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Campylobacter infection in 682 bulgarian patients with acute enterocolitis, inflammatory bowel disease, and other chronic intestinal diseases.

The aim of the study was to assess Campylobacter infections in 309 patients with acute enterocolitis, 272 patients with relapses of chronic enterocolitis, 70 patients with inflammatory bowel disease (involving Crohn's disease and ulcerative colitis) and 31 patients with other chronic intestinal illnesses. Isolation and identification were performed conventionally. Limited agar dilution method was used for susceptibility testing of the strains. Campylobacter species were isolated in patients with acute enterocolitis (7.8%), chronic enterocolitis (6.2%), Crohn's disease (6.2%), ulcerative colitis (3.7%), and irritable bowel syndrome (8.3%). Hippurate-positive Campylobacter jejuni isolates accounted for 62.2% of Campylobacter strains. One tetracycline resistant Campylobacter upsaliensis isolate was detected from a girl with acute enterocolitis. Resistance rates to erythromycin (31.1%) and clarithromycin (22.2%) were high, whereas those to amoxicillin/clavulanate (4.4%), ampicillin/sulbactam (13.3%), tetracycline (24.4%) and ciprofloxacin (22.2%) were relatively low. Resistance to erythromycin and either tetracycline or ciprofloxacin was detected in 8.9% and 6.7%. The involvement of Campylobacter infection in relapses of chronic intestinal disorders and the susceptibility patterns of the strains strongly emphasize the role of Campylobacter as a cause of infection in this group of patients.

Acute Disease↗

Enterocolitis in Hirschsprung's disease: a controlled study of the etiologic role of Clostridium difficile.

Cytopathic toxin neutralized by Clostridium sordellii antiserum was found in the feces of seven out of 13 children with Hirschsprung's disease complicated by enterocolitis (54%). Clostridium difficile was isolated from ten of these 13 children (77%). The frequency of fecal toxin positivity, the magnitude of toxin titers, and the isolation rate of C difficile were all significantly greater in children with Hirschsprung's enterocolitis than in children whose Hirschsprung's disease was not complicated by enterocolitis or in children without Hirschsprung's disease. It is suggested that C difficile may be causally related to enterocolitis in Hirschsprung's disease, but the age distribution of positive results indicates that the major etiologic role is confined to children under three years of age. Vancomycin was found to be an effective form of treatment in the children with enterocolitis in whom it was employed.

Bacteriological Techniques↗

Impaired gastrointestinal mucosal defense in Hirschsprung's disease: a clue to the pathogenesis of enterocolitis?

Twelve patients with Hirschsprung's disease were studied to investigate why some children develop enterocolitis. Previous studies have failed to explain this adequately; they have also failed to explain why enterocolitis can occur many years after definitive surgery. Six of the 12 patients had enterocolitis. By assessing immunological mucosal defense, it was shown that these patients had a marked deficiency in transfer of secretory IgA across the gastrointestinal mucosal cell, and thus were prone to mucosal invasion of both pathogenic and commensal organisms. The abnormalities were detected upon initial investigation (at presentation) prior to the onset of enterocolitis, and persisted into later life. The significance of these findings with reference to predicting which children are prone to develop enterocolitis and their long-term susceptibility to recurrence are discussed.

Digestive System↗

CDX-1 and CDX-2 are expressed in human colonic mucosa and are down-regulated in patients with Hirschsprung's disease associated enterocolitis.

Caudal type homeobox gene-1 and -2 (CDX-1 and CDX-2), homologues of the Drosophila homeobox gene caudal, encode transcription factors in endoderm derived tissues of the intestine. CDX genes control proliferation and differentiation of intestinal mucosal cells and colon cancer cells. Hirschsprung's Disease (HD) or congenital intestinal aganglionosis, a major developmental anomaly of intestine, which causes functional intestinal obstruction, is frequently associated with enterocolitis. Aetiology of HD-associated enterocolitis (HDEC) remains obscure. Reduction of gut mucosal enteroendocrine cells, and inefficient transfer of the secretory immunoglobulin A across the gut mucosal cell were shown to be associated with enterocolitis in HD patients suggesting that mucosa may directly involve in the pathophysiology of HDEC. This study aims to ascertain whether the CDX-1 and CDX-2 genes, that control the proliferation and differentiation of mucosal cells, play a role in HDEC. Using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridisation, we analysed the expression of CDX-1 and CDX-2 genes in colon specimens of normal controls, necrotising enterocolitis (NEC) infants, and HD patients with and without enterocolitis. We showed for the first time that CDX-1 and CDX-2 genes were expressed in the colonic mucosal epithelium in normal, NEC and in HD infants. However, the expressions of both genes were reduced in patients with HDEC. Our findings suggest that reduced expression of CDX-1 and CDX-2 genes in mucosa may be associated with the development of HDEC.

CDX2 Transcription Factor↗

Laparotomy versus peritoneal drainage for necrotizing enterocolitis and perforation.

BACKGROUND: Perforated necrotizing enterocolitis is a major cause of morbidity and mortality in premature infants, and the optimal treatment is uncertain. We designed this multicenter randomized trial to compare outcomes of primary peritoneal drainage with laparotomy and bowel resection in preterm infants with perforated necrotizing enterocolitis. METHODS: We randomly assigned 117 preterm infants (delivered before 34 weeks of gestation) with birth weights less than 1500 g and perforated necrotizing enterocolitis at 15 pediatric centers to undergo primary peritoneal drainage or laparotomy with bowel resection. Postoperative care was standardized. The primary outcome was survival at 90 days postoperatively. Secondary outcomes included dependence on parenteral nutrition 90 days postoperatively and length of hospital stay. RESULTS: At 90 days postoperatively, 19 of 55 infants assigned to primary peritoneal drainage had died (34.5 percent), as compared with 22 of 62 infants assigned to laparotomy (35.5 percent, P=0.92). The percentages of infants who depended on total parenteral nutrition were 17 of 36 (47.2 percent) in the peritoneal-drainage group and 16 of 40 (40.0 percent) in the laparotomy group (P=0.53). The mean (+/-SD) length of hospitalization for the 76 infants who were alive 90 days after operation was similar in the primary peritoneal-drainage and laparotomy groups (126+/-58 days and 116+/-56 days, respectively; P=0.43). Subgroup analyses stratified according to the presence or absence of radiographic evidence of extensive necrotizing enterocolitis (pneumatosis intestinalis), gestational age of less than 25 weeks, and serum pH less than 7.30 at presentation showed no significant advantage of either treatment in any group. CONCLUSIONS: The type of operation performed for perforated necrotizing enterocolitis does not influence survival or other clinically important early outcomes in preterm infants. (ClinicalTrials.gov number, NCT00252681.).

Birth Weight↗

Concentrations of IL-10 in preterm human milk and in milk from mothers of infants with necrotizing enterocolitis.

BACKGROUND: Despite the protective effects of human milk against necrotizing enterocolitis, the incidence is highest in the extremely premature infant, and only minimally decreased with feeding human milk. This suggests that certain protective agents may be lower in milk from mothers delivering extremely premature infants. The anti-inflammatory cytokine IL-10 was one possibility. AIM: We hypothesized that low concentrations of IL-10 in preterm milk contribute to the development of necrotizing enterocolitis in extremely premature infants. METHODS: IL-10 in human milk collected at weeks 1, 2, and 4 postpartum was measured by ELISA in mothers of infants born extremely premature at 23-27 wk gestation (group EP), premature at 32-36 wk gestation (group P), and term at 38-42 wk gestation (group T). Single milk samples were collected from a separate group of mothers whose infants developed necrotizing enterocolitis. RESULTS: There were no significant differences in concentrations of milk IL-10 among groups EP, P, or T. Concentrations of IL-10 declined as lactation progressed (p < 0.001). IL-10 in milk was frequently undetected in all groups, but even more so in the milk of the group of women whose infants had necrotizing enterocolitis (86%) than in groups EP (40%) and P (27%) (p < 0.01). CONCLUSION: IL-10 was present in preterm milk from most women, and the concentrations in preterm and term milk were not significantly different. A paucity of IL-10 in human milk was found in certain mothers in each group, especially in those whose infants developed necrotizing enterocolitis.

Adult↗

Epidemiologic characteristics of necrotizing enterocolitis: a population-based study.

The authors studied retrospectively the epidemiologic characteristics of necrotizing enterocolitis occurring among Georgia infants born during 1977 and 1978; 148 cases of necrotizing enterocolitis were identified. The highest incidence rate for necrotizing enterocolitis occurred among infants weighing 751-1000 g at birth and declined with increasing birth weight to less than 0.2 cases per 1000 live births among infants weighing more than 2500 g at birth. The overall incidence rate for blacks was significantly greater than that for whites (1.6 vs. 0.5 cases per 1000 live births, p = 0.01). The overall case fatality ratio was 38.5%; there were no differences in these ratios between blacks and whites. Necrotizing enterocolitis accounted for 15% of all deaths after the first week of life for infants weighting 1500 g or less at birth. If Georgia incidence rates and fatality ratios are applied to 1978 US births, it is estimated that 2210 cases of necrotizing enterocolitis with over 900 associated deaths would have occurred.

Birth Weight↗

Neutropenic enterocolitis in adults: systematic analysis of evidence quality.

OBJECTIVE: Neutropenic enterocolitis is a life-threatening complication occurring most frequently after intensive chemotherapy in acute leukaemias. The literature is heterogeneous and a systematic review is lacking. METHODS: Following a systematic search we categorised all relevant reports according to their quality and extracted evidence to answer the questions: Which diagnostic criteria are appropriate? What is the incidence of neutropenic enterocolitis? Are there good quality studies supporting specific interventions: Which empiric antimicrobial therapy is recommendable? Is neutropenic enterocolitis without surgical emergency complications an indication for bowel resection? RESULTS: We found and analysed 145 articles of these reports: 64 were reports of single cases, 30 papers reported of two or three cases, 13 were narrative reviews, 34 were retrospective case series of more than three cases and four were prospective diagnostic studies. There were no prospective trials or case control studies on the therapy of neutropenic enterocolitis. There was no consensus on diagnostic criteria. We discuss the difficulty to define diagnostic criteria without having a disease definition. Histology is mostly not available in the living patients. We suggest applying a combination of clinical and radiological criteria: fever, abdominal pain and any bowel wall thickening >4 mm detected by ultrasonography (US) or computed tomography. We calculated a pooled incidence rate from 21 studies of 5.3% (266/5058; 95% CI: 4.7%-5.9%) in patients hospitalised for haematological malignancies, for high-dose chemotherapy in solid tumours or for aplastic anaemia. CONCLUSIONS: This systematic review provides diagnostic criteria for neutropenic enterocolitis, presents a quantitative synthesis on its incidence and discusses its treatment recommendations. Prospective studies are clearly warranted.

Adult↗

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↗

Efficacy of Saccharomyces boulardii for treatment of horses with acute enterocolitis.

OBJECTIVE: To evaluate the viability of Saccharomyces boulardii after PO administration in clinically normal horses and its efficacy as a treatment for horses with acute enterocolitis. DESIGN: Prospective study. ANIMALS: 5 clinically normal horses and 14 horses with acute enterocolitis. PROCEDURE: Feces were collected from 5 clinically normal horses and submitted for microbial culture for 2 days prior to administration of a lyophilized form of S. boulardii (25 or 50 g, PO, q 12 h) for 10 days. Feces were collected for microbial culture 5 and 10 days after treament initiation and 10 days after treatment was discontinued. Fourteen horses with acute enterocolitis were randomly allocated to receive a placebo or S. boulardii (25 g), PO, every 12 hours for 14 days. RESULTS: S. boulardii was not detected in feces of clinically normal horses. After administration, yeast survived within the gastroinestinal tract but did not permanently colonize it. In horses with acute enterocolitis, the severity and duration of gastrointestinal tract disease during hospitalization were significantly decreased in horses receiving S. boulardii, compared with horses receiving the placebo. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of S. boulardii may help decrease the severity and duration of clinical signs in horses with acute enterocolitis.

Acute Disease↗

[An elderly case of cytomegalovirus enterocolitis associated with a malignant tumor].

An 83-year-old man was given a diagnosis of left parotid cancer in our hospital in November 1997. He refused to undergo a surgical procedure because of his advanced age. Therefore chemotherapy and radiotherapy were used. Chemotherapy with CAP (Cyclophosphamide, Adriacin, and CDDP) was conducted on 6 occasions between December 1997 to July 2000. Prednisolone (15 mg) was administered daily from July 15, 2000. The patient started suffering from diarrhea on August 2, 2000. As the patient also began to suffer high grade fevers and stomachaches, he was admitted on a diagnosis of acute enterocolitis. He had bloody stool on August 11. On emergency colonoscopy, an ulceration with bleeding was located in the lower rectum. The biopsy specimen revealed intranuclear inclusion bodies and positively staining cells for monoclonal antibody to cytomegalovirus through the immunohistochemical technique, and it was diagnosed as cytomegalovirus enterocolitis. He was treated with ganciclovir. One month later, his clinical symptoms had improved. Cytomegalovirus enterocolitis is an opportunistic infection, so immunocompromised hosts (such as cancer patients, patients using immunosuppressants, old people) have a greater probability of contracting cytomegalovirus infection. A ganciclovir is an effective treatment. A cytomegalovirus enterocolitis should considered in the differential diagnosis of enterocolitis, when alimentary symptoms like diarrhea or bloody stool are found in immunocompromised hosts.

Aged↗

[The prevention and treatment of enterocolitis in children with Hirschsprung's disease].

Enterocolitis remains the most grave and very dangerous complication of Hirschsprung's disease. Its etiology is not fully understood. It can occur in children both before and after surgery. The article focuses on the course of enterocolitis in 35 pediatric patients with Hirschsprung's disease. The clinical course varied from symptom-free course to an aggregate of manifest symptoms of enterocolitis and rapid progression of pathological changes. In all above pediatric patients, a therapeutic and prophylactic complex of measures was inaugurated involving urgent decompression of colon with irrigations and symptomatic therapy as well. Early diagnosis of Hirschsprung's disease is regarded as a mainstay in enterocolitis prophylaxis. The most effective method of prophylaxis and treatment of enterocolitis is decompression of a stretched colon with the aid of the irrigation technique.

Adolescent↗

[Protein changes in the jejunal juice and endointestinal exudation of albumin-I 131 in acute infectious enterocolitis].

The phenomenon of endointestinal protein exudation in acute infectious enterocolitis is studied. Total proteins were determined in 30 cases of acute enterocolitis and 50 of bacillary dysentery in the acute stages of the disease and convalescence. The proteinogram of the jejunal juice was performed in the acute stage and convalescence in 20 patients. In 16 patients and 5 controls endointestinal albumin elimination was determined quantitatively by means of 131I labeled albumin. The results showed increase in the total protein content in the jejunal juice in the course of acute infectious enterocolitis and bacillary dysentery and a return to normal values in convalescence. Electrophoresis of the jejunal juice in acute infectious enterocolitis showed the absence of fraction III with alpha1-globulin migration, and increased fractions I, II and IV probably due to the loss of endointestinal albumin, also confirmed by quantitative albumin determinations with 131I labeled albumin. In conclusion, patients with acute infectious enterocolitis present a marked loss of endointestinal albumins in the acute stage of the disease, with a return to normal values in convalescence.

Albumins↗

Early enteral feeding does not affect the incidence of necrotizing enterocolitis.

To begin to determine the optimal time for initiating enteral feedings, 34 sick, very low birth weight infants were prospectively selected from all neonates of less than 1,500 g (N = 116) and randomly divided into two groups. Infants were fed either on day 1 (early) or 7 (late) of life, according to a feeding protocol which included parenteral nutrition and a scheduled progression from sterile water to 2.5% dextrose, half-strength, and finally full-strength formula over seven days. The incidence of necrotizing enterocolitis and subsequent hospital course were compared. Initiating enteral feedings on day 1 did not significantly increase the incidence of necrotizing enterocolitis, produce a clustering of cases, or induce an earlier onset of necrotizing enterocolitis. The overall incidence of necrotizing enterocolitis in sick, very low birth weight neonates was 29% (5/17) and 35% (6/17) in the early and late groups, respectively, compared with 4.2% (2/47) in minimally sick, very low birth weight neonates. No significant differences between groups were seen in obstetrical complications, birth weight, gestational age, Apgar scores, presence of patent ductus arteriosus or intraventricular hemorrhage, use of umbilical catheterization, and respiratory or oxygen requirements. Infants fed enterally from day 1 did show a significantly higher energy and protein intake during the second week of life. These data show that providing dilute, early enteral calories does not adversely affect the incidence of necrotizing enterocolitis.

Enteral Nutrition↗

An outbreak of Clostridium difficile necrotizing enterocolitis: a case for oral vancomycin therapy?

During a 2-month period, 13 infants in this neonatal intensive care unit developed necrotizing enterocolitis, increasing the prevalence in inborns from 5.2 to 20.5/1,000 live births. Fifty-seven perinatal and neonatal factors, many of which have previously been associated with necrotizing enterocolitis, were compared between the infants with necrotizing enterocolitis and 17 unaffected inborn control infants admitted concurrently. Clostridium difficile cytotoxin was detected in the stools of 12 affected infants (92.3%) in comparison with two control infants (11.8%) (P less than .001), and the organism was isolated in eight affected neonates (61.5%) compared to none of the control infants (P less than .001). The outbreak was terminated upon institution of oral vancomycin therapy in cases and infant contacts, and strict antiinfective measures in the neonatal intensive care unit. This indicates an etiologic role of C difficile in the outbreak. Oral vancomycin in the management of necrotizing enterocolitis was assessed by therapeutic response, drug levels, and occurrence of side effects. Oral vancomycin therapy is indicated in necrotizing enterocolitis outbreaks in units where C difficile is endemic.

Clostridium Infections↗

Diagnosis of Clostridium difficile-associated enterocolitis in Sweden. Laboratory and epidemiological aspects.

Over a 32-week period 1979, 256 fecal samples from 132 patients with antibiotic-associated enterocolitis were analyzed for the presence of C. difficile bacteria and/or toxin. The toxin test was positive in 35 patients (27%) and the bacterium was present in 14 patients (11%). Seventy-three patients with enterocolitis were investigated with regard to age, sex, antibiotic therapy, and clinical symptoms by analysis of their records. A positive toxin titre had an apparent predictive value of 69% for pseudomembranous enterocolitis or other serious colitis, while a negative titre had a 74% predictability for a non-serious disease. Many different types of antibiotics were found to be associated with enterocolitis. Incubation times of more than two weeks from the onset of the antibiotic therapy were noted in 12% of the cases. Vancomycin was administered orally in the treatment of 17 patients, with good results in all but two cases. Two case reports are presented in which relapses occurred upon renewed antibiotic treatment. It is concluded that routine diagnosis of C. difficile in faeces, especially through direct detection of toxin, may be useful in the clinical management of antibiotic-associated enterocolitis.

Aged↗

Antibiotic-induced lethal enterocolitis in hamsters: studies with eleven agents and evidence to support the pathogenic role of toxin-producing Clostridia.

Clindamycin-induced enterocolitis in hamsters was studied, using a tissue culture assay to detect clostridial toxin. It was found that animals with lethal enterocolitis had a cytopathogenic substance in cecal contents and blood that was neutralized by clostridial antitoxins. Cultures of the cecal flora yielded numerous species of clostridia, but only 1 organism was detected which produced a toxin which was cytopathic in tissue culture. This organism, Clostridium difficile, was consistently present in high concentrations, and the cell-free supernate of these strains caused enterocolitis if injected intracecally into hamsters. Ten additional antimicrobials were tested ih hamsters. Ampicillin, vancomycin, erythromycin, cephalosporins, and oral gentamicin caused lethal enterocolitis in most recipients, and all animals which died had evidence of clostridia toxin in cecal contents at necropsy. Tetracycline and metronidazole were well tolerated, and the animals given these antimicrobials had no evidence of the toxin. We conclude that toxin-producing clostridia are responsible for lethal enterocolitis due to a variety of antimicrobials in hamsters.

Ampicillin↗

Unexpected death from enterocolitis after surgery for Hirschsprung's disease.

Unanticipated death from enterocolitis occurred in five children 3 weeks to 20 months after uncomplicated reconstruction for Hirschsprung's disease. In each case the presenting symptoms of enterocolitis were mild and were misinterpreted by examining physicians. Within 2 to 12 days of onset of symptoms, unexpected death occurred. Although fatal enterocolitis is a well-known complication of Hirschsprung's disease, emphasis is usually placed on preoperative enterocolitis. Fatal postoperative enterocolitis is not a new entity associated with Hirschsprung's disease, but physician awareness of this possibility is obviously deficient. We strongly recommend extensive parent education and better postoperative communication between the surgeon and the referring physician.

Diagnostic Errors↗