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Studies in animal models of enterocolitis have failed to confirm the purported metabolic and functional benefits of bowel rest induced by use of an elemental diet. Recent reports have demonstrated that glutamine-supplemented diets ameliorate or reverse many of the adverse effects of experimentally induced enterocolitis. Human studies are needed to confirm these findings.
Administration of chemotherapy is limited by host toxicity, which is often manifested by severe enterocolitis. This study evaluated the effects of a liquid, elemental, chemically defined diet (ED) supplemented with 2% glutamine (Glu-ED) compared with a polypeptide diet (PPD) on the morbidity and mortality after methotrexate (MTX) administration. Fischer 344 rats (n = 80) were fed either a regular rat chow diet (RD), a 2% glycine supplemented elemental diet (Gly-ED), a 2% glutamine-supplemented elemental diet (GLU-ED), and a glycine-supplemented polypeptide diet(Gly-PPD) for 7 days prior to administration of MTX (20 mg/kg, ip). After 72 hours, eight rats per group were killed; portal vein and vena cava blood, mesenteric lymph nodes (MLN), liver, small intestine, and cecum were sampled for bacterial culture. Remaining animals were followed to calculate survival. One hundred percent of the Gly-PPD and 25% of the Glu-ED animals survived compared with 0% of the Gly-ED animals. Our data showed that ED resulted in an increased quantity of intestinal Gram-negative bacteria and diminished intestinal mucosal height and mucosal DNA/protein content. The polypeptide diet prevented intestinal mucosal atrophy, avoided MTX-induced enterocolitis and significantly improved animal survival compared with an elemental diet with or without glutamine supplementation.
To evaluate the role of immunologic mechanisms in one specific syndrome of food intolerance in infants, food protein-induced enterocolitis, we measured class-specific serum antibodies to three food proteins, ovalbumin, soy, and cow milk, prior to diagnostic food challenges in 18 infants suspected to have this syndrome. Infants with positive challenge reactions to egg, soy, or cow milk had 5-10 times higher levels of IgA antibody directed against that food than did the infants with negative challenges. Levels of IgG antibody to soy and egg were also significantly higher (greater than 10-fold) in infants with positive challenge responses. There was no significant difference in levels of IgM food antibodies between the two groups. IgA anti-soy antibody levels rose in all 12 infants tested 2-10 weeks after a single soy feeding (challenge). However, IgM anti-soy antibody increased in the five infants who had a negative response to the challenge feeding and decreased in those seven with a positive response. The difference between the two groups was statistically significant (P less than 0.01). Some correlation existed (r = -0.68) between the increase in IgA anti-soy antibody and the decrease in IgM anti-soy antibody for infants with positive soy challenges. Although a pathogenic role for these antibodies is not proven, the findings suggest an altered immunologic response to ingestion of food antigens in infants with food protein-induced enterocolitis.
The intestinal contents of 17 neonates with necrotizing enterocolitis were analyzed for pH, carbohydrate, protein, and bacteria. The intraluminal pH was less than 5.0 (16/17). Sufficient carbohydrate and bacteria capable of fermenting the carbohydrate to organic acids were found. The intraluminal protein content was greater than 5 g/dl. The variables of acid and protein were then examined in a rabbit intestinal loop model. The hemorrhagic response in individual loops was measured using Cr51 tagged red blood cells such that the microliters of blood per centimeter intestine could be determined. Loops with organic acid and protein had significantly (p less than 0.01) more intramural blood than control loops. Organic acid (possibly generated by bacterial mixed acid fermentation of carbohydrate) in the presence of protein promotes intramural hemorrhage similar to that seen in neonates with necrotizing enterocolitis.
Necrotizing enterocolitis (NEC) is a significant neonatal public health problem that affects low-birth weight infants in neonatal intensive care units throughout the country. As the survival rate of low-birth weight infants continues to increase and as the number of low-birth weight births remains unchanged, we can anticipate that NEC will continue to be a cause of significant morbidity and mortality in the future. Despite many reports about NEC that describe demographic risk factors and short-term or long-term outcome, there is a paucity of basic science information about neonatal gastrointestinal physiology and pathophysiology in human preterm and even full-term infants. It has become increasingly evident that we need a much better understanding about the developmental aspects of gastrointestinal function in health and disease before we can achieve further advances in our understanding of and thus rational therapy for and prevention of NEC. The purpose of the National Institute of Child Health and Human Development conference "Necrotizing Enterocolitis: Basic Science Approaches to Gut Maturation and Pathogenesis" was to bring together basic science investigators, clinical epidemiologists, and clinical scientists to identify important areas of research that need to be applied to the problem of NEC. The concept of applying the "bench to bedside" type of collaborative research was emphasized and encouraged because many clinical neonatologists may have little scientific interaction with basic scientists. In addition, many basic scientists may be unaware of NEC and the implications for targeted research related to this disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Necrotising enterocolitis may occur as a complication of granulocytopenia of any aetiology. The clinical presentation may be non-specific and the diagnosis therefore depends heavily on radiographic findings, particularly changes seen by CT. In immune-compromised patients being investigated for possible abdominal sources of fever, CT may be particularly helpful in elucidating bowel sources of infection. Two cases of necrotising enterocolitis demonstrated by CT are presented. The two cases were in immune-compromised patients with malignant disorders who presented with fever. The CT findings of this disorder are presented.
Necrotizing enterocolitis is the principal cause of surgical referral in preterm neonates and the most common gastrointestinal emergency among infants. Its pathophysiology is unclear and it carries high levels of mortality and morbidity. This article provides an overview of necrotizing enterocolitis including risk factors, preventative strategies and medical and surgical management.
Necrotizing enterocolitis is a disease of the newborn that may involve the small intestine and/or the colon, and the stomach. To our knowledge, massive necrosis of the small intestine with concomitant involvement of the esophagus has never been reported. A case of a 6-month-old boy with necrotizing enterocolitis and pan-necrosis of the small intestine, cecum, and the lower third of the esophagus is presented. After 70 days of treatment, intestinal transit was established by an anastomosis between the first centimeter of jejunum and the ascending colon. Finally, esophageal transit was established by a total gastric transposition with cervical esophagogastric anastomosis. The patient was maintained under total parenteral nutrition, and after 19 months he developed fulminant hepatic failure due to parenteral nutrition; he then underwent combined liver and small bowel transplantation. After 2 months, the patient died due to undefined neurologic complications, probably related to infection or immunosuppressive therapy.
Necrotizing enterocolitis (NEC) occasionally deviates from the classical presentation of the disease. Small bowel dilatation and pneumatosis are frequently present prior to the actual onset of the clinical presentation. Pneumatosis intestinalis, an important diagnostic sign of NEC, is quite variable; it may be present, persist, worsen, or disappear; or at times it may not be present at all. A severe complication of necrotizing enterocolitis is perforation which in 50 percent of the cases presented without obvious free intra-abdominal air. Accumulation of fluid in the abdomen is stressed as strong evidence for perforation and a strong indication for surgery. The varying features indicate that NEC has a clinical spectrum that extends from benign to severe, and recognition of all these variations will lead to better diagnosis and to a better understanding of the disease. The clinical and roentgenologic variations make classification difficult but the variety most likely represents the combination of a great number of susceptible children and a greater recognition of the disease.
This study demonstrates that the diagnosis of necrotizing enterocolitis can sometimes be made before the full-blown clinical and radiographic findings are manifest. Of 12 infants with films available prior to diagnosis of the disease, nine had early selective dilatation of small bowel and little or no air in the colon. Necrotizing enterocolitis should be foremost in the differential diagnosis when this finding is coupled with signs such as abdominal distention, acidosis, and diarrhea.
Three patients, 1-11 months of age, who underwent open heart surgery with cardiopulmonary bypass and profound hypothermia, developed necrotizing enterocolitis postoperatively leading to death. Pneumatosis intestinalis and portal vein gas were demonstrated radiographically. Necrotizing enterocolitis has not been previously reported as a complication of cardiopulmonary bypass and profound hypothermia.
In this report we focus on the importance of an accurate diagnosis of gastrointestinal complications during chemotherapy for acute myeloid leukemia. The leukemic infiltrtion of the digestive system may cause mucosal ulcers which can lead to bleeding or perforation. The immune system deficiency in this cohort of patients may result in necrotic enterocolitis (leukemic typhlitis), perianal inflammation, abscesses, and peritonitis. We describe a 37-year old male who presented in June 2004 with 2-month history of fever, weakness and sore throat, treated with antibiotic therapy. Physical examination demonstrated palor. The peripheral blood count at admittance was as follow: Hemoglobin 87 g/l, WBC 63 x 10(9)/l, and platelets 56 x 10(9)/l. The peripheral blood differential count showed: myeloblasts 4%, polymorphonuclear neutrophils (PMN) 20%, monocytes 60%, lymphocytes 16%. The diagnosis of acute myeloid leukemia (AML) was confirmed by bone marrow aspirate, which presented an almost total infiltration by monocytoid blasts, AML type M5 according to FAB classification. Immunophenotypic evaluation by flow cytometry showed that the blast cells reacted with antibodies to CD33, CD13, CD14, CD64, CD15, cytogenetics showed normal karyotype. Induction treatment consisting of cytarabine 2 x 200 mg intravenously in push on days 1-8, vepeside 200 mg i.v. on days 1-5, adriblastine 90 mgon days 1,3 and 5. On day 15 of chemotherapy the patient got fever 38.5 degrees C, abdominal pain and diarrhea (10 stools daily). Broad-spectrum antibiotic therapy with ceftriaxone and amikacin was promptly instituted but condition worsened, abdominal pain extended to all abdomen while the fever and diarrhea persisted. Ultrasonography on day 18 documented bowel wall thickness of colic tract, part of duodenum and jejunum. Owing to suspicion of neutropenic enterocolitis, antibiotic therapy intensified with teicoplanin, fluconazole, metronidazole and pipril. Patient was neutropenic and thrombocytopenic, although daily platelet transfusion from a single donor were given. We started with granulocyte colony stimulating factor (G-CSF) 5 g/kg, which was adiminstered for 7 days. After 7 days neutrophil value reached 1 x 10(9)/l, but fever persisted, abdominal distension and diarrhea progressively improved. The fever peristed and central venous catheter was removed on day 30. After removal of the catheter the patient was getting better: the fever disappeared. The blood count showed Hb 91 g/l, WBC 3,4 x 10(9)/l, platelet 114 x 10(9)/l and normal leukocyte differential count. We emphesize the importance of collaboration between the hematologist and the surgeon in monitoring gastrointestinal complications during and after chemotherapy for acute leukemias and value of abdominal ultrasonography evaluation.
Neutropenic enterocolitis (NE) is an unusual acute complication of neutropenia, associated with leukemia and lymphoma. It has been observed mainly in the first phase of therapy when drugs are used in maximally tolerated dose. This is a case report of neutropenic enterocolitis in a patient with acute lymphoblast leukemia who received prednisone, vincristine, daunorubicin and L-asparaginase, with perforation of cecal and terminal ileum. Perforation and defect intestine wall was excised and sutured directly in two layers. Protective proximal loop ileostomy was performed at that time.
The purpose of this study was to determine the presence of virulence factors (heat-labile, heat-stable enterotoxin, verotoxin, invasiveness, localized, aggregative and diffuse adherence) among E. coli strains isolated from sporadic cases and outbreaks of enterocolitis, which belonged to serogroups characteristic for enteropathogenic E. coli. Serogroup was determined in 57.2% of 622 strains isolated from sporadic cases, and among them virulence factors were detected in 23.6%. Serogroup was also determined in 73.3% of 90 outbreaks isolates tested and virulence factors were detected in 97% of them. The detection rate of virulence factors rarely exceeded 50% among strains belonging to any of serogroup that was determined. The obtained data suggested that the identification of E. coli as a causative agent of enterocolitis by serogroup determination was a reliable method in outbreaks, but not in sporadic cases of this disease.
Two homosexual Danish men with the acquired immunodeficiency syndrome (AIDS) contracted cryptosporidium enterocolitis. One patient died in another opportunistic infection, the other developed severe chronic enterocolitis with malabsorption. The cryptosporidia escape detection on routine stool examination, but are easily demonstrated by a modified Ziehl-Neelsen stain. It is suggested that this procedure should be applied when persons from AIDS high risk groups or patients with other forms of immunological incompetence develop prolonged diarrhoea.
Repeated recurrence of Clostridium difficile-associated enterocolitis is uncommon but troublesome for the afflicted patient. The patient described here received vancomycin treatment several times but always had a relapse of C. difficile enterocolitis 2-3 weeks after discontinuation of treatment. She did not form serum antibodies to C. difficile cytotoxin (toxin B). Rectal infusion of enemas prepared from fresh faeces resulted in final cure.
AIM: To study the value of colonoscopy and selective angiography in diagnosing ischemic enterocolitis. METHODS: Among the 16 cases under study, 10 cases had hypertension and a history of coronary artery disease (one was hospitalized for sub-ventricular-wall infarction). The blood pressure of 10 of the 16 cases ranged from 13.9-23.8 to 13.3-14.6 kPa (170-180/100-110 mmHg). Two cases had chronic auricular fibrillation, and in four cases, a cardiogram showed left-front branch conduction block. Sixteen patients were examined by colonoscopy. Among them, 14 cases had a long course of angiocardiac disease, and were further examined by selective mesenteric inferior angiography. RESULTS: The colonoscopy revealed local mucous hyperemia edema and blood on contact. Lesions were found in the sigmoid colon in four cases, in the descending colon in eight cases and in splenic flexure in four cases, which suggests that the lesion always appeared in the left part of colon. There were different degrees of inflammatory cell infiltration, submucous bleeding, edema, fibro-embolism and hemosiderosis by biopsy in the 16 patients whose membranes affect part of the enteral wall. Of the 14 patients examined by mesenteric inferior angiography, 3 cases showed mesenteric amphraxis inferior and formation of collateral circulation. There were different degrees of stenosis in the other 11 subjects' mesenteric inferior cavities which grew slim and their branches were stenotic, so the radiographic image was not complete and the ends of some branches even cannot be seen. CONCLUSION: The colonoscopy and the selective mesenteric inferior angiography are both helpful in the diagnosis of ischemic enterocolitis.
We report 2 cases of adenovirus enterocolitis in pediatric patients who underwent bone marrow transplantation. The first case involved a 17-year-old adolescent boy with combined immunodeficiency and non-Hodgkin lymphoma who developed chronic graft versus host disease and persistent adenovirus duodenitis. Case 2 involved a 3-year-old boy who received a mismatched unrelated bone marrow transplant for metachromatic leukodystrophy; the boy developed severe graft versus host disease and died of multiorgan failure. At autopsy, diffuse hemorrhagic enterocolitis with changes of severe graft versus host disease and extensive mucosal invasion by adenovirus was found. Awareness and early recognition of this uncommon complication of concomitant graft versus host disease and adenovirus infection could impact therapy and outcome of patients with bone marrow transplant.