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PubMedDate not supplied

Food protein-induced enterocolitis syndrome: report of one case.

We report a 76-day old infant who got diarrhea within the first week of life. He was treated as acute gastroenterocolitis and kept on feeding with regular infant formula. Because the symptoms persisted, the feeding formula was shifted to soy-based formula then to the highly-hydrolyzed formula and got improvement. But severe bloody diarrhea, vomiting, dehydration and fever developed after feeding with regular infant formula again. Based on the history and clinical presentations, cow's milk allergy was suspected. He received total parenteral nutrition for 5 days then fed with highly-hydrolyzed formula with slowly increasing amount. Thereafter tests for total eosinophil counts, total serum IgE, milk specific IgE antibodies and milk extract skin prick test were all unremarkable. Under the impression of food protein-induced enterocolitis syndrome (FPIES), a double-blind placebo-controlled food challenge (DBPCFC) with infant formula was performed. Regular infant formula induced severe vomiting, diarrhea, fever, acidosis and elevation of absolute neutrophil counts (ANC) of peripheral blood by 27,640/mm3. Based on the laboratory findings and challenge results, the patient fit the diagnostic criteria of food protein-induced enterocolitis syndrome.

Enterocolitis↗

PubMed2000

[NEC--neonatal necrotising enterocolitis--methods of treatment and outcome: a comparative analysis of Scottish (Glasgow) and Polish (Western Pomerania) cases].

The aim of the work was to perform a comparative analysis of medical files of 125 neonates with necrotising enterocolitis treated between 1990 and 1995 in two regional centres: Glasgow (Scotland) and Western Pomerania (Poland), and to search for factors constituting an indication for surgery in NEC. The following data contained in the medical documentation of NEC cases have been analyzed: maternal risk factors, perinatal abnormalities, neonatal risk factors, procedures performed in the neonate, feeding practices, clinical and radiological signs, time of onset of the disease, clinical staging of NEC according to Bell (modified by Walsh and Kliegman), methods of treatment, postoperative course and outcome. The analysis was performed in the whole material and in the subgroup of newborns weighing < 1500 g (low/extremely low birth weight babies). Glasgow neonates with NEC had significantly lower birth weight, gestational age, platelet count, and sodium level when compared to Pomeranian newborns, while the latter had significantly lower leukocyte count and shorter time of onset of the disease. In the subgroup of newborns weighing less than 1500 g, Glasgow neonates had significantly lower birth weight, gestational age, platelet count, and sodium level when compared to Pomeranian newborns, while the latter had significantly lower 1 minute Apgar score, pH and base excess (BE) values. Glasgow clinical NEC stage was significantly more severe (IIB-IIIB) when compared to Pomeranian neonates. A higher proportion of full-term neonates in the present study--31.2%--was diagnosed with NEC than in the literature. Hyponatremia with severe acidosis and low platelet count (especially below 100 x 10(9)/L) may constitute an easily available laboratory finding serving as an indicator for surgical intervention in NEC. Statistical analysis revealed that the selection of treatment was influenced in the Glasgow group by birth weight and in the Pomeranian group by the clinical stage of NEC. Overall mortality was 32.8% in the whole group of 125 neonates, 34.4% in the Glasgow and 31.2% in the Pomeranian group. However, Glasgow neonates had significantly lower birth weight and gestational age and were more severely ill. The mortality in the subgroup of Scottish neonates with primary peritoneal drainage was 55.5%, the majority presenting with significantly lower birth weight and stage IIIB of necrotising enterocolitis. In conservatively treated neonates, mortality was 13% in the whole group, 9% in the Glasgow group and 15% in the Pomeranian group. Overall mortality in neonates treated surgically was 46.6%. In the Glasgow group it was 23% without and 42% with primary peritoneal drainage, respectively. Surgical mortality in the Pomeranian group was 42%. Overall mortality was 5.6% in full-term newborns, 3.2% in the Glasgow group and 7.8% in the Pomeranian group. Primary peritoneal drainage is a valuable, mildly invasive method of initial, and in some cases final, treatment in severely ill NEC babies, especially with low birth weight. This method was not used in the Pomeranian group.

Anastomosis, Surgical↗

PubMed2001

[An extremely low birth weight infant with pulmonary atresia complicated with necrotizing enterocolitis].

We experienced an extremely low birth weight (ELBW) infant complicated with pulmonary atresia and necrotizing enterocolitis. She was born at 25 weeks of gestation with a birth weight of 752 g. Five hours after birth, she manifested cyanosis and was diagnosed as having pulmonary atresia with intact ventricular septum (PAIVS). Infusion of lipo-prostaglandin E1 (PGE1) was started to keep the ductus open along with infusion of dopamine and dobutamine. At 8 days of life she developed hypotension and metabolic acidosis, and the diagnosis of intestinal perforation was made by free air in the abdomen. The excessive shunt flow to the pulmonary vasculature via the ductus was suspected to have caused an inadequate systemic flow leading to the intestinal ischemia and necrotizing enterocolitis. Lipo-PGE1 was discontinued to decrease the shunt flow through the ductus. Brock's operation (closed transventricular pulmonary valvotomy) was performed at the age of 8 and 11 days and the ligation of the ductus arteriosus was performed at the age of 13 days. Propranolol was administered to inhibit the pulmonary outflow tract constriction along with catecholamines to stabilize hemodynamics. She recovered slowly and her trachea was extubated at 58 days of life.

Anesthesia↗

PubMed1975

Importance of multiple episodes of hypoxia or cold stress on the development of enterocolitis in an animal model.

Necrotizing enterocolitis, a highly lethal disease in the newborn infant characterized by ischemic necrosis of the gastrointestinal tract frequently leading to perforation, is seen primarily in low birth weight infants who have undergone stress, such as hypoxia. In an animal model it was demonstrated that cold stress was as effective as hypoxia in producing the disease in formula-fed newborn rats. Breast milk was completely protective in both cold- and hypoxic-stressed animals. Presumably cold stress produces the same selective circulatory ischemia as does hypoxia. The experiment further supports the concept that any insult or stress which decreases mesenteric blood flow may initiate the changes leading to necrotizing enterocolitis. It was shown also that the incidence of the disease in formula-fed rats was related directly to the number of episodes of either cold or hypoxic stress. These results suggest that a critical amount of ischemia is necessary to initiate these changes and may help to explain the fact that not all infants exposed to hypoxia or cold stress developthe disease.

Animals↗

PubMed2002

CT findings in eosinophilic enterocolitis with predominantly serosal and muscular bowel wall infiltration.

A 44-year-old female presented with tenderness of her abdomen, vomiting, intestinal obstruction, hypoalbuminemia and blood eosinophilia. Gastroscopy was normal and colonoscopic biopsies showed only non-specific inflammation of the colonic mucosa and submucosa. CT revealed large amounts of ascites and bilateral pleural effusions but eosinophil counts in the ascites were normal. At CT the jejunum was dilated and showed marked prominence of the valvulae whereas the ileum and the colon presented with a diffuse and hypoattenuating bowel wall thickening. The bowel wall thickening was most pronounced in the colon which especially showed also an impressive thickening and hyperenhancement mainly of its outer bowel wall layers. Parasitic infection could be excluded as well as a specific allergic response. In context with the known blood eosinophilia the diagnosis of an eosinophilic enterocolitis was suspected already by CT but finally only surgical full thickness biopsies could confirm the rare diagnosis of an eosinophilic enterocolitis with predominantly serosal and muscular bowel wall infiltration.

Adult↗

PubMed2001

[A case of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis: anti-ganglioside antibody levels with or without Guillain-Barré syndrome].

A 38-year old man developed enterocolitis one day after he had ingested raw chicken. Nine days later, his grip strength weakened. Eleven days later, he was admitted to our hospital with weakness of four limbs, dysphagia and dysarthria. Serum anti-Campylobacter jejuni antibody and anti-ganglioside antibodies (GM1, GD1a, GD1b, GalNAc-GD1a) were positive, and motor action potentials were not evoked at all extremities. He was diagnosed as having Guillain-Barré syndrome. After receiving immune absorption therapy and plasma exchange therapy, the patient improved. Another person who had also consumed the same raw chicken developed colitis only. Five weeks later, the anti-GalNAc-GD1a-IgG antibody titers (O.D. 490 nm) of the patient and the other man who developed colitis were 0.324 and 0.118, respectively. It was suggested that the pathogenesis of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis may be related to the type and titer of anti-ganglioside antibodies and also to the sensitivity of the individual.

Adult↗

PubMed1976

Carbohydrate malabsorption in necrotizing enterocolitis.

A prospective investigation was conducted to determine if infants with necrotizing enterocolitis had evidence of carbohydrate intolerance prior to the onset of clinical symptoms of advanced disease. Stool specimens were examined for fecal reducing substances with Clintest tablets from well, full-term infants and sick premature infants. Only two of 45 (4.4%) formula-fed, full-term infants demonstrated higher than 2+ fecal reducing substances. Ten of 14 (71%) formula-fed premature infants who developed necrotizing enterocolitis had higher than 2+ reducing substances detected in their stools. Daily measurement of fecal reducing substances can be a useful adjunct in the management of sick premature infants.

Carbohydrate Metabolism↗

PubMed2002

[Diagnosis and characteristics of the clinical course of necrotizing enterocolitis in children].

Necrotizing enterocolitis (NEC) is a disease of unknown etiology affecting mainly premature newborns and occurring in about 1 to 7% of all admissions to neonatal intensive care units. Among the greatest problems is the early diagnosis and adequate and timely treatment, surgery included. In the last quarter of the century the survival rate of premature infants was gradually increasing in national regions and worldwide and accordingly there is an increasing number of babies with NEC. To date, to treat patients with the diagnosed enterocolitis is a complicated problem. The mortality rate among the children remains high. In the period from 1978 to 2000 432 patients with NEC were admitted to the St. Petersburg Center of Neonatal Surgery in the Children Hospital N 1,300 of them requiring surgical interventions. The author's personal experience with the diagnosis and treatment of the disease allowed three main forms of the clinical course of the disease to be established: superacute, acute and subacute.

Critical Care↗

PubMed1976

Disseminated intravascular thrombosis as the cause of ischaemic enterocolitis.

Disseminated intravascular thrombosis was diagnosed in a woman aged 63 years. At autopsy the typical appearances of ischaemic enterocolitis were found, together with thrombi in other organs. This case illustrates the previously postulated connection between intravascular thrombosis and ischaemic enterocolitis.

Disseminated Intravascular Coagulation↗

PubMed1999

Interleukin-10 inhibits inducible nitric oxide synthase in an animal model of necrotizing enterocolitis.

BACKGROUND: Nitric oxide (NO) and its role in surgical inflammation are well documented; demonstrating the role of NO in necrotizing enterocolitis (NEC) and ways in which it may be suppressed may provide avenues for immune modulation in the treatment of NEC. AIMS: We sought to demonstrate an increase in inducible nitric oxide synthase (iNOS) mRNA and nitric oxide in an experimental model of necrotizing enterocolitis. In addition, we hypothesized that interleukin-10 (IL-10) would attenuate this response. METHODS: Newborn rats were treated with 25 microliters intraperitoneal IL-10 or vehicle prior to laparotomy, 1 h superior mesenteric artery (SMA) occlusion, 50 micrograms/kg intraluminal platelet activating factor administration, and SMA reperfusion. iNOS mRNA and nitric oxide levels were measured in the liver, small bowel, and serum and compared using Student's t-test. RESULTS: Small bowel iNOS mRNA increased after NEC induction from 0.058 +/- 0.02 to 0.144 +/- 0.05 relative intensity units (RIU) at 2 h (p < 0.01) and from 0 to 0.09 +/- 0.02 RIU at 6 h (p < 0.03). Liver mRNA increased from 0.026 +/- 0.002 to 0.485 +/- 0.09 RIU (p < 0.002) and from 0 to 0.069 +/- 0.02 RIU (p < 0.0001) at 2 and 6 h, respectively. Serum nitric oxide increased in NEC induced animals at 2 h from 28.04 +/- 10.5 to 45.18 +/- 6.8 microM (p < 0.001). IL-10 suppressed iNOS mRNA and nitric oxide expression at 2 h in small bowel, liver, and serum by 60%, 89%, and 11%, respectively. CONCLUSIONS: IL-10 decreases iNOS mRNA response in experimental NEC. This down-regulation may be an avenue for anti-inflammatory intervention in NEC.

Animals↗

PubMedDate not supplied

Enteral immunotherapy in the treatment of chronic enterocolitis in interleukin-10-deficient mice.

BACKGROUND/AIMS: Transgenic IL-10-deficient mice (IL-10 ko mice) spontaneously develop a chronic inflammatory bowel disease that is reminiscent of Crohn's disease. In a randomized, prospective, comparative study, we evaluated the effect of local, endoluminal immunotherapy by duodenal injection of mouse recombinant IL-10 (rm IL-10), in IL-10 ko mice with chronic enterocolitis; the first of its kind. METHODOLOGY: Sixteen IL-10 ko mice received a monoinjection of rm IL-10 into the duodenum while a control group of 16 IL-10 ko mice received an injection of physiological saline. Histology of the entire bowel and plasma concentrations of IL-4, IL-6, IL-10, tumor necrosis factor-alpha, and interferon-gamma were analyzed on the 3rd or 7th postoperative day. RESULTS: The histological features of the specimens from IL-10 ko mice were, non-specific, segmentary and located mainly in the ileum. Lesions were of more significance in mice injected with physiological saline than in those receiving IL-10 in the proximal ileum, near to the site of injection. Plasma concentrations of IL-6 were higher in IL-10 ko mice than in the control group. CONCLUSIONS: This study confirms that there is hyperproduction of Th1 cytokines in IL-10 ko mice and also suggests that endoluminal administration of IL-10 may be envisaged for the treatment or prevention of enterocolitis.

Animals↗

PubMedDate not supplied

[Physical factors in the treatment of chronic enterocolitis in children].

It is a review of long-term investigations in the field of treating chronic enterocolitis in children admitted to Pyatigorsk sanatoria. The disease is proposed to be managed with different therapeutic factors: sinusoidal currents, mud, radon, oral mineral water. Such combination proved beneficial as it corrected the principal pathogenetic mechanisms of chronic enterocolitis: inflammation, dysbacteriosis, malabsorption syndrome, enzymatic defects, etc.

Child↗

PubMed1992

Combined Sarcocystis and gram-positive bacterial infections. A possible cause of segmental enterocolitis in Thailand.

Between 1981 and 1990, 22 intestinal specimens surgically resected due to segmental enterocolitis were collected and examined. Grossly, the specimens were classified into 3 groups 1) Acute inflammation with hemorrhage and necrosis 2) Constrictive lesion 3) False diverticulum with perforation. Mostly, there was unisegmental involvement, distributed in jejunum, ileum and ileocolon. Microscopically, small parasitic structures, interpreted to be unconventional excystation stage of Sarcocystis hominis, (Railliet and Lucet, 1891) Dubey 1976, were present on the luminal border and within the crypt-lining epithelial cells. At the ulcerated area, tissue invasion by Gram-positive bacteria were always seen and considered as second pathogen. Source of the parasite was likely from cyst-containing beef available in markets, (Bos indicus and Bubalus bubalis) along with consumption of undercooked beef. Antismooth muscle antibody, IgG class, with the titer ranging from 1:16-1:256 were detected in 45 per cent of the patients. This is considered as autoimmunity against intestinal smooth muscle damaged previously from subclinical inflammatory condition. Present information suggests a long-standing existence of Sarcocystis in the patients' intestine, associated with Gram-positive bacterial infection, as the mechanism producing segmental enterocolitis found in the Central region.

Adolescent↗

PubMed1992

Sarcocystis infection and actinomycosis in tumorous eosinophilic enterocolitis.

Intramural masses were resected from jejunum and ileocecal portion of a 49-year-old, female patient with partial gut obstruction. Histopathological examination indicated the masses to be tumorous eosinophilic enterocolitis. Recent and late development phases of Sarcocystis in relation to bradyzoite infection have been observed and considered to be responsible for eosinophilic inflammation. Concomitant intestinal actinomycosis, known to produce tumorous lesion without eosinophilia, appears as an attractive natural model in producing tumorous eosinophilic enterocolitis. Pertaining to parasitic development, it is suggested that persisting sporulated oocyst may undergo spontaneous excystation in the host's intestinal wall, along with complex sporogony.

Actinomycosis↗

PubMed1992

Management of neutropenic enterocolitis in the patient with cancer.

Neutropenic enterocolitis is a life-threatening condition often seen in patients experiencing prolonged periods of neutropenia from conditions such as leukemia and lymphoma and from aggressive chemotherapy regimens. Its exact pathologic process remains unclear; however, it has been proposed that direct cytotoxic damage occurs to the bowel mucosa with subsequent microbial invasion complicated by the lack of adequate neutrophil response. The damage may progress to bowel perforation and septic shock. Early recognition and management by healthcare team members are crucial for the improved prognosis of these individuals. Controversy continues to exist concerning management options and the timing of these interventions. This article outlines nursing and medical management of the patient with neutropenic enterocolitis.

Enterocolitis↗

PubMedDate not supplied

[Necrotizing enterocolitis in the preterm infant: etiopathogenic considerations].

Necrotizing enterocolitis (NE) represents the most frequent gastrointestinal emergency encountered in neonatal intensive care units. This necrotic-inflammatory bowel disease affects primarily premature patients and it is recorded as an important cause of neonatal morbidity and mortality. The NE aetiology seems to be multifactorial: prematurity, enteral feeding, hypoxia and micro-organisms toxicity are registered as the most important risk factors, able to trigger the phlogistic and necrotic way at the basis of necrotizing enterocolitis. Despite the NE first report was in the past century, the correct pathogenic sequence of this neonatal disease is still hypothetical.

Enteral Nutrition↗

PubMed2005

[Role of peritoneal drainage in very low birth weight with enterocolitis].

UNLABELLED: Peritoneal drainage (PD) has been proposed as a temporizing procedure for perforated necrotizing enterocolitis (NEC) in very low birth weight neonates. This operation was designed for patients considered too unstable to undergo laparotomy (LAP). Since the introduction of PD some investigators have suggested that it may serve as a definitive therapy. The aim of our study is to determine the efficacy of PD for the stabilization of patients with complicated NEC and its utility as a definitive surgical treatment. METHODS: We review the clinical records from all the patients treated in our unit because of NEC that required surgical therapy. We analyze the mean blood pressure, cardiac and respiratory rate, inspired oxygen concentration, mean airway pressure, diuresis, and arterial blood gases measured 6 and 12 hours after the initial surgical treatment. We divide patients in two different groups according to the initial surgical procedure, peritoneal drainage (PD) or laparotomy group (LAP). Data is shown as media +/- standard deviation, statistical analyses were performed using analysis of variance (ANOVA) for repeated measures and Mann-Withney test. RESULTS: From January 1997 to January 2001 we treated 13 patients with necrotizing enterocolitis that required surgical treatment. Among this group 6 patients were managed initially with PD and 7 with LAP. The gestational age media was 29.07 +/- 3.81 weeks and the birth weight mean 1199.76 +/- 521 gr., without any significant differences between the two groups DP and LAP. All patients improved haemodynamically and respiratory 6 and 12 hours after the surgical treatment. Nevertheless, the mean blood pressure improved even more in the DP group (p<0.005). The DP group showed an improvement in all parameters 6 hours after the drainage was placed, but this effect wasn't maintained for the next 12 hours onwards. From the 12 hours after PD all patients suffered a steady worsening that required further surgical procedures. The overall mortality was 3 patients (23%), without differences between the two groups. The surgical techniques performed (bowel resection, diversion) were similar for both groups. DISCUSSION: DP allows the stabilization for very critically ill patients with complicated NEC. However, this stabilization is temporary. This improvement lasts for a few hours providing a better status for the definitive surgical treatment for the perforated NEC. In our experience DP could not be considered as a definitive surgical treatment.

Child, Preschool↗

PubMedDate not supplied

Neutropenic enterocolitis in an advanced epithelial ovarian cancer patient treated with paclitaxel/platinum-based chemotherapy: a case report and review of the literature.

BACKGROUND: Literature data show that neutropenic enterocolitis is a rare but severe complication that can occur in cancer patients treated with chemotherapy and especially with taxanes. CASE REPORT: A 60-year-old woman with stage Illc epithelial ovarian cancer developed neutropenic fever, abdominal pain, severe diarrhoea, nausea, vomiting and oral mucositis one week after the first postoperative cycle of paclitaxel (175 mg/m2 3-hour infusion) plus carboplatin-based chemotherapy. Abdominal X-ray showed diffuse dilatation of the ileal and colonic loops with air/fluid. The patient soon recovered after intensive supportive care. For the second cycle the dose of paclitaxel was reduced by 20%, but nine days later the patient again developed severe neutropenia with fever, abdominal colicky pain, diarrhoea and vomiting. The culture of blood samples collected on admission was found to be positive for Escherichia coli, whereas stools resulted negative for both enteric rods and Clostridium difficile toxin. The patient recovered with intensive supportive care, and chemotherapy was continued with single-agent carboplatin. DISCUSSION: The increasing use of paclitaxel in first-line as well as in the salvage treatment of epithelial ovarian cancer could increase the occurrence of neutropenic enterocolitis in patients with this malignancy. The importance of symptoms such as neutropenic fever, abdominal pain and tenderness and severe diarrhoea should be stressed in patients who receive taxane-based chemotherapy, and intensive supportive care management should be started immediately.

Antineoplastic Combined Chemotherapy Protocols↗