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PubMed1984

Intestinal lesions containing coronavirus-like particles in neonatal necrotizing enterocolitis: an ultrastructural analysis.

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. Coronavirus-like particles, enclosed in intracytoplasmic vesicles of damaged epithelial cells of the intestinal mucosa, were observed in the small intestine, appendix, and colon. The ultrastructural study, supported by bacteriologic findings, suggests the role of coronavirus-like particles in the appearance of the lesions. Secondary proliferation of mainly anaerobic bacteria, probably responsible for pneumatosis, may aggravate the disease.

Appendix↗
PubMed1981

[Hypothermia, respiratory distress and umbilical catheterization as risk factors in necrotizing enterocolitis (author's transl)].

Fourteen patients diagnosed of neonatal necrotizing enterocolitis (NNE) admitted into the neonatal unit since August 1977 are presented. They were matched to a control group of 130 newborn infants born during that same period of time for sex, weight and gestational age. All patients were formula fed except for three who followed mixed feeding. NNE was closely associated to hypothermia (p less than 0.005), respiratory distress (p less than 0.001) and umbilical catheterization (p less than 0.005). Umbilical catheters introduced for reasons other than distress did not increase the incidence of NNE. Low birth weight infants were more frequently affected than those weighing over 2,500 gm (ratio, 27:1). Evolution was lethal in six cases. The remaining eight are presently under follow up with no evidence of disease.

Catheterization↗
PubMed1976

Neonatal necrotizing enterocolitis--a personal experience.

An increasing incidence of neonatal necrotizing enterocolitis over a 2 1/2 year period is demonstrated. Following a brief discussion of pathogenic and etiologic factors, 41 cases are reviewed retrospectively. Clinical, laboratory, and radiographic diagnostic aids are discussed. Surgical and nonsurgical methods of therapy and their results are presented. In conclusion, guidelines and indications for conservative and operative treatment are outlined.

Birth Weight↗
PubMed2001

Effect of polyunsaturated fatty acid (PUFA) supplementation on intestinal inflammation and necrotizing enterocolitis (NEC) in a neonatal rat model.

Inasmuch as long-chain polyunsaturated fatty acids (PUFA, metabolites of the essential n-3 and n-6 fatty acids) are known to modulate inflammation, we hypothesized that supplementation of formula with these compounds would prevent necrotizing enterocolitis (NEC) and intestinal inflammation in our neonatal rat model. Newborn rats were stressed with asphyxia and formula feeding, and randomly assigned to control formula, control with PUFA supplementation, and PUFA with nucleotides. Animals were followed for 72--96 h and assessed for death, gross and histologic NEC, intestinal apoptosis, endotoxemia, and intestinal mRNA synthesis of phospholipase A(2)-II (rate-limiting enzyme for platelet activating factor production), platelet activating factor receptor, and inducible nitric oxide synthase. We found that PUFA reduced the incidence of death and NEC compared with the other groups (NEC 8 of 24 versus 17 of 24 control and 13 of 23 PUFA + nucleotides, p < 0.05). Furthermore, PUFA reduced plasma endotoxemia at 48 h (25 +/- 4 EU/mL versus 276 +/- 39 EU/mL in control and 170 +/- 28 EU/mL in PUFA + nucleotide), intestinal phospholipase A(2)-II expression at 24 h, and platelet activating factor receptor expression at 48 h. Formula supplementation had no effect on apoptosis of intestinal epithelium or intestinal inducible nitric oxide synthase expression. Addition of nucleotides with PUFA abrogated the beneficial effects of PUFA on intestinal inflammation. We conclude that PUFA reduces the incidence of NEC and intestinal inflammation in a neonatal rat model.

Animals↗
PubMed2001

The role of recombinant human erythropoietin in lipid peroxidation and platelet-activating factor generation in a rat model of necrotizing enterocolitis.

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). Three groups, each consisting of eight 1-day-old Wistar albino rat pups, were studied; Group 1, hypoxia-reoxygenation; Group 2, hypoxia-reoxygenation and rhEPO pretreatment; Group 3, control. rhEPO was given 750 U/kg/week by intraperitoneal injection three times a week for 2 weeks. On day 15th of life, hypoxia was induced by placing rat pups in a 100% CO2 chamber for 5 min. After hypoxia, the rat pups were reoxygenated for 10 min with 100% oxygen and returned to their mothers. All pups were killed at 4h following hypoxia-reoxygenation. The abdomen was opened and representative samples of injured areas were taken for histopathologic examination. MDA and PAF levels were determined in the intestine. Significantly increased intestinal MDA content was found in Group 1 rat pups compared to Group 2 and Group 3 pups (p < 0.001 and p < 0.001, respectively). However, PAF concentrations were highly elevated in the intestine of Group 1 and Group 2 pups (p>0.05) when compared to the intestine of Group 3 pups (p < 0.001 and p < 0.001, respectively). Histopathologic findings did not differ between Groups 1 and 2. The present study demonstrates that oxygen-derived free radicals and PAF are involved in the pathophysiological mechanism of the development of NEC. This study also shows that administration of rhEPO significantly decreases lipid peroxidation; however, PAF generation was not inhibited in hypoxia-induced bowel necrosis.

Animals↗
PubMed1981

Survival after necrotizing enterocolitis of leukemia treated with oral vancomycin.

A 56-yr-old female with chronic lymphocytic leukemia developed hemolytic anemia and thrombocytopenia. Prednisone therapy was instituted, but her disease was further complicated by the development of necrotizing enterocolitis. No specific enteropathogens were identified, and the stools were consistently negative for Clostridium difficile toxin. Treatment with vancomycin was instituted and resulted in complete recovery. In view of the high mortality and poor results of treatment in necrotizing enterocolitis, it is postulated that a further trial of this drug is justified.

Administration, Oral↗
PubMed2002

Nitric oxide synthase isoenzyme activities in a premature piglet model of necrotizing enterocolitis: effects of nitrergic manipulation.

Nitric oxide (NO) plays a major role in gut mucosal protection and motility. Having demonstrated the protective effects of intravenous L-arginine (L-arg) and the NO donor, sodium nitroprusside (SNP), in an in-vivo premature piglet intraluminal model of necrotizing enterocolitis (NEC) that incorporates both mucosal damage and intestinal dysmotility, we measured the effects on NO synthase (NOS) isoenzyme activities during i.v. manipulation of the nitrergic system in the NEC-injured gut. In newborn premature Yorkshire piglets, NEC was induced in four groups by intraluminal injection of acidified casein solution in closed test loops of bowel separated by normal saline-injected control loops. Group 1 (n = 4) underwent no further treatment. Group 2 (n = 4) received concomitant continuous i.v. L-arg, a NO substrate. Group 3 (n = 6) received concomitant continuous i.v. SNP, a NO donor. Group 4 (n = 5) received concomitant continuous i.v. N-omega-nitro-L-arginine-methyl-ester (L-NAME), a non-selective NO inhibitor. Control and test gut specimens were harvested after 3 h. NO synthase activity in frozen gut segments was assessed using the (14)C-L-arg to (14)C-L-citrulline conversion assay. Total NOS (TNOS), constitutive NOS (cNOS), and inducible NOS (iNOS) activities were compared. The mean and standard error were calculated for each specimen. Group means were used to compare test and control gut enzyme activities in the different treatment groups. One-way analysis of variance and the Bonferroni post test were used to compare differences among groups. A P value of less than 0.05 was considered significant. In the L-NAME group, cNOS activity was lower than in the untreated NEC group. The SNP group had higher iNOS and TNOS activities than the L-arg group; cNOS was also higher in test and control loops in the SNP versus both L-arg and L-NAME groups. However, in L-arg control loops, cNOS activity was greater than in the L-NAME group. SNP and L-arg treatment of NEC did not significantly modify NOS isoenzyme activities. Thus, in this premature piglet 3-h model of NEC, i.v. L-NAME significantly decreases cNOS activity and correlates with our previously published histopathologic findings confirming the protective role of cNOS-derived NO in NEC-injured gut mucosa. In order to further elucidate the mechanisms involved in the mucosal protection afforded by i.v. L-arg and SNP in this NEC model, studies of a longer duration have been undertaken.

Animals↗
PubMed2005

Epidemiology of necrotizing enterocolitis--Part I: Changing regional trends in extremely preterm infants over 14 years.

OBJECTIVES: Advances in perinatal care include exogenous surfactant, unequivocal acceptance of antenatal steroids and in utero and ex utero transfers to tertiary centres. Increased survival of extremely premature infants may change the incidence and outcome of necrotizing enterocolitis (NEC). Our aim was to examine the trends in the incidence of NEC, surgery and mortality in infants of 24-28 weeks gestation in a retrospective regional review of three epochs over a span of 14 years. METHODS: Radiologically or surgically proven NEC cases were determined from the New South Wales Neonatal Intensive Care Unit Study database. Three epochs were examined. A total of 360 infants were admitted in 1986-87 (Epoch 1), 622 in 1992-93 (Epoch 2) and 673 in 1998-99 (Epoch 3). RESULTS: There was an increase in neonatal intensive care unit admissions and a decrease in early and overall mortality of these very premature infants across the epochs. None of the early deaths was due to NEC. The incidence of NEC decreased in post day 5 survivors: 33 cases in Epoch 1 (12%), 60 cases in Epoch 2 (12%) and 34 cases in Epoch 3 (6%, P < 0.001). There was no change in surgical intervention (45%, 57% and 41%, respectively) or mortality due to NEC (37%, 27% and 32%). The reduced incidence of NEC was not singularly influenced by antenatal steroids, exogenous surfactant or outborn delivery. In a multivariate analysis, only later epoch of birth was independently associated with reduced NEC risk. CONCLUSIONS: With improved care and survival of extremely premature infants, the incidence of NEC has decreased, but it remains a disease of high mortality and morbidity.

Enterocolitis, Necrotizing↗
PubMed1979

[The etiology of necrotizing enterocolitis in the newborn].

Apparently there are different causes for necrotizing enterocolitis (NEC) in the newborn infant. Besides it may be that NEC only is caused by the interaction of several factors such as perinatal complications, medical measures, an aggressive oral alimentation and an adverse colonization of the bowel and that a critical degree of stress is required to initiate enterocolitis. This assumption would help to explain, why one newborn infant can stand an episode of perinatal stress without falling ill, while the other develops the disease a short time later. Probably NEC starts with an intestinal mucosa damage caused by ischemia or local noxae, and only subsequent invasion by the bowel flora into the damaged tissue and gas formation within the bowel wall lead to the picture of necrotizing inflammation and pneumatosis intestinalis.

Catheterization↗
PubMed2005

Postoperative outcomes of extremely low birth-weight infants with necrotizing enterocolitis or isolated intestinal perforation: a prospective cohort study by the NICHD Neonatal Research Network.

OBJECTIVE: Purposes of this study were: 1) to compare mortality and postoperative morbidities (intra-abdominal abscess, wound dehiscence, and intestinal stricture) in extremely low birth weight (ELBW) infants who underwent initial laparotomy or drainage for necrotizing enterocolitis (NEC) or isolated intestinal perforation (IP); 2) to determine the ability to distinguish NEC from IP preoperatively and the importance of this distinction on outcome measures; and 3) to evaluate the association between extent of intestinal disease determined at operation and outcome measures. BACKGROUND: ELBW infants who undergo operation for NEC or IP have a postoperative, in-hospital mortality rate of approximately 50%. Whether to perform laparotomy or drainage initially is controversial. Also unknown is the importance of distinguishing NEC from IP and the current ability to make this distinction based on objective data available prior to operation. METHODS: A prospective, multicenter cohort study of 156 ELBW infants at 16 neonatal intensive care units (NICU) within the NICHD Neonatal Research Network. RESULTS: Among the 156 enrolled infants, 80 underwent initial peritoneal drainage and 76 initial laparotomy. Mortality rate was 49% (76 of 156). Ninety-six patients had a preoperative diagnosis of NEC and 60 had presumed IP. There was a high level of agreement between the presumed preoperative diagnosis and intraoperative diagnosis in patients undergoing initial laparotomy (kappa = 0.85). The relative risk for death with a preoperative diagnosis of NEC (versus IP) was 1.4 (95% confidence interval, 0.99-2.1, P = 0.052). The overall incidence of postoperative intestinal stricture was 10.3%, wound dehiscence 4.4%, and intra-abdominal abscess 5.8%, and did not significantly differ between groups undergoing initial laparotomy versus initial drainage. CONCLUSIONS: Survival to hospital discharge after operation for NEC or IP in ELBW neonates remains poor (51%). Patients with a preoperative diagnosis of NEC have a relative risk for death of 1.4 compared with those with a preoperative diagnosis of IP. A distinction can be made preoperatively between NEC and IP based on abdominal radiographic findings and the patient's age at operation. Future randomized trials that compare laparotomy versus drainage would likely benefit from stratification of treatment assignment based on preoperative diagnosis.

Drainage↗
PubMed1986

[Necrotizing enterocolitis. Pathogenesis and iatrogenic factors].

Following clinical observations, measurements of osmolarity of liquid drugs, and determination of blood loss due to sampling in very low birthweight infants, the following hypothesis on iatrogenic factors contributing to the pathogenesis of necrotizing enterocolitis is proposed: Due to diagnostic blood sampling during intensive care, premature infants may become severely anemic. Therefore their intestinal perfusion is reduced, causing hypoxia and hypoperfusion in the submucosa. Especially in infants with oral feeding and hyperosmolar medication, mechanical factors, hyperosmolarity and infection can affect the mucosa from the luminal side. Simultaneous hypoperfusion and hyperosmolar load may contribute to the pathogenesis of necrotizing enterocolitis. This hypothesis, which needs experimental verification, explains the different incidence of the disease in different hospitals.

Blood Volume↗
PubMed1988

Occult blood in stools and necrotizing enterocolitis. Is there a relationship?

A prospective study was undertaken to determine the incidence of occult hematochezia in enterally fed low-birth-weight neonates (less than 1800 g at birth). The relationship of this occult hematochezia to the development of necrotizing enterocolitis (NEC) was then analyzed. Daily stool specimens from 95 neonates were tested for occult blood during the first six weeks of life. Fifty-four (58%) of the 95 neonates had one or more blood-positive stools. Six neonates (6.3%) developed NEC. Necrotizing enterocolitis occurred in only two of the 54 neonates with one or more blood-positive stools vs four of the 41 neonates with blood-negative stools only. Presence of occult blood in the stools did not correlate with development of NEC.

Enteral Nutrition↗
PubMed2002

Plasma concentration of intestinal- and liver-FABP in neonates suffering from necrotizing enterocolitis and in healthy preterm neonates.

Both early diagnostic and prognostic assessment of the acute abdomen in preterm infants are hampered by the lack of a sensitive and specific parameter for intestinal injury. In this prospective clinical study we wanted to estimate the value of intestinal (I-) and liver (L-) fatty acid binding protein (FABP) in diagnosing necrotizing enterocolitis (NEC). Using highly sensitive and specific sandwich ELISAs which employ recombinant human I- and L-FABP as standard proteins (limit of detection 0.1 ng/ml plasma), the L-FABP concentration (median 7.6 ng/ml) was determined to be about 3 fold that of I-FABP (median 2.52 ng/ml) in plasma of healthy preterm infants. I- and L-FABP concentrations significantly increased with birth weight (1.6 and 5.0 ng/ ml per kg, respectively). At onset of symptoms, I-FABP concentration was significantly higher in infants who later developed severe NEC compared to healthy infants and those, whose illness remained confined to stage I or II. L-FABP was significantly elevated compared to the control group at onset of symptoms regardless of the further course of NEC. In conclusion, I-FABP appears to be a specific parameter for early detection of intestinal injury leading to severe NEC stage III. L-FABP, however, is a promising sensitive marker even for stage I of NEC.

Animals↗
PubMed1992

Mucormycosis of the neonatal gut: a "new" disease or a variant of necrotizing enterocolitis?

Mucormycosis is an opportunistic infection that has been mainly described in adults with preexisting disease affecting immune status, eg, diabetes, leukemia, lymphoma, and renal failure on peritoneal dialysis. Few cases have been described in neonates. The presentation of mucormycosis as a cause of neonatal necrotizing enterocolitis is an unusual phenomenon. Three fatal cases of mucormycosis of the gut in premature infants in the period 1990 to 1991 are described. It is not clear whether this should be considered a separate disease or a variant of necrotizing enterocolitis. All three patients died soon after laparotomy from septic shock and the histological diagnosis of mucormycosis was made too late for effective chemotherapy.

Enterocolitis↗
PubMed2003

The therapeutic effect of recombinant human trefoil factor 3 on hypoxia-induced necrotizing enterocolitis in immature rat.

Trefoil peptides are a new class of regulatory peptides involved in mucosal protection and repair in the gastrointestinal tract. Among them, trefoil factor 3 (TFF3) (intestinal trefoil factor) is known to be cytoprotective in the gut. The aim of this study was to determine the effect of recombinant human trefoil factor 3 (rhTFF3) on hypoxia-induced necrotizing enterocolitis (NEC) in immature rats. In the present study, thirty-two 1-day-old Wistar rat pups were randomly divided into four groups. Group 1 served as nonhypoxic controls. Group 2 rats were subjected to hypoxia reoxygenation (H/O) and then were returned to their mothers. Groups 3 and 4 rats were subjected to H/O, were returned to their mothers, and were treated with rhTFF3 intraperitoneally (0.5 mg) and subcutaneously (0.2 mg), respectively, for the next 3 days. All animals were killed on day 4, and intestine specimens were obtained to determine the histological changes, tissue level of interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), malondialdehyde (MDA), prostaglandin E2 (PGE2), tromboxane B2 (TXB2), and nitric oxide (NO). In addition, the effects of rhTFF3 on abundance of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) were also investigated. In neonatal NEC (group 2), necrosis of villi and crypts and, in some cases, transmural necrosis was observed under light microscopy. Tissue level of interleukin-8, tumor necrosis factor-alpha, malondialdehyde, prostaglandin E2, tromboxane B2, and nitric oxide were significantly higher than group 1. In addition, abundance of inducible nitric oxide synthase and cyclooxygenase 2 was markedly increased. In groups 3 and 4, only very slight intestinal injury was observed. The tissue level of interleukin-8, tumor necrosis factor-alpha, malondialdehyde, prostaglandin E2, tromboxane B2, and nitric oxide were significantly decreased in comparison to the group 2. Meanwhile, the abundance of inducible nitric oxide synthase and cyclooxygenase 2 was also marked decreased in comparison to group 2. The current study suggests a therapeutic role of TFF3 in an experimental model of NEC. Our findings may open a new insight into the treatment of NEC in newborns.

Aging↗
PubMed2001

Altered nitric oxide production in the premature gut may increase susceptibility to intestinal damage in necrotizing enterocolitis.

BACKGROUND/PURPOSE: Nitric oxide (NO) mediates enteric smooth muscle relaxation and mucosal protection. The authors have identified an ontogenically determined pattern of enteric NO neural maturation that may render the distal gut of premature piglets susceptible to injury. METHODS: NO synthase (cNOS and iNOS) activities were measured in the developing piglet gut wall and compared with gut from an intraluminal model of necrotizing enterocolitis (NEC) at different times. RESULTS: In premature animals, iNOS activity was significantly higher 3 hours after NEC induction compared with similarly treated 3-day-old piglets. INOS levels continued to rise 6 hours after NEC induction in prematures. Premature animals (labor induced by prostaglandins) failed to show such a rise in iNOS. In 3 day olds, iNOS levels increased significantly 16 hours after injury compared with the 3-hour group. CONCLUSIONS: iNOS production increases in premature piglets with NEC compared with full-term NEC animals and continues to rise in the presence of intestinal damage regardless of developmental status. Maternal administration of prostaglandins attenuates this rise in iNOS activity. Elevated NO production in premature gut may contribute to increased susceptibility to damage in NEC.

Age Factors↗
PubMed2000

Erythropoietin and the incidence of necrotizing enterocolitis in infants with very low birth weight.

BACKGROUND/PURPOSE: The presence of erythropoietin (Epo) in human milk and the expression of Epo receptors on intestinal villous enterocytes of neonates suggest that Epo has a role in growth and development of the gastrointestinal tract. On this basis, the authors hypothesized that recombinant Epo (rEpo) given for prevention or treatment of the anemia of prematurity would protect against necrotizing enterocolitis (NEC). METHODS: A retrospective cohort study was conducted from a university neonatal intensive care unit of 483 very low birth weight (500 to 1,250 g) neonates born from July 1, 1993 to January 1, 1998. RESULTS: A total of 260 neonates received rEpo, and 223 did not (control group). The rEpo and control groups were similar in gender distribution (52% v. 48% boys), gestational age (26.8+/-2.1 v. 27.6+/-2.9 weeks; mean +/- SD), birth weight (895+/-198 v. 911+/-208 g), 1 and 5 minute Apgar scores (4.2 and 6.1 v4.7 and 6.7), and incidence of severe intraventricular hemorrhage (8.9% v. 10.3%). The rEpo group had a lower incidence of NEC (12 of 260, 4.6% v. 24 of 223, 10.8%; P = .028, 95% confidence interval for difference: -0.108 to -0.015). CONCLUSION: In very low birth weight infants, the incidence of NEC is lower in those who received rEpo.

Enterocolitis, Necrotizing↗
PubMed1995

Trends in pediatric ostomy surgery: intestinal diversion for necrotizing enterocolitis and biliary diversion for biliary hypoplasia syndromes.

Ostomies are placed in children for different indications than in the older population. Many ostomies of childhood are placed because of congenital or neonatal problems that require temporary or long-term diversion to stabilize the neonatal patient. Necrotizing enterocolitis, the most common reason for placement of neonatal colostomies and ileostomies, is increasing in frequency as more prematurely born infants survive. Recently, there has been an increase in treatment of various biliary hypoplasia syndromes with biliary cutaneous diversion. Children with biliary hypoplasia syndromes are a challenging group of patients who frequently can be helped by ostomies. This article reviews current information on biliary cutaneous diversion for the biliary hypoplasia syndromes and intestinal diversion for necrotizing enterocolitis.

Bile Ducts↗