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At least 289 records · Page 16Linked to original sources
PubMed2006

Cytomegalovirus enterocolitis complicated by perforated appendicitis in a premature infant.

A 9-week-old, former 30-week estimated gestational age premature infant had recurrent episodes of abdominal distention. Laparotomy revealed partial small bowel obstruction caused by ileocecal inflammation with stenosis, and a perforated appendix with fistulization into the cecum. The resected appendix and ileocecal junction showed intranuclear and intracytoplasmic viral inclusions, and were cytomegalovirus positive by immunoperoxidase staining, which implicated cytomegalovirus as the etiology of the recurring bouts of enterocolitis with appendicitis. Cytomegalovirus is frequently overlooked in the differential diagnosis of enterocolitis and chronic gastrointestinal symptoms in infants, but should be included as in older immunocompromised patients.

Appendicitis↗
PubMed2007

Heparin-binding epidermal growth factor-like growth factor promotes enterocyte migration and proliferation in neonatal rats with necrotizing enterocolitis.

PURPOSE: We have shown that heparin-binding epidermal growth factor-like growth factor (HB-EGF) decreases experimental necrotizing enterocolitis (NEC). Intestinal epithelial cell (IEC) migration (restitution) and proliferation are key elements in recovery from intestinal injury. Here, we investigated whether the beneficial effects of HB-EGF are mediated, in part, by its ability to affect these processes. METHODS: Necrotizing enterocolitis was induced in newborn rats by exposure to stress (hypoxia, hypothermia, hypertonic feedings, and lipopolysaccharide), with pups receiving different doses of HB-EGF (0, 25, 50, 100, 200, 400, 600, and 800 microg/kg). To investigate the effect of HB-EGF on enterocyte proliferation and migration, bromodeoxyuridine was administered intraperitoneally 18 hours before sacrifice, with intestine subjected to bromodeoxy-uridine immunohistochemistry. RESULTS: The incidence and severity of experimental NEC decreased, and the survival rate increased, with increasing doses of HB-EGF. Results were confirmed using scanning electron microscopy. Migration of IEC in breast-fed pups was 7.07 microm/h, decreased significantly to 2.29 microm/h in stressed pups, and was significantly improved at 5.95 microm/h in pups subjected to stress but treated with HB-EGF (P < .05). Quantification of IEC proliferation revealed 208 (+) cells per high-power field (HPF) in breast-fed pups, which decreased significantly to 99 (+) cells per HPF in stressed pups and increased to 190 (+) cells per HPF in stressed pups treated with HB-EGF (P < .05). CONCLUSIONS: These results demonstrate that HB-EGF protects newborn rats from experimental NEC in a dose-dependent fashion. The ability of HB-EGF to protect the intestines from NEC is due, in part, to the ability of HB-EGF to preserve enterocyte migration and proliferation.

Animals↗
PubMed2004

Neutropenic enterocolitis (typhilitis) associated with docetaxel therapy in a patient with non-small-cell lung cancer: case report and review of literature.

Neutropenic enterocolitis (NE) is an unusual acute complication of neutropenia, most often associated with leukemia and lymphoma which is characterized by segmental cecal and ascending colon ulceration that may progress to necrosis, perforation, and septicemia. We present a case of neutropenic enterocolitis in a patient with non-small-cell lung cancer who received docetaxel and flavopiridol as part of a phase I clinical trial and review cases in the literature where docetaxel was involved. Given the increased use of docetaxel and other taxanes in the treatment of advanced lung cancer, physicians should be aware of this potential toxicity of therapy.

Aged↗
PubMed2005

Lactoferrin-enhanced anoikis: a defense against neonatal necrotizing enterocolitis.

Enteral nutrition with human milk lowers the incidence of necrotizing enterocolitis in preterm human infants. Lactoferrin, the major whey protein in human milk, has many functions related to host defense against bacterial infection. Here, we hypothesize that lactoferrin also helps terminate bacterial invasion of enterocytes via a detachment-induced apoptosis called anoikis. Death of infected epithelia by anoikis prevents local spread of bacterial pathogens because the bacteria are trapped within the cell. Such infected, apoptotic and sloughed epithelia also cannot infect the lower gastrointestinal tract, and the epithelia exit the body in the stool. Currently, anoikis is a phenomenon related to the renewal of enterocytes, and it is not recognized as an anti-bacterial host defense. We suggest that anoikis of infected enterocytes is a process in which lactoferrin plays an important role. In a pilot study in which neonatal rats were pre-treated with intra-gastric recombinant human lactoferrin, we found evidence of epithelia with anoikis in ileal fluid after enteric infection. This finding was rarely seen in infected neonatal rats without pre-treatment with lactoferrin. Quantitative analysis of intestinal lavage specimens and quantitative stereology of apoptotic epithelia in this model will be required to verify the theory. We propose that oral use of recombinant human lactoferrin might have these hypothesized and other anti-bacterial effects in preterm infants, and hence, this protein might prevent necrotizing enterocolitis in preterm infants who cannot take human milk.

Animals↗
PubMed2006

Fatal enterocolitis in Asian elephants (Elephas maximus) caused by Clostridium difficile.

Two cases of fatal enteritis caused by Clostridium difficile in captive Asian elephants are reported from an outbreak affecting five females in the same zoo. Post mortem examination including histopathology demonstrated fibrinonecrotic enterocolitis. C. difficile was isolated by selective cultivation from two dead and a third severely affected elephant. Four isolates were obtained and found positive for toxin A and B by PCR. All isolates were positive in a toxigenic culture assay and toxin was demonstrated in the intestinal content from one of the fatal cases and in a surviving but severely affected elephant. PCR ribotyping demonstrated that the C. difficile isolates shared an identical profile, which was different from an epidemiologically unrelated strain, indicating that the outbreak was caused by the same C. difficile clone. It is speculated that the feeding of large quantities of broccoli, a rich source of sulforaphane, which has been shown to inhibit the growth of many intestinal microorganisms may have triggered a subsequent overgrowth by C. difficile. This is the first report of C. difficile as the main cause of fatal enterocolitis in elephants. The findings emphasize the need to regard this organism as potentially dangerous for elephants and caution is recommended concerning antibiotic treatment and feeding with diets containing antimicrobials, which may trigger an expansion of a C. difficile population in the gut.

Animals↗
PubMed2003

Are localized intestinal perforations distinct from necrotizing enterocolitis?

BACKGROUND/PURPOSE: Localized intestinal perforation (LP) is thought to be a distinct entity when compared with perforation associated with necrotizing enterocolitis (NEC). Studies have indicated that LP is more amenable to percutaneous drainage and associated with a better outcome. We sought to determine whether LP and NEC could be distinguished based on clinical parameters alone. METHODS: A retrospective review of 40 neonates with gastrointestinal perforations between January 1990 and May 1998 was performed. All had undergone laparotomy and had histologic specimens available for evaluation. RESULTS: Twenty-one neonates had necrotizing enterocolitis (NEC), and 19 had localized perforation (LP) based on histologic criteria. More neonates with LP were exposed to prenatal indomethacin (37% v 5%; P <.05), received intravenous dexamethasone (42% v 10%; P <.05), had umbilical artery catheters (63% v 14%; P <.05), and had a higher white blood cell (WBC) count (27.1 +/- 23.1 v 14.3 +/- 11.5; P <.05). More neonates with NEC had pneumatosis intestinalis (47% v 11%; P <.05). No significant differences existed in enteral feeding (16% LP v 38% NEC) or overall mortality rate (37% LP v 38% NEC). No statistical differences in the timing of perforation or clinical presentation were found. CONCLUSIONS: NEC and LP are difficult to distinguish based on clinical parameters alone. The authors did find associations between LP and prenatal indomethacin, intravenous dexamethasone, umbilical artery catheters, and a higher WBC count. Mortality rate and clinical outcome were nearly identical in both groups. Pneumatosis intestinalis, thought to be pathognomonic for NEC, was seen on abdominal radiograph in 2 babies with histologically proven LP.

Adult↗
PubMed1978

Hirschsprung's enterocolitis, prostaglandins, and response to cholestyramine.

An infant with Hirschsprung's enterocolitis developed a fulminant secretory diarrhea unresponsive to all conventional therapy until cholestyramine was administered. A 12-fold decrease in prostaglandin E (PGE) levels in the colostomy fluid was documented in response to cholestyramine therapy. It is postulated that increased PGE activity, enterotoxin, and bile acid malabsorption may be involved in the enterocolitis of Hirschsprung's disease.

Cholestyramine Resin↗
PubMed1983

Hexosaminidase: a marker for intestinal gangrene in necrotizing enterocolitis.

Detection of intestinal ischemia, prior to necrosis, is a major clinical problem. The lysosomal acid hydrolase, hexosaminidase (HEX), is known to be elevated in intestinal infarction. To determine if this enzyme could differentiate between partial intestinal ischemia and full-thickness intestinal gangrene, the following rat study was designed. Partial segmental intestinal ischemia was created by ligating alternate vascular bundles over a short (6 vessel) segment of the small-bowel mesentery, and complete segmental intestinal vascular occlusion was achieved by ligating the blood supply to the ileocecal segment. Preoperative serum HEX values were obtained from 15 animals. The rats were separated into one sham-operated and two intestinal ischemia groups. At four hours after surgery HEX values were determined. Total HEX activity was significantly elevated four hours after insult in both partial and complete intestinal ischemia, (P less than 0.005 and P less than 0.001 respectively). Total HEX activity was greater in complete intestinal ischemia than in partial ischemia, (P less than 0.05). Three neonates with intestinal perforation, secondary to necrotizing enterocolitis, were evaluated. The mean preoperative HEX activity was 1421 nmol/hr/mL serum and the mean post-resection HEX activity was 808 nmol/hr/mL serum. These data suggest that serum HEX activity may be a good marker for intestinal gangrene in neonates with necrotizing enterocolitis.

Animals↗
PubMed1986

A mouse model for the study of necrotizing enterocolitis.

A mouse model for the study of necrotizing enterocolitis is presented. It is a model of temporary intestinal ischemia and consists of occluding both superior mesenteric vessels with a bulldog clamp for varying periods of time. The resultant lesions resemble the intestinal lesions seen in necrotizing enterocolitis in respect to the gradual development of the necrotizing lesions and their patchy distribution. We also studied the effect of intravenous saline and low molecular weight dextran in preventing the development of these ischemic lesions. In moderate ischemia, saline and dextran show a similar protective effect, and in severe ischemia, both show a protective effect, with dextran being more effective than saline.

Animals↗
PubMed1988

Natural history and pathophysiology of enterocolitis in the piebald lethal mouse model of Hirschsprung's disease.

A breeding colony of piebald lethal mice was established in order to study the natural history of congenital megacolon in a mouse model of Hirschsprung's disease and to investigate mucosal defense mechanisms and secretory functions in enterocolitis complicating congenital megacolon. In experiment 1, 214 mice were studied, 53 of which had congenital megacolon. All piebald lethal mice with congenital megacolon (S1/S1) died at 3 to 11 weeks of age. Two distinct patterns of mortality were identified. A majority of mice (64%) became acutely ill at 3 to 4 weeks of age and died, whereas the remainder died between 9 and 11 weeks of age. The former group of mice exhibited clinical and histologic evidence of severe enterocolitis while the latter group had massive abdominal distension and classical megacolon. In experiment 2, piebald mice with congenital megacolon were killed at the time of acute illness. Significant histologic and immunohistochemical differences were seen in the ganglionic colon between piebald mice with early clinical onset of acute illness and piebald mice with the classical clinical picture of congenital megacolon. In the former group of mice the number of immunocytes in the lamina propria was significantly higher than in control mice (P less than .001), immunoglobulin-producing cells were equally distributed throughout the lamina propria and IgA-containing cells were by far the most abundant cell type identified in the colon. In the latter group of mice, immunocyte responses were significantly low and the distribution of immunocytes markedly different, with the immunoglobulin-producing cells being located only at the deep layer of lamina propria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The pathophysiology of Hirschsprung's-associated enterocolitis: importance of histologic correlates.

To more clearly define the pathophysiology of Hirschsprung's-associated enterocolitis (HAEC), this study comprehensively evaluates the gastrointestinal tissue of a group of infants with clinical HAEC. A pathologic grading system that demonstrates a progressive sequence of histologic changes specific for HAEC is established. The grading system correlates closely with clinical enterocolitis and may prove to be a useful method for early detection of infants at risk for the development of clinical HAEC. A significant alteration of intestinal mucins with an increase in neutral mucins and a decrease in acidic-sulfomucins was identified in HAEC tissue specimens. Enterocyte-adherent organisms were present in 39% of HAEC tissue specimens. The pathogenesis of HAEC may result from an alteration in intestinal mucins that may allow for the subsequent adherence of enteropathogenic organisms to enterocytes. The enterocyte-adherent organisms have the potential to induce an enterocolitic process and may contribute to both the intestinal and systemic manifestations of HAEC.

Enterocolitis↗
PubMed1976

Neonatal pneumatosis coli: a mild form of neonatal necrotizing enterocolitis.

A distinctive form of necrotizing enterocolitis was observed in seven newborn infants in a 4 1/2-year period. Characteristically these patients had gross blood in the stools, but other local and systemic signs were mild or absent. Radiography mainly revealed submucosal intramural intestinal gas which was limited to the colon (pneumatosis coli). There was no evidence of small bowel involvement as judged by the absence of small intestinal pneumatosis or distension. This form of colonic disease should be recognized as a benign variety of neonatal necrotizing enterocolitis that carries a favorable prognosis and responds to medical management without sequelae.

Enterocolitis, Pseudomembranous↗
PubMed1982

The prevalence of Clostridium difficile and toxin in a nursery population: a comparison between patients with necrotizing enterocolitis and an asymptomatic group.

During a period when certain neonates in our nursery developed necrotizing enterocolitis, we studied stool specimens from a population of symptomatic and asymptomatic patients for the presence of Clostridium difficile and its toxin. The presence of the organism among nursery personnel and in the nursery environment was also evaluated. Results showed that five symptomatic neonates and 17 asymptomatic neonates in a population of 37 patients studied in our neonatal intensive care and intermediate care nurseries had positive stool cultures for C. difficile. Toxin was detected in stool from four of five symptomatic patients and was present at dilutions of greater than 1/125 in stool from six asymptomatic patients who were culture positive for C difficile. The organism was not found in stool samples from any nursery personnel but was recovered from the hand culture of a nursery worker and from the inanimate environment. Although our findings support the notion of nosocomial spread of C difficile, we were unable to clearly implicate the organism as the cause of necrotizing enterocolitis in our nursery.

Bacterial Toxins↗
PubMed1997

Plasma L-arginine concentrations in premature infants with necrotizing enterocolitis.

OBJECTIVE: To determine whether L-arginine concentrations (the substrate for nitric oxide synthesis) are lower in premature infants in whom necrotizing enterocolitis (NEC) develops than in unaffected infants. METHODS: We measured arginine and nutritional intake, plasma arginine, glutamine, total amino acids, and ammonia concentrations in 53 premature infants (mean gestational age +/- SD: 27 +/- 1.7 weeks) at risk of NEC. Measurements were done on days 3, 7, 14 and 21 and just before treatment in infants with NEC. RESULTS: Necrotizing enterocolitis developed in 11 infants between postnatal days 1 and 26. On day 3, plasma arginine concentrations were decreased compared with normal published values (mean +/- SE, 41 mumol/L +/- 4). Arginine concentrations increased with day of life of measurement (p < 0.001) and arginine intake (p < 0.001). Plasma arginine concentrations were significantly lower at the time of diagnosis in infants with NEC compared with control subjects, even after adjusting for arginine intake and day of life (p = 0.032). Plasma glutamine and total amino acid concentrations were not significantly different in infants with NEC compared with control subjects. Plasma ammonia concentrations were elevated on day 3 (mean +/- SE, 72 +/- 3.3 mumol/L) and decreased with postnatal age (p < 0.001) and increasing plasma arginine concentrations (p < 0.001). CONCLUSION: Plasma arginine concentrations are decreased at the time of diagnosis in premature infants with NEC. The potential benefit of arginine supplementation in the prevention of the disease deserves evaluation.

Age Factors↗
PubMed1996

Necrotizing enterocolitis: the search for a unifying pathogenic theory leading to prevention.

During the past two decades, necrotizing enterocolitis has emerged as a major cause of mortality and morbidity in premature infants. The specific cause of the disease remains enigmatic, but several putative risk factors provide clues to a pathophysiology that seems to be multifactorial. With the use of newly developed scientific tools, an understanding of the basic pathophysiologic cascade that causes necrotizing enterocolitis is emerging, providing hope for improved treatment and prevention.

Anti-Bacterial Agents↗
PubMed1992

Necrotizing enterocolitis in infancy.

The most common gastrointestinal emergency in the newborn is necrotizing enterocolitis. Premature babies are the most likely victims, but it also occurs in full-term infants. Although great strides have been made in elucidating some of the factors responsible for necrotizing enterocolitis, such as intestinal ischemia, bacterial overgrowth, and feeding dysfunction, the exact etiology is as yet unclear. The timing and indications for surgery differ from institution to institution, but the long-term outcome is similar in most large series. The overall mortality rate remains about 20% to 40%, and of the survivors, about one half seem to have no sequelae, the remaining infants having neurologic and gastrointestinal deficits of various degrees of significance.

Enterocolitis, Pseudomembranous↗
PubMed2003

Faecal calprotectin concentrations and diagnosis of necrotising enterocolitis.

Calprotectin has been proposed as a useful marker of inflammatory bowel disease in children. We did a pilot study to establish whether it can be used to aid diagnosis of necrotising enterocolitis in preterm infants. Patients with clinical features of necrotising enterocolitis had raised faecal calprotectin concentrations at the time of diagnosis compared with matched controls (288.4 mg/L [SD 49.1] and 98.0 mg/L [60.6], respectively; p=0.0006). Faecal calprotectin might be a useful marker of gastrointestinal mucosal inflammation in neonates.

Case-Control Studies↗
PubMed1978

Fulminant necrotising enterocolitis associated with Clostridia.

5 infants with no growth of bacteria on cultures of blood and peritoneal fluid recovered from necrotising enterocolitis after medical treatment alone. 12 infants with positive cultures required surgery. 5 of these 12, who did not harbour clostridia, had a mild clinical course and all 5 survived segmental bowel resection. The 7 infants who harboured clostridia had a more severe clinical course and 4 died. In 3 of 4 infants with Clostridium perfringens, the necrotising enterocolitis was fulminant, characterised by severe pneumatosis intestinalis, extensive gangrene, early intestinal perforation, and a fatal outcome.

Ascitic Fluid↗