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PubMed2005

Necrotizing enterocolitis after antipsychotic treatment involving clozapine and review of severe digestive complications -- a case report.

A case of necrotizing enterocolitis in a 19-year old man treated for schizophrenic disorder, induced by a drug association involving clozapine and requiring surgical treatment, is presented. To our knowledge only few reports have described the occurrence of this complication with atypical antipsychotics. Evidence for linking this complication to clozapine was reinforced by the absence of any viral or bacterial infection. The authors present a review of similar cases, stress the potential hazards induced by such drug combinations and discuss supposed mechanisms of this enterocolitis.

Adult↗
PubMedDate not supplied

[Pathogenetic concepts of neonatal necrotizing enterocolitis].

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 hypoxemia, the uptake, transport, delivery and consumption of oxygen, the digestion of carbohydrates and proteins and in intestinal motility between premature and term infants exist. The diving-reflex too is important for intestinal pathophysiology in these patients. The central key of the pathogenesis is the evident vascular damage. Infectious agents, inflammatory mediators, circulatory insufficiency, feeding excess is followed by the initial mucosal damage. This results in an increased intestinal permeability also for inflammatory mediators, endotoxins, bacteria and gas. Ileus, stasis and gas production cause endotoxinemia and abdominal distension. Increased intraluminal pressure with or without activation of inflammatory mediators leads to an important vascular dysregulation. Consecutively these multiple facts cause the "ischemic looking" hemorrhagic necrosis, we call necrotizing enterocolitis.

Acute-Phase Proteins↗
PubMed1989

The role of radiology in Campylobacter enterocolitis.

A series of 18 patients with diarrhoea and positive stool cultures for Campylobacter jejuni is presented. The most important radiological features were thickening of ileal mucosal folds, of interhaustral indentations and of the ileocaecal valve, lymphoid hyperplasia and microulcerations. Radiology, as well as endoscopy, are both nonspecific in Campylobacter jejuni enterocolitis. The importance of radiology is to exclude more typical features of other causes of inflammatory bowel diseases. Moreover, before the result of the stool culture is available, the radiological features should suggest the suspicion of an acute infectious enterocolitis by Campylobacter jejuni as possible diagnosis.

Adult↗
PubMed1983

Necrotizing enterocolitis as a result of cow's milk allergy?

A three-day-old newborn developed necrotizing enterocolitis in absence of the usual precipitating factors. Colonic perforation necessitated surgical intervention. After recovery cow's milk allergy was diagnosed. Probably this food allergy was the cause of the development of the necrotizing enterocolitis.

Animals↗
PubMed1981

[Atresia and obliteration of the small bowel in cases of necrotizing enterocolitis (author's transl)].

As a result of necrotizing enterocolitis, one patient developed multiple obliterations of jejunum and ileum, partly over long stretches of bowel. In a second case of a neonate with enterocolitis necroticans, an ileum atresia formed in the second and third weeks of life, completely interrupting the continuity of the intestine. In the literature, we could only find one report comparable with each case.

Enterocolitis, Pseudomembranous↗
PubMed2003

Early feeding after necrotizing enterocolitis in preterm infants.

OBJECTIVE: To report our experience with an early initiation of enteral feedings after necrotizing enterocolitis (NEC). STUDY DESIGN: Over a 4-year period, all inborn infants with NEC Bell stage II or greater received enteral feedings, increased by 20 mL/kg/d, once no portal vein gas had been detected on ultrasound for 3 consecutive days (group 1). Infants were compared with a historic comparison group (group 2). RESULTS: Necrotizing enterocolitis rates were 5% (26/523) in the early feeding group and 4% (18/436) in the comparison group. One early feeding infant and two comparison group infants died of NEC, whereas two and one, respectively, had recurrent NEC. Enteral feedings were restarted at a median of 4 days (range, 3-14) versus 10 days (range, 8-22) after onset of NEC. Early feeding was associated with shorter time to reach full enteral feedings (10 days [range, 7-31] vs 19 days [range, 9-76], P<.001), a reduced duration of central venous access (13.5 days [range, 8-24] vs 26.0 days [range, 8-39], P<.01), less catheter-related septicemia (18% vs 29%, P<.01), and a shorter duration of hospital stay (63 days [range, 28-133] vs 69 days [range, 36-150], P<.05). CONCLUSION: Early enteral feeding after NEC was associated with significant benefits and no apparent adverse effects. This study was underpowered, however, to exclude a higher NEC recurrence risk potentially associated with this change in practice.

Enteral Nutrition↗
PubMed2000

Inflammation in the developing human intestine: A possible pathophysiologic contribution to necrotizing enterocolitis.

Necrotizing enterocolitis (NEC), a major cause of morbidity and mortality in premature infants, occurs after the introduction of oral feedings in conjunction with initial bacterial colonization of the gut and is hypothesized to be due to an immature (inappropriate) enterocyte response to bacterial stimuli. To test this hypothesis, we compared the enterocyte IL-8 response to inflammatory stimuli [lipopolysaccharide (LPS) and IL-1beta] in immature vs. mature human small intestine. Initial in vitro studies comparing confluent Caco-2 cells, a model for mature human enterocytes, with a primary human fetal intestinal cell line (H4 cells) demonstrated that after inflammatory stimulation fetal cells secreted more IL-8 (LPS, 8-fold; IL-1beta, 20-fold) than Caco-2 cells. IL-8 mRNA activity in fetal compared to Caco-2 cells was proportionately increased by the same magnitude with both stimuli. To validate the in vitro observations, small intestinal organ cultures from fetuses vs. older children were exposed to LPS and IL-1beta. Again in human organ cultures from fetuses compared to older children, IL-8 secretion was greater (LPS, 2.5-fold; IL-1beta, 200-fold) and mRNA activity after stimulation was comparably higher, suggesting that increased transcription of the IL-8 gene may account for the excessive response. Using immunohistochemical staining to identify the cellular source of IL-8, activity was noted predominantly in villous and crypt epithelium but also in a few immunoresponsive lymphoid cells. The observation that immature human enterocytes react with excessive pro-inflammatory cytokine production after inflammatory stimulation may help in part explain why prematures exposed to initial colonizing bacteria develop necrotizing enterocolitis.

Adenocarcinoma↗
PubMed1990

Necrotizing enterocolitis: an overlooked life-threatening complication of acute diarrhoeal illness in infants and children.

A 7-month-old girl developed necrotizing enterocolitis with extensive pneumatosis intestinalis following an acute diarrhoeal illness. This was preceded by the use of an anti-motility drug and repeated attacks of paralytic ileus. It is noteworthy that all the published cases of necrotizing enterocolitis following acute diarrhoeal illness in infants and children are from tropical countries. This might be related to the use of anti-diarrhoeal drugs and associated malnutrition resulting in hypokalaemia and hypoalbuminaemia.

Diarrhea, Infantile↗
PubMedDate not supplied

Neutropenic enterocolitis in children with acute lymphoblastic leukemia.

Neutropenic enterocolitis is an acute, life-threatening inflammation of the small and large bowel, often seen in children with malignancies during periods of prolonged or severe neutropenia. During the period 1990-1995, 180 children were treated at the authors' center for acute lymphoblastic leukemia using a standard chemotherapy protocol. Among them, 11 children (6.1%) aged 4 to 12 years, were diagnosed clinically to have neutropenic enterocolitis. Eight had severe neutropenia (absolute neutrophil count < 10(8)/L and 5 had prolonged neutropenia (> 7 days duration). The symptoms included diffuse abdominal pain (10 children), oral mucositis (7), hematochezia (7), diarrhea (6), hematemesis (5), and right lower quadrant tenderness (4). Three children had radiological evidence of free intraperitoneal gas and an additional 3 children were found on surgical exploration to have cecal perforation. Laparotomy was performed on 8 children (73%), 4 of whom survived. Among the 3 children managed conservatively, 1 died awaiting surgical exploration, while the other 2 did well. The overall survival was 55%. The authors recommend an approach to management that respects the heterogeneity of the disease.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1982

Campylobacter-associated enterocolitis in childhood. Report of a fatal case.

The full clinical range of Campylobacter fetus enterocolitis has become apparent only recently. This case study describes the clinical and pathologic findings in a chronically ill child who developed signs of inflammatory bowel disease. Following a negative bacteriologic culture, Crohn's disease was diagnosed by roentgenographic criteria. A trial of immunosuppressive therapy failed, and a repeat of microbiologic examination identified a heavy growth of Campylobacter fetus ss. jejuni. Various complications developed and the patient died with a coagulopathy and a widespread enterocolitis. The role of the Campylobacter in this clinical setting of inflammatory bowel disease is discussed in light of current understanding.

Campylobacter Infections↗
PubMed1996

Increased risk of necrotizing enterocolitis in premature infants with patent ductus arteriosus treated with indomethacin.

OBJECTIVE: The authors evaluated the risk of necrotizing enterocolitis (NEC) in very low birth weight infants receiving indomethacin (INDO) to close patent ductus arteriosus (PDA). BACKGROUND DATA: Controversy exists regarding the best method of managing very low birth weight infants with PDA and whether to employ medical management using INDO or surgical ligation of the ductus. METHODS: Two hundred fifty-two premature infants with symptomatic PDA were given intravenously INDO 0.2 mg/kg every 12 hours x 3 in an attempt to close the ductus. Patients were evaluated for sex, birth weight, gestational age, ductus closure, occurrence of NEC, bowel perforation, and mortality. RESULTS: There were 135 boys and 117 girls. The PDA closed or became asymptomatic in 224 cases (89%), whereas 28 (11%) required surgical ligation. Ninety infants (35%) developed evidence of NEC after INDO therapy. Fifty-six were managed medically; surgical intervention was required in 34 of 90 cases (37.8%) or 13% of the entire PDA/INDO study group. Bowel perforation was noted in 27 cases (30%). Factors associated with the onset of NEC included gestational age < 28 weeks, birth weight < 1 kg, and prolonged ventilator support. The overall mortality rate was 25.5%, but was higher in infants with NEC versus those without. The highest mortality was noted in perforated NEC cases. The PDA/INDO patients were compared with a control group of 764 infants with similar sex distribution, birth weights, and gestational ages without PDA who did not receive INDO. Necrotizing enterocolitis occurred in 105 of 764 control patients (13.7%), including 13 (12.3%) with perforation. The overall mortality rate of controls was 25%, which was similar to the overall 25.5% mortality rate in the PDA/INDO study group. CONCLUSION: These data indicate that there is increased risk of NEC and bowel perforation in premature infants with PDA receiving INDO. Mortality was higher in the PDA/INDO group with NEC than those PDA/INDO infants without NEC.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Molecular mechanisms contributing to necrotizing enterocolitis.

OBJECTIVE: To examine the cellular mechanisms involved in the pathogenesis of necrotizing enterocolitis (NEC). SUMMARY BACKGROUND DATA: Necrotizing enterocolitis is a major cause of death and complications in neonates; the cellular mechanisms responsible for NEC are unknown. The inducible form of cyclooxygenase (i.e., COX-2) is activated by the transcription factor nuclear factor (NF)-kappaB and is thought to play a role in inflammation. METHODS: Segments of perforated and adjacent uninvolved small intestine from neonates with NEC were analyzed for COX-2 expression by immunohistochemistry. NEC was induced in weanling (18 days old) rats by occlusion of superior mesenteric vessels for 1 hour and intraluminal injection of platelet activating factor (50 micro/kg). Small intestine was harvested for protein extraction. Western immunoblot was performed to determine expression of COX-2. Gel shift assays were performed to assess NF-kappaB binding activity. RESULTS: Immunohistochemical analysis showed increased COX-2 protein expression in the perforated intestinal sections of all 36 neonates but not in adjacent normal intestine. Increased expression of COX-2 protein and NF-kappaB binding activity was noted in the small intestine of weanling rats at 0 and 3 hours after induction of NEC. CONCLUSIONS: Increased COX-2 expression was identified in all neonatal intestinal segments resected for perforated NEC. In addition, a coordinate induction of COX-2 expression and NF-kappaB binding was noted in a rodent model of NEC. These findings suggest that the COX-2/NF-kappaB pathway may play a role in the pathogenesis of NEC. Therapeutic agents that target this pathway may prove useful in the treatment or possible prevention of NEC.

Animals↗
PubMed2003

Neonatal necrotizing enterocolitis: an overview.

PURPOSE OF REVIEW: Necrotizing enterocolitis represents a disease entity that remains quite challenging for neonatologists all around the world, in that its aetiology has yet to be revealed, but it is the cause of death for many premature infants each year, affecting up to 28% of very low birthweight infants. This is an attempt to improve the management of affected babies and stimulate more research concerning new diagnostic tools. RECENT FINDINGS: Current trends in the field of (early) diagnosis, such as: (1) imaging techniques, e.g. contrast radiography, portal vein ultrasonography, magnetic resonance, radionuclide scanning; (2) gastrointestinal tonometry; (3) the detection of biochemical markers, cytokines, growth factors; and (4) the determination of the mean peak hydrogen: carbon dioxide ratio excreted in breath, are only some of those mentioned. Various novel preventive techniques are also presented, among which platelet-activating factor acetyl hydrolase activity enhancement, platelet-activating factor receptor antagonists and probiotics, such as Bifidobacterium infantis and Lactobacillus acidophilus, seem quite promising. Regarding treatment, the use of oxygenated perfluorocarbon has added to the limited alternatives available. These data along with other recent discoveries concerning the risk factors and pathogenesis of this disease create a full picture of the current opinion on this topic. SUMMARY: Keeping in mind that the key to confronting such a devastating disorder as necrotizing enterocolitis is early diagnosis and prevention, both clinically applicable and experimental advances are presented with the hope of improving the survival rates of patients affected.

Enterocolitis, Necrotizing↗
PubMed1995

Diffusely increased colonic F-18 FDG uptake in acute enterocolitis.

A 60-year-old woman with a remote history of colon carcinoma was studied with F-18 FDG PET imaging 5 days after admission for acute toxigenic enterocolitis. Marked and diffusely increased uptake was noticed throughout the ascending and transverse colon, which was noticed to be edematous and thickened on contrast CT examination. The study emphasizes the need to consider nonneoplastic entities, such as enterocolitis in the differential diagnosis of intensely hypermetabolic colonic lesions on F-18 FDG PET examinations.

Acute Disease↗
PubMed1979

Small intestinal changes in enterocolitis complicating Hirschsprung's disease.

Hirschsprung's disease is one of the more common causes of childhood bowel obstruction. The disease can cause enterocolitis which, untreated, may result in considerable mortality. We describe our evaluation of two infants who suffered from intractable diarrhea of infancy secondary to Hirschsprung's disease. We found that mucosal damage to the small bowel and disaccharidase deficiency are among the most important mechanisms producing this complications. Therefore, management of enterocolitis including parenteral alimentation should proceed as soon as the complication is observed.

Biopsy↗
PubMed1999

Eosinophilic enterocolitis and visceral neuropathy with chronic intestinal pseudo-obstruction.

A patient is described who was found to have both eosinophilic enterocolitis and visceral neuropathy with chronic idiopathic intestinal pseudo-obstruction. The etiology and pathogenesis of this rare combined disorder of the gastrointestinal tract are discussed. Although eosinophilic enterocolitis is amenable to conservative treatment, surgery may be necessary for palliation in selected patients with pseudo-obstruction due to visceral neuropathy.

Adult↗
PubMed2002

Cytomegalovirus enterocolitis in an immunocompetent individual.

We report a rare case of cytomegalovirus (CMV) enterocolitis in a healthy 57-year-old woman. In March 1999, she developed hematochezia, diarrhea, and abdominal pain. Total colonoscopy on March 17th showed multiple aphthoid lesions and friable mucosa from the terminal ileum to the rectum and a shallow ulcer on the ileocecal valve. Repeat total colonoscopy on April 19th showed faded aphthoid lesions in the terminal ileum, and biopsy specimen revealed CMV inclusion bodies. Symptoms and endoscopic findings improved without any specific medication. In previous reports, the definition of "immunocompetent individual" varied. Here, we define immunocompetent individual as one who has no associated diseases, is not under immunosuppressive therapy, has no recent history of operation, is negative for human immunodeficiency virus antibody, is not pregnant, has no obvious infectious course, and is less than 70 years of age. This is the ninth report of CMV enterocolitis in an immunocompetent individual in the world literature.

Colonoscopy↗
PubMedDate not supplied

Evaluation of hexosaminidase activity as a potential biochemical marker in serum for necrotizing enterocolitis.

The presence of increased serum activity of the lysosomal hydrolase hexosaminidase has been suggested to be potentially useful in the diagnosis of neonatal necrotizing enterocolitis (NEC). In the present study, serum activity of hexosaminidase was measured in 19 neonates with NEC and compared to developmental patterns of enzyme activity determined in 61 neonates without NEC. Infants with NEC were studied at intervals starting at the onset of disease and continuing until 6 weeks after diagnosis. In normal infants, serum activity of hexosaminidase increases with increasing gestational and postnatal ages. However, infants with NEC had relatively lower serum hexosaminidase activity than these control infants of similar gestational and postnatal ages. Necrotizing enterocolitis is not associated with increased serum activity of hexosaminidase.

Enterocolitis, Pseudomembranous↗