necrotizing enterocolitis cases and 23 matched and 10 random controls. Enterococcus spp., Staphylococcus epidermidis, and Escherichia coli were the most common aerobic bacterial species
Low-fat, high-carbohydrate parenteral nutrition (PN) may potentially reverse liver disease in long-term PN-dependent infants.
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BACKGROUND
Parenteral nutrition-associated cholestasis (PNAC) is a complication of long-term parenteral nutrition (PN). Removal of lipids may reverse PNAC but compromises the energy to ensure infant growth. The purpose of this study was to test whether a low-fat, high-carbohydrate PN regimen, which
Metabolomic signatures distinguish the impact of formula carbohydrates on disease outcome in a preterm piglet model of NEC.
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Major risk factors for necrotizing enterocolitis (NEC) include premature birth and formula feeding in the context of microbial colonization of the gastrointestinal tract. We previously showed that feeding formula composed of lactose vs. corn syrup solids protects against NEC in preterm pigs;
Feeding associated neonatal necrotizing enterocolitis (Primary NEC) is an inflammatory bowel disease.
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Neonatal necrotizing enterocolitis which develops after feeding preterm infants is characterized by severe intestinal inflammation and profound systemic metabolic acidosis. The fermentation of undigested dietary carbohydrate by colonic flora yields gases (CO2 and H2) and short chain organic acids.
Necrotizing enterocolitis: intraluminal biochemistry in human neonates and a rabbit model.
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The intestinal contents of 17 neonates with necrotizing enterocolitis were analyzed for pH, carbohydrate, protein, and bacteria. The intraluminal pH was less than 5.0 (16/17). Sufficient carbohydrate and bacteria capable of fermenting the carbohydrate to organic acids were found. The intraluminal
An intraluminal model of necrotizing enterocolitis in the developing neonatal piglet.
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The most common risk factors for the development of necrotizing enterocolitis (NEC) are prematurity and enteral feeding. Most models of NEC involve ischemic insult resulting in generalized necrosis, different from the classical ileocecal predilection of NEC. This anatomic predisposition is explained
Bacterial community structure and functional contributions to emergence of health or necrotizing enterocolitis in preterm infants.
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BACKGROUND
Preterm infants represent a unique patient population that is born functionally immature and must accomplish development under the influence of a hospital environment. Neonatal necrotizing enterocolitis (NEC) is an inflammatory intestinal disorder affecting preterm infants. The purpose of
Pulmonary Epithelial TLR4 Activation Leads to Lung Injury in Neonatal Necrotizing Enterocolitis.
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We seek to define the mechanisms leading to the development of lung disease in the setting of neonatal necrotizing enterocolitis (NEC), a life-threatening gastrointestinal disease of premature infants characterized by the sudden onset of intestinal necrosis. NEC development in mice requires
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