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PubMed2004

Interferon-alpha reduces the development of experimental necrotizing enterocolitis.

Cytokines had important role in the pathogenesis of necrotizing enterocolitis (NEC). The aim of this study is to investigate if IFN-alpha has a prophylaxic effect on experimental NEC development in newborn rat pups. Twenty eight Wistar Albino newborn rat pups were divided into three groups. Control group rats were breast-fed, NEC group and interferon (IFN) group rat pups were hand-fed with premature newborn formula. IFN-alpha was administered subcutaneously at a dose of 50,000 IU/rat/day in IFN group. NEC was induced experimentally by cold stress twice a day in IFN and NEC groups. On the fourth day, the rats were killed, and all the intestine were removed to determine the tissue level of malonaldehyde (MDA) and histologic changes. The microscopic lesions in the NEC group rats were virtually the same as those seen in neonatal NEC, with severe separation of submucosa and/or lamina propria, loss of villi and in some cases necrosis to extention the muscularis. In contrast, in the rats treated with IFN, lesions were moderate separation of submucosa and/or lamina propria, edema in submucosal and muscular layers. Intestinal injury score and MDA levels in NEC group were significantly higher than in the IFN group (P<0.05). In conclusion it was suggested that IFN-alpha was effective in reducing the severity of NEC in rat pups.

Animals↗
PubMed2004

The role of the glutathione antioxidant system in gut barrier failure in a rodent model of experimental necrotizing enterocolitis.

BACKGROUND: Evidence suggests that intestinal barrier failure in necrotizing enterocolitis results in part from overproduction of nitric oxide and other toxic oxidant species that result in enterocyte death and intestinal barrier failure. We hypothesize that the glutathione detoxifying system is important in maintaining intestinal barrier integrity by protecting against nitrosative stress. METHODS: Newborn rats were subjected to hypoxia (5% O2, tid) and fed formula by gavage (NEC), or were breast-fed without hypoxia (BF). Rats were killed and the distal ilea were harvested for RNA, protein, and morphologic studies. RNA underwent cDNA microarray analysis. To assess glutathione in protecting against nitrosative stress, IEC-6 cells were exposed to SIN-1 and/or L-buthionine-(S,R)-sulfoximine (BSO), a glutathione inhibitor. Cells were analyzed for glutathione-S-transferase activity, apoptosis and mitochondrial function. RESULTS: BF controls developed normal intestinal architecture, whereas NEC animals sustained damage to the intestinal epithelium. Microarray analysis demonstrated that 93 genes were overexpressed in NEC compared with controls. In the array, glutathione-S-transferase pi and alpha 2, GSH-dependent detoxifying enzymes, RNA were upregulated compared with BF controls. IEC-6 cells exposed to SIN-1/BSO produced an increase in apoptosis. Poly ADP-ribosylpolymerase cleavage and apoptosis-inducing factor (AIF) nuclear localization, markers of apoptosis, were seen in IEC-6 cells exposed to SIN-1/BSO as opposed to media controls. CONCLUSION: These data support the hypothesis that GSH antioxidant system plays a crucial role in gut barrier protection by attenuating enterocyte death.

Animals↗
PubMed1999

Bifidobacterial supplementation reduces the incidence of necrotizing enterocolitis in a neonatal rat model.

BACKGROUND & AIMS: Neonatal necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature infants partly caused by intestinal bacterial proliferation. Because bifidobacteria are thought to reduce the risk for intestinal disturbances associated with pathogenic bacterial colonization, we hypothesized that exogenous bifidobacterial supplementation to newborn rats would result in intestinal colonization and a reduction in the incidence of neonatal NEC. METHODS: Newborn rat pups were given Bifidobacterium infantis (10(9) organisms per animal daily), Escherichia coli, or saline control and exposed to the NEC protocol consisting of formula feeding (Esbilac; 200 cal. kg(-1). day(-1)) and asphyxia (100% N(2) for 50 seconds followed by cold exposure for 10 minutes). Outcome measures included stool and intestinal microbiological evaluation, gross and histological evidence of NEC, plasma endotoxin concentration, intestinal phospholipase A(2) expression, and estimation of intestinal mucosal permeability. RESULTS: Bifidobacterial supplementation resulted in intestinal colonization by 24 hours and appearance in stool samples by 48 hours. Bifidobacteria-supplemented animals had a significant reduction in the incidence of NEC compared with controls and E. coli-treated animals (NEC, 7/24 B. infantis vs. 19/27 control vs. 16/23 E. coli; P < 0.01). Plasma endotoxin and intestinal phospholipase A(2) expression were lower in bifidobacteria-treated pups than in controls, supporting the role of bacterial translocation and activation of the inflammatory cascade in the pathophysiology of NEC. CONCLUSIONS: Intestinal bifidobacterial colonization reduces the risk of NEC in newborn rats.

Animals↗
PubMed2002

Long-term follow-up of patients with necrotizing enterocolitis.

BACKGROUND/PURPOSE: Despite the rise in the incidence of necrotizing enterocolitis (NEC), there is a paucity of data regarding long-term patient outcome. The authors examined functional outcome of infants with NEC (n = 103) treated at our institution between 1991 and 1995. METHODS: The authors reviewed the medical records of infants who were treated both operatively and nonoperatively, n = 103. Variables examined included gestational age, birth weight, Bell stage (I through III), operations performed, and mortality rate. Telephone interviews assessed school enrollment, developmental delay, bowel function, and nutritional status. RESULTS: Children treated operatively had a lower gestational age than those in the nonoperative group. Likewise, birth weight in the operative group was significantly lower. Sixty-three percent of patients had stage III, and the remainder had stage II disease. The telephone response rate was 61%. Mean age at follow-up was 7.5 +/- 2.5 years. All children ate by mouth. Nearly all children were toilet trained. All children were less than the 50th percentile for height and weight, and the majority (83%) were enrolled in school full time. CONCLUSION: Infants with stage II and III NEC who are treated operatively or nonoperatively have a favorable long-term outcome.

Body Height↗
PubMed2000

Reduced serum amino acid concentrations in infants with necrotizing enterocolitis.

OBJECTIVE: To determine whether premature infants who have necrotizing enterocolitis (NEC) have deficiencies in glutamine (GLN) and arginine (ARG), which are essential to intestinal integrity. STUDY DESIGN: A 4-month prospective cohort study of serum amino acid and urea levels in premature infants was done. Serum amino acid and urea levels were measured by high-pressure liquid chromatography and enzymatic methods, respectively, on samples obtained on days of life 3, 7, 14, and 21. RESULTS: Infants in the control (n = 32) and NEC groups (n = 13) were comparable for birth weight, gestational age, and Apgar scores. NEC began on mean day of life 14.5 (95% CI, day of life 11 to 18). Median values of GLN were 37% to 57% lower in the NEC group on days 7, 14, and 21 compared with those in the control group (P <.05). On days 7 and 14, median values of ARG, GLN, alanine, lysine, ornithine, and threonine were decreased 36% to 67% (P <.05) in the NEC group. Total nonessential amino and total essential amino acids were 35% to 50% lower in the NEC group on days 7 and 14 (P <.05). Infants in the NEC group had significant reductions in GLN and ARG 7 days before the onset of NEC. CONCLUSIONS: Infants who have NEC have selective amino acid deficiencies including reduced levels of GLN and ARG that may predispose to the illness.

Age Factors↗
PubMed2004

Early intestinal bacterial colonization and necrotizing enterocolitis in premature infants: the putative role of Clostridium.

Necrotizing enterocolitis (NEC) is among the most severe conditions that can affect preterm infants. Although the etiology of NEC remains unknown, initial bacterial colonization could play a pivotal role in the development of NEC. To further explore the putative relationship between pathogen microorganisms and NEC, we conducted a prospective case-control study in 12 preterm infants with a new approach based on molecular techniques. Over an inclusion period of 24 mo, 12 neonates of <34 wk gestational age admitted to the neonatal unit were enrolled. The group included three cases of NEC, and nine control infants without evidence of NEC who were matched for gestational age and birth weight. Stool samples were collected at weekly intervals from all infants. PCR and temporal temperature gradient gel electrophoresis of 16S ribosomal DNA were used to detect the establishment of bacterial communities in the digestive tract. A salient feature of the bacteriological pattern was observed only in the three infants who later developed NEC: A band corresponding to the Clostridium perfringens subgroup could be detected in early samples, before diagnosis. There was no evidence for this specific band in any of the nine controls. To our knowledge, the current report is the first to demonstrate that the use of molecular techniques based on the study of bacterial 16S rRNA genes allowed the recognition of C. perfringens species in the first 2 wk of life of three infants who later displayed symptoms of NEC. A significant temporal relationship was thus established between early colonization by Clostridium and the later development of NEC. Compared with conventional bacteriological culturing methods, the use of this new molecular approach to analyze the gastrointestinal ecosystem should therefore allow a more complete and rapid assessment of intestinal flora. Although the current data do not constitute definitive proof that the identified bacterial species was a causative agent in the development of NEC, they outline the promise of this new technique based on molecular biology, and suggest that large-scale studies on a much wider population at high risk for NEC may be warranted.

Birth Weight↗
PubMed2006

Genetic basis for necrotizing enterocolitis--risk factors and their relations to genetic polymorphisms.

Necrotizing enterocolitis (NEC) is a common, life-threatening neonatal gastrointestinal disease; it affects approximately 11% of extremely premature neonates. The etiology of NEC is multifactorial. Risk factors may roughly be grouped into four main categories: prematurity; transient ischemia of the intestine; local/systemic inflammation predisposing the bowel to injury, and therapeutic interventions. Recent studies have shown that carrier state of genetic polymorphisms may be associated with perinatal morbidity, including NEC. In perinatal disorders, the significance of genetic variants of cytokines, the renin-angiotensin-aldosterone system, and surfactant proteins have been investigated most widely. Positive findings indicate the implication of genetic polymorphisms of proinflammatory cytokines in premature birth; angiotensin converting enzyme in perinatal adaptation and angiotensin type 1 receptor in the closure of ductus arteriosus; surfactant proteins A and B in respiratory distress syndrome; interleukin (IL)-6 in sepsis, and IL-4-receptor alpha chain and IL-18 in NEC. This review provides an insight into the genetics of NEC and summarizes genetic data in light of pathologic processes leading to NEC.

Chorioamnionitis↗
PubMed2000

A cluster of necrotizing enterocolitis in term infants undergoing open heart surgery.

BACKGROUND: Necrotizing enterocolitis (NEC) is a serious gastrointestinal disease of unknown cause that predominantly affects premature infants, but it has been reported in term infants with congenital heart disease. METHODS: In August and September of 1997, 4 cases of NEC in term infants with congenital heart disease were identified among 24 infants undergoing cardiac surgical procedures at our institution. Because nosocomial NEC had not previously been identified among infants in our pediatric intensive care unit, a case-control study was conducted to identify risk factors for NEC. All infants less than 4 months old undergoing cardiac surgery without development of NEC during the epidemic period were selected as controls. RESULTS: The only significant risk factor associated with case-infants was a higher mean temperature gradient (rectal/toe) during the immediate 12-hour postoperative period (4.0 degrees C vs 2.0 degrees C, P <.01). Urine output was higher in control-infants in this postoperative period, although not statistically significant (11.9 mL/h vs 6.1 mL/h, P =.15). CONCLUSION: Although an infectious etiology cannot be ruled out, the cases of NEC in infants with congenital heart disease after cardiac procedures may have resulted from mesenteric ischemia associated with a low perfusion state in the perioperative period.

Anti-Bacterial Agents↗
PubMed2001

Intestinal permeability in newborns with necrotizing enterocolitis and controls: Does the sugar absorption test provide guidelines for the time to (re-)introduce enteral nutrition?

BACKGROUND: In necrotizing enterocolitis (NEC), (sub)mucosal edema, hemorrhage, ulceration, or necrosis will disturb intestinal integrity, as reflected by an increased intestinal permeability. Enteral substrate is therefore withheld for a variable period up to 3 weeks (in many clinics). The authors used the sugar absorption test to measure intestinal permeability changes in surgically treated necrotizing enterocolitis patients and surgical controls to evaluate the usefulness of this test in timing the (re-)introduction of enteral feeding in NEC patients as intestinal integrity recovers. METHODS: Changes in intestinal permeability to lactulose and rhamnose were evaluated prospectively in 13 children with NEC and 10 operated control patients. The patients were given 1 mL/kg body weight lactulose/rhamnose solution at different time intervals after admission. The lactulose to rhamnose (L/R) ratio was determined by gaschromatography in 4-hour urine samples. RESULTS: The L/R ratios in NEC patients were increased for prolonged periods of time with a tendency to decrease in the third week after the start of NEC. However, in some cases, the increased L/R ratios even exceeded the 3-week period of starvation. High peaks in the L/R ratio were seen in patients suffering from bowel perforation or sepsis. Compared with necrotizing enterocolitis patients, L/R ratios of control patients were increased only in the first days after surgery and normalized more rapidly. The results of the L/R tests in this study corroborated the clinical condition of the patients. CONCLUSIONS: The sugar absorption test shows an individual variability in the recovery of intestinal permeability in a group of seriously ill newborns with advanced stages of NEC. An individual approach in restarting enteral nutrition seems to be justified; however, the optimal time-point to restart enteral nutrition cannot be determined by the sugar absorption test alone. Combining parameters of intestinal integrity and function could enable a more accurate determination of this optimal timepoint. J Pediatr Surg 36:587-592.

Capillary Permeability↗
PubMed1990

Neonatal necrotizing enterocolitis associated with delta toxin-producing methicillin-resistant Staphylococcus aureus.

Delta toxin-producing coagulase-negative staphylococci previously have been associated with necrotizing enterocolitis in neonates. We identified three preterm infants (body weight, 845 +/- 59 g) infected with methicillin-resistant Staphylococcus aureus (MRSA) who had a similar clinical syndrome, characterized by pustular dermatitis, bacteremia and necrotizing enterocolitis accompanied by gastric residua, abdominal distention, hematochezia and pneumatosis intestinalis. MRSA was recovered from all three infants at infected skin sites, blood or venous catheters and from two of three infants in stool specimens. Two infants also had Staphylococcus epidermidis isolated from stool. All MRSA isolates had identical microbiologic profiles: four plasmids with identical molecular weights; coproduction of enterotoxins A and B; and the same antibiotic susceptibilities. Of one skin isolate, two blood isolates and two stool isolates of MRSA that were tested, all had characteristic delta toxin hemolytic activity. All culture supernatants of these isolates evaluated for delta toxin were positive by Western blot analysis. The two strains of S. epidermidis isolated from stool were negative for delta-like toxin by a standardized enzyme-linked immunoassay. The clustering of these cases, the similarity of the clinical syndrome, and the prior association of necrotizing enterocolitis with delta-like toxins produced by S. epidermidis, suggest that delta toxin-producing MRSA (or other S. aureus isolates) also may be etiologic agents in some cases of necrotizing enterocolitis in newborns.

Bacterial Toxins↗
PubMed1989

[Total colectomy in necrotizing enterocolitis].

Total colectomy in the neonatal period, after a necrotizing enterocolitis is not infrequent and implies a series of complex attitudes towards a good adaptation of the remaining small bowel. We present 9 cases of total colectomy in children with necrotizing enterocolitis of 11 cases surgically treated out of 57 cases. We describe the different types of surgical procedures used as well as the evolution of each patient.

Colectomy↗
PubMed1978

Relationships of mesenteric thromboembolism, oral feeding, and necrotizing enterocolitis.

Mesenteric blood vessels were examined in postmortem specimens of 30 selected infants. The infants had had necrotizing enterocolitis (16 cases) or other lesions (14 cases). Mesenteric thromboemboli were observed in 12 of the infants with necrotizing enterocolitis (P less than 0.001). Umbilical vessel catheters were apparently responsible for the emboli. Multiple instances of thrombosis and thromboembolism were detected in other organs. Ninety-four percent of infants with necrotizing enterocolitis were orally fed (P less than 0.001). Mesenteric thromboemboli were more frequent in infants who were fed via the digestive route while an umbilical arterial catheter was in place. Mesenteric thromboembolism in these infants was postulated to have been attributable to increased postprandial blood flow in the mesenteric vessels.

Catheterization↗
PubMed1982

Association of coronavirus infection with neonatal necrotizing enterocolitis.

From the clustered occurrence of numerous cases of necrotizing enterocolitis in newborns, it was possible to associate this disease significantly with infection due to coronavirus-like agents. Prematurity or low birth weight did not seem to affect the development of the disease, at least during the present epidemic. However, associated gas-producing bacteria could influence its severity and play a role in the appearance of pneumatosis. In many aspects the human disease is reminiscent of experimental necrotizing enterocolitis obtained by infection of germ-free newborn animals, as reported in the literature.

Antibodies, Viral↗
PubMed1990

Prevention of necrotizing enterocolitis in the rat with prenatal cortisone.

Cortisone acetate is known to accelerate maturation of the immature intestine. The effect of prenatal administration of cortisone acetate on the morbidity and mortality of necrotizing enterocolitis was examined in a rat pup model. Pregnant rats were administered cortisone acetate, 20 mg/100 g of body weight, or normal saline by daily IP injection from day 18-21 of gestation. Rat pups were taken from the mothers before suckling was initiated, fed a simulated rat milk formula, and subjected to daily ischemic insults to produce an animal model of necrotizing enterocolitis. Both morbidity and the mortality rates were significantly improved with prenatal cortisone treatment. Maturation of the intestinal mucosal barrier was accelerated with the cortisone treatment as measured by decreased serum concentrations of a fed antigen, ovalbumin. Aerobic bacterial colonization of the small intestine and translocation of bacteria to the liver were decreased in the pups pretreated with steroids. These changes observed in a rat model of necrotizing enterocolitis may explain the decreased incidence of necrotizing enterocolitis in human infants born to mothers who received corticosteroids late in gestation.

Animals↗
PubMed1973

Necrotizing enterocolitis--a medical approach to treatment.

Ten cases of necrotizing enterocolitis occurred among 5400 infants delivered consecutively during a two and one-half year period at the Halifax Infirmary. Since this disease involved such extensive areas of the intestinal wall, medical management was employed exclusively, even when intestinal perforation occurred. Nine of the ten infants survived.In this series there was a high incidence of prematurity, prolonged interval between rupture of the placental membranes and delivery, severe asphyxia neonatorum and subsequent hypotension and metabolic acidosis. Blood cultures grew Klebsiella aerobacter or E. coli in 7/10 infants. Only two of these organisms were sensitive to kanamycin and all were resistant to ampicillin. Administration of ampicillin to the mothers did not protect these infants against necrotizing enterocolitis. Edema of the gut wall appeared to be an important early sign. Stricture formation occurred in 4/10 cases, all in the terminal ileum. These infants were operated upon only after the acute stage of the disease had subsided.

Acidosis↗
PubMed1997

The epidemiology of necrotizing enterocolitis infant mortality in the United States.

OBJECTIVES: This study examined trends and risk factors for infant mortality associated with necrotizing enterocolitis in the United States. METHODS: Necrotizing enterocolitis-associated deaths and infant mortality rates from 1979 through 1992 were determined by means of US multiple cause-of-death and linked birth/infant death data. RESULTS: Annual necrotizing enterocolitis infant mortality rates decreased from 1979 through 1986 but increased thereafter and were lower during the 3-year period before (1983 through 1985;11.5 per 100,000 live births) the introduction of surfactants than after (1990 through 1992; 12.3 per 100,000). Low-birthweight singleton infants who were Black male, or born to mothers younger than 17 had increased risk for necrotizing enterocolitis-associated death. CONCLUSIONS: As mortality among low-birth weight infants continues to decline and smaller newborns survive early causes of death, necrotizing enterocolitis-associated infant mortality may increase.

Age Distribution↗
PubMed2004

[Necrotizing enterocolitis during pregnancy in a woman operated on at six months of Hirschsprung's disease].

Necrotizing enterocolitis is a rare and severe complication of Hischsprung's disease. Aggravation of unknown or undertreated Hischsprung's disease may be seen during pregnancy. To our knowledge, the following case is the first combining those two elements: necrotizing enterocolitis in a 20 years old women operated on of Hischsprung's disease when she was six months. The final diagnosis was made 24 hours later. Definitive treatment was a three-stage ileal pouch-anal anastomosis.

Adult↗