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PubMed2004

Infrequency of microsatellite instability in complete and incomplete gastric intestinal metaplasia.

Chronic inflammation may be associated with microsatellite instability (MSI). To test the hypothesis that MSI frequently occurs in gastric intestinal metaplasia, we examined gastric biopsies from 58 subjects from an area of high risk for gastric cancer. These were selected to have 2 types of intestinal metaplasia: complete (31 subjects) and incomplete or mixed-type (27 subjects). None of the subjects had gastric cancer, but 95% had chronic inflammation with Helicobacter pylori. We used laser capture microdissection to retrieve metaplastic glands to compare with lymphocytes microdissected from the adjacent gastric mucosae in the same subjects. We performed microsatellite analysis using 6 microsatellite loci, including BAT26. None of the cases were found to have reproducible MSI, and only 1 case showed loss of heterozygosity at 1 marker, D3S1067. To test the sensitivity of our assay, we mixed templates to produce bands of different mobility and found that we could detect an aberrant microsatellite pattern if only 2% of the DNA showed that pattern. Our results indicate that MSI is a rare event in intestinal metaplasia in subjects who do not have gastric cancer.

Base Pair Mismatch↗
PubMed2005

Amelioration of intestinal reperfusion injury by moderate hypothermia is associated with serum sICAM-1 levels.

BACKGROUND: The aim of this study was to investigate the effects of moderate hypothermia on various serum markers involving in inflammation after intestinal ischemia-reperfusion (IR). MATERIALS AND METHODS: The model of 30 min intestinal ischemia +90 min reperfusion was used. Three groups of rats were studied, n=7-8 per group: 1) sham at normothermia, 36.5 to 37.5 degrees C; 2) IR at normothermia and; 3) IR at moderate hypothermia, 32 to 33 degrees C. Serum levels of TNF-alpha, lipopolysaccharide-inducible CXC chemokine (LIX), and soluble intercellular adhesion molecule-1 (sICAM-1) were determined using ELISA technique. Histological features of terminal ileum were also graded. RESULTS: Intestinal IR at normothermia caused remarkable tissue injury together with an elevation in serum TNF-alpha, LIX, and sICAM-1 levels. Moderate hypothermia significantly decreased the degree of mucosal damage and attenuated the elevation of serum sICAM-1 levels. However, there were no significant differences in serum TNF-alpha and LIX levels between IR at normothermia and IR at hypothermia. CONCLUSIONS: Intestinal IR at normothermia induces the elevation of serum TNF-alpha, LIX, and sICAM-1 levels. Moderate hypothermia protects the small intestine from reperfusion injury. This beneficial effect is associated with serum sICAM-1 levels but not with serum TNF-alpha and LIX levels. We speculate that one of the mechanisms, by which hypothermia blunts the tissue injury, is at the step of firm adhesion between leukocytes and endothelial cells.

Animals↗
PubMed2000

Assessment of intestinal permeability in rats by permeation of inulin-fluorescein.

The measurement of intestinal permeability is widely used to assess different aspects of mucosal barrier disorders and related disease states, and has been proposed for evaluation of disease activity. To provide a simple method for assessment of intestinal permeability, we examined the permeation of inulin-fluorescein (InFl) in rat models of small intestinal injury and colitis. Small intestinal or colonic inflammation was induced by either i.p. administration of indomethacin or rectal administration of trinitrobenzene sulfonic acid (TNBS), respectively. For monitoring of intestinal permeability, InFl was administered orally or rectally to rats with small intestinal or colonic inflammation, respectively, and its level in blood was determined by the fluorescence intensity in the plasma. In small intestinal injury, InFl reached its peak in plasma 3 h after oral administration, while in colitis the InFl peak was reached 1 h after rectal administration. The highest permeability was observed at 72 h or 12 h after induction of small intestinal or colonic inflammation, respectively. In small intestinal injury the InFl permeation, as measured by its plasma level prior to sacrifice, was in agreement with intestinal damage evaluated after sacrifice. In colitis, the permeability at 12 h after induction of the disease correlated well with mortality. These findings demonstrate that InFl can be used as a novel, safe and easy-to-use probe for the evaluation of gut permeation and follow-up of gastrointestinal injury.

Animals↗
PubMed2005

Inlet patch: heterotopic gastric mucosa--another contributor to supraesophageal symptoms?

OBJECTIVE: To determine prospectively the incidence of an inlet patch (IP) in children requiring esophagogastroduodenoscopy (EGD) and assess the prevalence of presenting symptoms between children with and without an IP. STUDY DESIGN: All patients undergoing EGD in a 2-year period were assessed for the presence of an IP with biopsy confirmation. IP, distal esophagus, and stomach biopsy specimens were blindly reviewed by a pathologist for the presence and degree of inflammation and intestinal metaplasia. Symptoms from children with and without an IP were compared. RESULTS: From 407 EGDs done by a single endoscopist, 24 patients had confirmed IP (incidence of 5.9%). The presence and degree of inflammation were always relatively greater in the columnar mucosa of the IP than in the antral/body gastric mucosa in the same patient (P = .0027) Inflammation was similar in the squamous epithelium around the IP and in the distal esophagus (P=.46). Two patients had intestinal metaplasia of the IP. The patients with IPs had a higher prevalence of respiratory symptoms than the control group (P = .03). CONCLUSIONS: Children with IPs may have a higher frequency of respiratory symptoms. Periodic surveillance should be performed in children with intestinal metaplasia of an IP.

Adolescent↗
PubMed2005

Pitfalls in the diagnosis of intestinal tuberculosis: a case report.

An 18-year-old long-term Norwegian resident of Somali origin was submitted to hospital with bloody diarrhoea, fever, weight loss and abdominal pain. On initial colonoscopy, colitis with segmental appearance was seen. Apart from a single polymerase chain reaction (PCR) from gastric aspirate staining, PCR and culture for acid-fast bacilli revealed negative results from the multiple samples taken including sputum, gastric fluid, stool, urine and intestinal mucosa. On physical examination and CT scan, there was no evidence of ascites, lymph node enlargement or pathologic pulmonary findings. Although the diagnosis was uncertain, tuberculostatic therapy was initiated. As the conformational testing of the PCR and the microbiological work-up remained negative and the patient's condition did not improve, tuberculostatic treatment was stopped and Crohn's disease was stated as the most likely diagnosis. Although the patient improved clinically under therapy with prednisolone, newly appearing fistulas deriving from the ascending colon were noted on follow-up. Thus tuberculostatic treatment was restarted. However, signs of an acute abdomen appeared and laparotomy was performed, thereby revealing a peritoneal spread of nodules. Resection of the ileum and ascending colon was performed. Diagnosis of intestinal tuberculosis with peritoneal spread was made by histology from resected bowel specimens showing caseating granulomas and a positive PCR result. The patient's condition improved after resection of the highly inflamed bowel segments and tuberculostatic therapy. Our case report shows the difficulty of proving intestinal tuberculosis by microbiological testing, macroscopic features on colonoscopy, histology, imaging such as CT scan and by empirical therapy. Therefore, in cases of colonic inflammation, where intestinal tuberculosis is an important differential diagnosis, a more aggressive diagnostic approach such as explorative laparoscopy should be considered.

Adolescent↗
PubMed2001

Clinical, clinicopathologic, radiographic, and ultrasonographic characteristics of intestinal lymphangiectasia in dogs: 17 cases (1996-1998).

OBJECTIVE: To characterize the clinical, clinicopathologic, and imaging findings in dogs with intestinal lymphangiectasia and to compare the histologic grade of lymphangiectasia with clinicopathologic and imaging abnormalities. DESIGN: Retrospective study. ANIMALS: 17 dogs with a histologic diagnosis of intestinal lymphangiectasia. PROCEDURE: Medical records of dogs with a histologic diagnosis of intestinal lymphangiectasia were reviewed for signalment, history, clinical signs, results of exploratory laparotomy, and clinicopathologic, radiographic, ultrasonographic, and histologic findings. RESULTS: Mean age of dogs was 8.3 years; the most common clinical signs were diarrhea, anorexia, lethargy, vomiting, and weight loss. Abnormal physical examination findings included dehydration, ascites, and signs of pain on palpation of the abdomen. The most notable clinicopathologic findings were low serum ionized calcium concentration and hypoalbuminemia. Abdominal ultrasonography was performed in 12 dogs and revealed intestinal abnormalities in 8 dogs and peritoneal effusion in 7 dogs. Exploratory laparotomy revealed abnormalities in 9 of 16 dogs including thickened small intestine, dilated lacteals, lymphadenopathy, and adhesions. On histologic examination of the small intestine, concurrent inflammation was observed in 15 of 17 dogs, crypt ectasia in 5 of 17, and lipogranulomas in 2 of 17. CONCLUSIONS AND CLINICAL RELEVANCE: Intestinal lymphangiectasia in dogs appears to be a heterogeneous disorder characterized by various degrees of panhypoproteinemia, hypocholesterolemia, lymphocytopenia, and imaging abnormalities. In most dogs, the severity of hypoalbuminemia appears to offer the best correlation with severity of histologic lesions of lymphangiectasia. Imaging abnormalities are common in dogs with intestinal lymphangiectasia but are not specific enough to differentiate this disorder from other gastrointestinal disorders, nor are they predictive of histologic severity.

Abdomen↗
PubMed1990

Glucocorticoid treatment in ileal Crohn's disease: relief of symptoms but not of endoscopically viewed inflammation.

The effect of prednisolone (20-30 mg daily for six to nine weeks) was studied in eight patients with Crohn's disease and recurrent, preanastomotic ileal inflammation, in respect of symptoms, endoscopic findings and phospholipase A2 activity in the ileal mucosa. The Harvey-Bradshaw Crohn's disease activity index improved significantly, mainly because of reduced frequency of loose stools and diminution of abdominal pain. Endoscopy revealed no corresponding decrease in ileal inflammation, which in all cases persisted after treatment. The phospholipase A2 activity in the ileal mucosa was not altered by prednisolone. In two of three patients with concomitant colitis colonic inflammation improved. The study confirmed earlier reports of good symptomatic relief from glucocorticoid treatment in Crohn's disease of the small bowel, but endoscopy suggests that this improvement was not the result of resolution of small intestinal mucosal inflammation.

Adult↗
PubMed1999

Oral spermine administration inhibits nitric oxide-mediated intestinal damage and levels of systemic inflammatory mediators in a mouse endotoxin model.

Enhanced intestinal nitric oxide production observed during sepsis is thought to play a central role in lipopolysaccharide-induced intestinal damage. In contrast intestinal polyamines, both from endogenous and exogenous origin, are essential for the maintenance of mucosal integrity. Polyamines have been shown to inhibit lipopolysaccharide-induced nitric oxide release in vitro and have been claimed to exert additional antiinflammatory actions. In this study, the effect of the polyamine spermine on the release of the proinflammatory mediators nitric oxide and tumor necrosis factor-alpha by a murine macrophage cell line was investigated. Furthermore, we investigated whether oral spermine administration inhibits lipopolysaccharide-induced intestinal inducible nitric oxide synthase and nitrotyrosine expression and modulates the release of inflammatory mediators. Our results show that although spermine inhibited lipopolysaccharide-induced nitric oxide release in a murine macrophage cell line, no effect on tumor necrosis factor-alpha release was observed. In addition, oral spermine administration inhibited intestinal inducible nitric oxide synthase and nitrotyrosine expression suggesting a protective effect of spermine on lipopolysaccharide-induced intestinal damage. In parallel a decrease in serum levels of the proinflammatory mediators nitrate, nitrite, and interferon-gamma and an increase in the antiinflammatory cytokine interleukin-10 was observed, although tumor necrosis factor-alpha levels were unaffected. These results indicate that spermine inhibits lipopolysaccharide-induced nitric oxide release in vitro as well as in vivo. Further, intraluminally derived polyamines modulate the systemic immune response. It is concluded that oral spermine administration might have therapeutic perspectives for several disorders characterized by systemic inflammation and intestinal damage.

Administration, Oral↗
PubMed2005

Obstruction in patients with colorectal cancer increases morbidity and mortality in association with altered nutritional status.

Intestinal obstruction aggravates the prognosis of colorectal cancer (CRC) patients. The aim of this study was to carry out a comparative analysis of nutritional status and inflammatory response in CRC patients with or without intestinal obstruction. The study was carried out on 43 patients with CRC. Twenty-three of these patients had intestinal obstruction. Anthropometric measurements, serum protein content, acute phase reactants, and diagnostic and risk nutritional indices were analyzed. The presence of intestinal obstruction reduced albumin (31 +/- 5.2 vs. 36 +/- 4.2 g/l; P = 0.0025) and prealbumin (0.13 +/- 0.047 vs. 0.21 +/- 0.042 g/l; P = 0.0001) and increased C-reactive protein (49 +/- 43.8 vs. 14 +/- 16.7 mg/l; P = 0.006) and alpha1-antitrypsin (189 +/- 34.7 vs. 148 +/- 35.4 mg/dl; P = 0.0011). Intestinal obstruction was related to malnutrition (86% vs. 33%; P = 0.019) and Mullen's prognostic nutritional index (48 +/- 21.7 vs. 31 +/- 17.9; P = 0.038) in CRC patients. Mullen's nutritional risk index was inversely correlated to total cholesterol (r = -0.51; P = 0.0002) and albumin (r = -0.81; P = 0.0001). No correlation was found between Duke's tumor stages and acute phase response, inflammatory parameters, and malnutrition. In conclusion, intestinal obstruction occurred more frequently in CRC patients with malnutrition. The increased morbidity and mortality of CRC patients was also associated with acute phase response, inflammation, and low serum cholesterol and triglyceride concentration.

Acute-Phase Proteins↗
PubMed2006

[Effect of intestinal ischemia/reperfusion injury on leptin and orexin-A levels].

OBJECTIVE: To explore the effect of intestinal ischemia/reperfusion (I/R) injury on leptin and orexin-A levels in peripheral blood and central secretory tissues, and investigate the roles of leptin and orexin-A in acute inflammatory responses. METHODS: An intestinal I/R injury rat model was established, and the rats were grouped according to duration of the reperfusion time following a 60-min ischemia. Radioimmunoassay was used to examine the protein levels of leptin in the serum and adipose tissue, and the protein levels of orexin-A in the plasma and hypothalamus. Reverse transcriptase-polymerase chain reaction was also performed to detect the mRNA expressions of adipose leptin and hypothalamus orexin-A. RESULTS: Compared with that before injury, serum leptin level of 60-min ischemia with 30-min reperfusion (I60'R30') group decreased significantly and that of I60'R360' increased significantly. Compared with the sham-operation group (sham) after injury, serum leptin level of I60'R360' group increased significantly, and adipose leptin protein levels of I60'R30' and I60'R90' groups decreased significantly, whereas that of I60'R360' group increased obviously. Compared with sham group after injury, adipose leptin mRNA expressions of I60'R30', I60'R240' and I60'R360' groups all increased significantly, while that of I60'R150' showed significant decrease. No significant changes were noted in the protein levels of orexin-A either in the plasma or hypothalamus after I/R injury. In comparison with sham group after injury, hypothalamus orexin-A mRNA expressions of I60'R30' and I60'R90' groups showed gradual but significant decrease, and till 150 min of reperfusion, the expression reached its lowest, followed then by slow recovery at 240 and 360 min, though still remaining significantly lower than that of sham group. CONCLUSION: Leptin and orexin-A have a time-dependent response to intestinal I/R injury, but the former appears to exhibit a faster response, and they may play a certain role in the metabolic disorders of acute inflammation.

Animals↗
PubMedDate not supplied

[HIV enteropathy].

HIV enteropathy is defined, according to authors, by intestinal histological anomalies presumed to be induced by HIV and/or the chronic diarrhea of AIDS progressing in the absence of any detectable intestinal infectious pathogen. HIV can certainly infect the mononuclear cells of the chorion of the intestinal mucosa, and probably certain colonocytes. The links between infection of these cells and HIV enteropathy remain very poorly understood. Certain authors attribute a preponderant role to possible abnormalities of enterocyte renewal induced by HIV, and others to intestinal mucosal inflammation induced by the infection and activation of lymphocytes of the mucosal chorion. Multifactorial, anatomical and functional, involvement of the mucosal barrier of the entire intestine is no doubt closest to the truth.

CD4-Positive T-Lymphocytes↗