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PubMed2006

Genetic polymorphisms of CD14, toll-like receptor 4, and caspase-recruitment domain 15 are not associated with necrotizing enterocolitis in very low birth weight infants.

OBJECTIVES: Inadequate response of the innate immune system to bacterial antigens present in the intestinal flora may play a role in the development of necrotizing enterocolitis (NEC). Pattern recognition receptors such as CD14, toll-like receptor (TLR) 4, and caspase-recruitment domain (CARD) 15 bind bacterial lipopolysaccharide and peptidoglycan, and their activation leads to production of inflammatory cytokines. Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants. PATIENTS AND METHODS: We determined the CD14 C-260T, TLR4 A +896G, C +1196T, and CARD15 G +2722C, C +2104T, 3020insC functional SNPs in dried blood samples from 118 VLBW infants (of those, 41 developed NEC) and from 146 healthy term newborns using polymerase chain reaction and restriction fragment length polymorphism methods. We tested the association between genotype and risk of NEC. RESULTS: No significant differences were found in the prevalence of CD14 -260T, TLR4 +896G, +1196T, and CARD15 +2722C, +2104T, 3020insC alleles between VLBW infants and healthy term newborns (P = NS). The frequencies of investigated genotypes were similar in infants with and without NEC (P = NS). Furthermore, we did not find any association between genotype and prematurity or sepsis, which are important risk factors of NEC. CONCLUSIONS: Carrier state of the tested CD14, TLR4, and CARD15 SNPs is not associated with NEC risk in VLBW infants.

Enterocolitis, Necrotizing↗
PubMed1998

Recurrent necrotizing enterocolitis associated with episodes of supraventricular tachycardia.

The case of a 5-month-old baby with congenital heart disease and recurrent episodes of refractory supraventricular tachycardia (SVT) is presented. Severe segmental necrotizing enterocolitis (NEC) developed in the patient after one prolonged episode of SVT that required a limited right hemicolectomy. Further episodes of SVT were associated with recurrence of NEC requiring multiple laparotomies. The pathogenesis and therapeutic implications of this process are discussed in view of the potentially multiple pathological processes involved.

Colectomy↗
PubMed1999

Necrotizing enterocolitis in infants born to women with severe early preeclampsia and absent end-diastolic umbilical artery doppler flow velocity waveforms.

The aim of this study was to determine the prevalence of necrotizing enterocolitis (NEC) in infants born to a homogeneous group of women with severe preeclampsia before 34 weeks' gestation and who had absent end-diastolic umbilical artery Doppler flow (AEDF) or normal umbilical Doppler flow velocities (NUFV). A total of 242 infants were entered into the study. The mean birth weight was 1260.5 g (SD = 339) and the mean gestational age 30.5 weeks (SD = 2.0). Sixty-eight (28%) infants had AEDF, 43 (18%) had umbilical artery Doppler flow velocities between the 95th and 99th percentile, and 131 (54%) had NUFV. Forty-one (18%) infants developed NEC, of whom 20 (8%) developed definite and advanced NEC (grade 2 and 3). Of these, 16(80%) had grade 2 and 4(20%) had grade 3. Twenty-one (8%) infants developed suspected NEC (grade 1). The mean onset of grade 1 NEC (7.2 days) occurred significantly earlier than in those with grades 2 and 3 NEC (18.7 and 23.3 days, respectively). Of the 21 infants with grade 1 NEC, 10 (48%) had AEDF and 9 (43%) had NUFV. None of the infants with grades 2 or 3 NEC had AEDF. We conclude that although chronically hypoxemic fetuses born to women with severe early onset preeclampsia and AEDF respond by redistributing blood flow to vital organs and away from the gut; the intestinal compromise is of insufficient magnitude to induce intestinal necrosis or NEC. Enteral feeding, however, should be introduced cautiously in infants with AEDF, as so-called suspected NEC developed significantly more often in these infants.

Blood Flow Velocity↗
PubMed2002

Laparotomy in very small premature infants with necrotizing enterocolitis or focal intestinal perforation: postoperative outcome.

BACKGROUND/PURPOSE: Laparotomy for peritonitis secondary to necrotizing enterocolitis (NEC) or focal intestinal perforation (FIP) has been supplanted by peritoneal drainage (PD) as the initial treatment in many institutions. Although proponents regard it as a safer alternative, early mortality is cited between 21% and 36%, with subsequent laparotomy required for worsening disease in 26% to 83% of patients. The current outcomes for initial laparotomy are analyzed and compared with those cited for PD. METHODS: A retrospective review of very small premature infants less than 1,500 g undergoing laparotomy for NEC or FIP between 1994 and 2000 was performed. RESULTS: Thirty-five neonates were identified with a median weight of 741 g (range, 460 g to 1,415 g) and a median age of 26 weeks (range, 23 to 33 weeks). Twelve patients had FIP and 23 had NEC including 5 with pan-intestinal necrosis (PIN). No deaths occurred during laparotomy or stoma closure. Seven (20%) patients died within the immediate 7-day postoperative period. Nine (26%) patients died in the 30-day postoperative period. CONCLUSIONS: With current peri-operative management, mortality rates for initial laparotomy and PD are comparable. Assessing the extent of disease and removing necrotic bowel at initial laparotomy can hasten recovery and eventual discharge while enabling informed surgical decision making and advice to parents.

Cause of Death↗
PubMed2006

Association of necrotizing enterocolitis with elective packed red blood cell transfusions in stable, growing, premature neonates.

The purpose of this study was to determine an association between packed red blood cell (PRBC) transfusions for anemia and necrotizing enterocolitis (NEC) in a subset of stable, growing, premature neonates. As part of a survey of current clinical practices over a 17-month period from June 1999 to October 2000, a chart review was performed to determine the relationship between elective PRBC transfusions and the occurrence of NEC. Demographic data were tabulated and compared between the NEC patients with a prior history of immediate blood transfusion (within 48 hours of onset of symptoms) and those NEC patients without a prior history of immediate blood transfusion. A total of 908 (inborn) neonatal admissions had received 751 PRBC transfusions during the study period; of these, 17 patients (1.8%) had developed radiographic, clinical, or surgical signs of NEC. Six cases of NEC (35%; six of 17 patients) were associated with PRBC transfusions (0.8%; six of 751 transfusions). The transfusion-associated NEC group developed presenting signs within 22 +/- 5 hours (median, 19; range, 12 to 38) of a PRBC transfusion at a mean age of 32 +/- 7 days. In contrast, the non-transfusion-associated NEC group (n = 11) had onset of NEC at a mean age of 12 +/- 7 days ( P < 0.05) after 185 +/- 91 hours (median, 180; range, 96 to 312; P < 0.02] of a transfusion. Prior to the onset of NEC, all of the neonates in the transfusion-associated NEC group were stable, growing, not ventilated, receiving full enteral feedings, and had no other active medical problems except anemia (hematocrit, 24 +/- 3%). In contrast, the nontransfusion NEC group was more often ventilated, was receiving < 50% of fluids by mouth, had lower Apgar scores, and was transfused for an average hematocrit of 37 +/- 7% ( P < 0.05). There was no significant difference in the type, storage, volume, or preservative used between the blood products in the two groups. We identified an unanticipated relationship between late-onset NEC in stable, growing, premature neonates who were transfused electively for anemia of prematurity.

Anemia, Neonatal↗
PubMedDate not supplied

Necrotizing enterocolitis complicated with perforation in extremely low birth-weight premature infants.

This study determined the incidence, clinical characteristics, treatment and outcome in extremely low birth-weight (ELBW) premature infants with perforated necrotizing enterocolitis (NEC). We retrospectively reviewed the medical records of ELBW (birth weight <1000 g ) premature infants with perforated NEC diagnosed and managed at National Taiwan University Hospital (NTUH) from January 1993 through December 2000. A total of 8 ELBW premature infants with perforated NEC were collected. The incidence of perforated NEC in ELBW premature infants was 5.1% (8 out of 158). The average age at onset of perforated NEC was 26 days. The most common clinical features were abdominal distention, decreased bowel sound and poor activity level. Dilated and fixed bowel loops, bowel wall thickening and ascites with stool-like substance drainage out from penrose drain tube were the predominant signs at the time of diagnosis of perforated NEC. Thrombocytopenia, elevated C-reactive protein and anemia were the major laboratory findings. All infants received a primary penrose drain in the acute stage of disease. The overall survival rate was 37.5% (3 out of 8). Death occurred due to nosocomial infection with sepsis in 3 patients and due to perforated NEC in 2 patients. Two of the three surviving patients started enteral feeding 19 and 41 days after the diagnosis of perforated NEC and tolerated oral feedings well; the third patient still required total parenteral nutrition two years after diagnosis. Although the clinical characteristics and radiographic findings of perforated NEC in ELBW premature infants were variable, brown color ascites with stool-like substance may be considered a significant sign of perforated NEC despite the absence of free air on radiography at the early stage of disease. Close observation of clinical symptoms and signs, more aggressive surgical intervention and prevention of the following nosocomial infection may have the opportunity to reduce the mortality due to perforated NEC.

Drainage↗
PubMed2006

The fear of necrotizing enterocolitis versus achieving optimal growth in preterm infants--an opinion.

UNLABELLED: Very-low-birthweight (VLBW) infants suffer marked growth delay despite well-intentioned efforts at combining enteral and parenteral nutrition. Fear of necrotizing enterocolitis (NEC) has traditionally influenced neonatologists toward delaying and progressing slowly with enteral feeding, while supporting the infant with parenteral nutrition. Current evidence suggests significant benefits of enteral feeding that is started early and advanced at rates of 20-35 ml/kg/d. CONCLUSION: We conclude that fear of inadequate growth should replace the fear of NEC in guiding nutritional strategies for these infants.

Animals↗
PubMed2005

Oral probiotics prevent necrotizing enterocolitis in very low birth weight neonates.

OBJECTIVE: To test the hypothesis that normalizing the intestinal flora by administration of prophylactic probiotics would provide a natural defense, thereby reducing both the incidence and severity of necrotizing enterocolitis (NEC) in preterm neonates. STUDY DESIGN: Neonates < or =1500 g birth weight were randomized to either receive a daily feeding supplementation with a probiotic mixture (Bifidobacteria infantis, Streptococcus thermophilus, and Bifidobacteria bifidus; Solgar, Israel) of 10(9) colony forming units (CFU)/day or to not receive feed supplements. NEC was graded according to Bell's criteria. RESULTS: For 72 study and 73 control infants, respectively, birth weight (1152 +/- 262 g vs 1111 +/- 278 g), gestational age (30 +/- 3 weeks vs 29 +/- 4 weeks), and time to reach full feeds (14.6 +/- 8.7 days vs 17.5 +/- 13.6 days) were not different. The incidence of NEC was reduced in the study group (4% vs 16.4%; P=.03). NEC was less severe in the probiotic-supplemented infants (Bell's criteria 2.3 +/- 0.5 vs 1.3 +/- 0.5; P=.005). Three of 15 babies who developed NEC died, and all NEC-related deaths occurred in control infants. CONCLUSION: Probiotic supplementation reduced both the incidence and severity of NEC in our premature neonatal population.

Administration, Oral↗
PubMed2000

Rectosigmoid pHi monitoring during experimental necrotizing enterocolitis.

BACKGROUND/PURPOSE: Gastric or rectosigmoid intramural pH (pHi) is considered a reliable indicator of splanchnic perfusion. The aim of this study was to evaluate whether rectosigmoid pHi reflects the severity of bowel damage in experimental necrotizing enterocolitis (NEC). METHODS: A total of 36 neonatal piglets, (median age, 3; range, 1 to 11 days; median weight, 2.5; range, 1.2 to 3.8 kg), were anesthetized, ventilated mechanically, and had invasive monitoring of hemodynamics. A sigmoid tonometer was inserted into the rectosigmoid colon. Enterocolitis was induced in 27 piglets by intraluminal injection of casein-d-gluconate (16.0 mL/kg) into terminal 100 cm of the ileum. Nine control piglets received an equal amount of intraluminal saline. NEC was graded macroscopically as follows: 0, no changes; 1, mild; 2, moderate; and 3, severe. Histology was evaluated according to Chiu scale from 0 to 5. RESULTS: The macroscopical bowel injury in caseine-injected piglets was as follows: grade 3 (n = 6), grade 2 (n = 9), grade 1 (n = 12). All control piglets showed macroscopically normal bowel (grade 0). All affected bowels showed histologic changes (Chiu's scale 2 to 4). All study animals had an initial drop of pHi after injection of casein or saline. In control piglets and those with mild NEC (grade 1) pHi tended to return to preinjection level. In animals with moderate or severe NEC (grade 2 to 3) the initial drop was deeper and the pHi continued to decrease significantly throughout the experiment (P < .05). In the arterial pH and mean blood pressure there were no statistically significant differences between piglets with no NEC and mild NEC, and these with moderate or severe NEC. CONCLUSION: Drop in rectosigmoid pHi was the most sensitive and earliest sign of severe mucosal necrosis of ileum in this experimental NEC model.

Animals↗
PubMed2005

Necrotizing enterocolitis in a premature infant as the presenting symptom of familial dysautonomia in the neonatal period: case report and review of the literature.

We present a case of a premature infant with early-onset necrotizing enterocolitis as the presenting symptom of familial dysautonomia. The diagnosis of familial dysautonomia in the neonatal period is usually rare and difficult, because many of the symptoms may be mild or nonspecific, whereas other characteristic signs and symptoms appear only later in life. The neonatologist should be aware of this rare diagnosis in the neonatal period, especially in the offspring of Ashkenazi Jews. The diagnosis is genetic. Preconception counseling to future parents belonging to populations at risk should include recommendation for genetic screening test to identify carriers of the mutations in the familial dysautonomia gene.

Dysautonomia, Familial↗
PubMed1989

Experimental cecitis in gnotobiotic quails monoassociated with Clostridium butyricum strains isolated from patients with neonatal necrotizing enterocolitis and from healthy newborns.

Using axenic quails fed a diet containing lactose, we have investigated the potentially pathogenic roles of six Clostridium butyricum strains of human origin. Three strains (CB155-3, CB1002, and CB203-1) isolated from neonatal necrotizing enterocolitis patients and two of three strains (CB19-1 and CB25-2) isolated from healthy newborns led to cecal or crop lesions or both similar to those observed in human neonatal necrotizing enterocolitis: thickening of the cecal wall with gas cysts, hemorrhagic ulcerations, and necrotic areas. The lactose-negative strain (CB46-1) did not develop any lesions. The neuraminidase-producing strain (CB155-3) caused lesions in all monoassociated quails, whereas the other strains caused lesions in 28 to 85% of animals. Removal of dietary lactose suppressed all pathological incidence. These results show that lactose fermentation is a prerequisite in these pathological changes and stress the roles played by both the strain and the host in the expression of C. butyricum enteropathogenicity.

Animals↗
PubMed1984

Neonatal necrotizing enterocolitis: an update.

We reviewed 91 cases of neonatal necrotizing enterocolitis (NNEC), which continues to be a devastating disease occurring in 2% to 4% of all newborn intensive care unit admissions. Onset now occurs in older infants (11.9 days). The morbidity is significant (22%), with strictures (8%) and recurrences (8%) the primary problems. Recurrences are more likely to require surgical intervention and result in a high mortality. Early diagnosis of necrotic bowel before perforation, peritoneal contamination, and sepsis is difficult and contributes to the still high, but improved, overall mortality of 36%.

Enterocolitis, Pseudomembranous↗
PubMed2004

Necrotizing enterocolitis and neurodevelopmental outcome in extremely low birth weight infants <1000 g.

OBJECTIVE: To determine the growth and neurodevelopmental outcome, as well as predictors of the latter in extremely low-birth-weight (ELBW) infants with definitive necrotizing enterocolitis (NEC). STUDY DESIGN: Case - control analysis. In all, 17 ELBW infants <1000 g with Stage 2 or 3 NEC were matched to 51 control infants without NEC. Demographics, clinical course, growth, and neurodevelopmental outcome were compared. RESULTS: Demographic and clinical characteristics of both groups were similar except that NEC infants had more culture-proven sepsis (59 vs 24%, p=0.02), longer intubation (36 vs 16 days, p=0.003) and longer hospital stay (134 vs 86 days, p<0.001). At 18 to 22 months corrected age BSID-II mental scores (MDI) were similar between groups (74+/-14 vs 81+/-13, p=0.2). However, the psychomotor index (PDI) (66+/-18 vs 88+/-14), the proportion with abnormal neurologic examination (54 vs 9%), subnormal height (38 vs 3%) and head circumference (23 vs 0%) were significantly higher in NEC infants (p<0.05). A logistic model identified NEC and chronic lung disease as predictors for abnormal PDI and MDI, respectively. CONCLUSIONS: NEC and its comorbidities are associated with severe neurodevelopmental and growth delay in ELBW infants.

Case-Control Studies↗
PubMed2004

Intestinal zygomycosis due to Absidia corymbifera mimicking necrotizing enterocolitis in a preterm neonate.

Zygomycosis is a rare fungal disease that occurs in compromised human hosts, including the preterm infant. The three clinical forms of zygomycosis are cellulitis, disseminated, and gastrointestinal, and the last often mimics necrotizing enterocolitis (NEC), complicating the diagnosis. This report details a case of primary gastrointestinal zygomycosis due to Absidia corymbifera, mimicking NEC, in a preterm infant, and emphasizes features that may lead to earlier diagnosis and treatment of future cases.

Absidia↗
PubMedDate not supplied

Cyanotic congenital heart disease and necrotizing enterocolitis: report of three cases.

Three infants with cyanotic congenital heart diseases (CCHD) had abdominal distension, poor activity at day 2, day 3, and day 23. The abdominal roentgenograms showed dilated bowel loops, pneumatosis intestinalis, and pneumoperitoneum. Necrotizing enterocolitis (NEC) was diagnosed. After medical and surgical intervention, one infant survived. In this report, we discuss the relationship between CCHD and NEC. The possible risk factors were also discussed, and it is recommended that NEC be a considered significant complication of infants with CCHD.

Enterocolitis, Necrotizing↗
PubMed2005

High-mobility group box 1 protein is an inflammatory mediator in necrotizing enterocolitis: protective effect of the macrophage deactivator semapimod.

High-mobility group box 1 (HMGB1) is a late mediator of endotoxemia known to stimulate the production of proinflammatory cytokines that are putative mediators of intestinal inflammation associated with necrotizing enterocolitis (NEC). We hypothesized that HMGB1 is also involved in the pathogenesis of NEC. We examined the expression of HMGB1 and the effect of the novel drug semapimod on intestinal inflammation in an experimental model of NEC in neonatal rats. Newborn rats were subjected to hypoxia and fed a conventional formula by gavage (FFH) or were breast fed (BF). Rats were killed on day 4, and the distal ileum was harvested for morphological studies and Western blot analysis. FFH newborn rats but not BF controls developed intestinal inflammation similar to the histological changes observed in human NEC. We found that the expression of HMGB1 and its receptor for advanced glycation end products (RAGE) as well as that of other apoptosis/inflammation-related proteins (Bad, Bax, inducible nitric oxide synthase, and cyclooxygenase 2) was upregulated in the ileal mucosa of FFH newborn rats compared with BF animals. Administration of the drug semapimod inhibited the upregulation of those proteins and partially protected the animals against the FFH-induced intestinal injury. Elevated levels of HMGB1 were also found in ileal samples from infants undergoing intestinal resection for acute NEC. Our results implicate HMGB1 and RAGE as important mediators of enterocyte cell death and hypoxia-induced injury in NEC and support the hypothesis that inhibitors such as semapimod might play a therapeutic role in chronic intestinal inflammation characterized by this animal model.

Animals↗
PubMed2006

Special circumstances: trophic feeds, necrotizing enterocolitis and bronchopulmonary dysplasia.

There are many unresolved issues regarding how to feed the extremely-low-birth-weight (ELBW) infant. Trophic feedings of small volumes of breast milk or formula do not appear to increase the incidence of necrotizing enterocolitis (NEC). For prevention of NEC, breast milk, antenatal steroids and fluid restriction each confers a benefit. Because the incidence of NEC is relatively low, to determine if a particular prevention strategy is effective, large numbers of infants would need to be enrolled in a prospective, randomized controlled trial, and such trials are rare. Candidate therapies for NEC prevention that warrant further study include oral immunoglobulins, probiotics, long-chain polyunsaturated fatty acids and arginine. Suboptimal nutrition in ELBW infants is common in the early postnatal period. This is also the most critical time for the development of bronchopulmonary dysplasia, when even brief periods of malnutrition have significant effects on lung development and growth.

Bronchopulmonary Dysplasia↗
PubMed2001

Bacterial toxins and enteral feeding of premature infants at risk for necrotizing enterocolitis.

Concordance between gram-negative enteric and other toxin-producing bacteria in blood and stool culture, endotoxin (lipopolysaccharide), and interleukin 6 (IL-6) was measured in 60 preterm infants (600-1600 g) as a clinical index in neonatal necrotizing enterocolitis (NEC). Escherichia coli, Klebsiella, Enterobacter, and Clostridium spp, identified by routine bacteriology, were each strongly associated with elevated concentrations of endotoxin (P < 0.01) in stool filtrates with Clostridium spp most strongly associated with NEC disease. Stool filtrate endotoxin (endotoxin units [EU] per gram) measured by a Limulus amebocyte lysate assay was age-dependent. Samples from stage I NEC (61%) and infants with advanced disease (67%) had notably elevated levels of stool endotoxin (>10 ln EU/g) compared with NEC-negative (47%) samples tested. Plasma and stool IL-6 generally tested at the low, nonmeasurable limit of the enzyme-linked immunosorbent assay (ELISA) for NEC-negative (88%) and stage I NEC (93%), although a small proportion of samples (25%) from infants with stage II or II NEC had elevated stool concentrations of IL-6. We conclude that identification of toxin-producing organisms and endotoxin elevations in stool filtrates are more useful than circulating levels of endotoxin in plasma in predicting mucosally limited disease in the gastrointestinal tract. The prognostic value of monitoring stool endotoxin in infants with overgrowth of gram-negative bacteria has implications for therapeutic strategies for patients with early and advanced stages of disease. Monitoring inflammatory cytokines (IL-6) in relation to endotoxin values in stool appears of limited clinical value in controlling this devastating disease in preterm neonates.

Bacterial Toxins↗