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Results for “Intestinal Inflammation”

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At least 1,783 records · Page 99Linked to original sources
PubMed1995

Importance of endoscopically visualized recurrent ileitis and small-bowel resection for symptoms in Crohn's disease.

BACKGROUND: The relationship between the endoscopic appearance of the ileal mucosa in Crohn's disease and the symptoms has not been studied. Although surgery is important, morbidity caused by intestinal resections and its relation to recurrent inflammation have been poorly evaluated. METHODS: The relationship of symptoms to various ileoscopic signs of inflammation and previous intestinal resection was prospectively studied in 75 postresection Crohn patients. RESULTS: Multivariate analysis showed that a combination of anastomotic width, pus, and length of previous small-bowel resection best explained a symptom score (r = 0.53, p < 0.001). Of 40 patients with the anastomosis strictured to less than 15 mm, only 9 had moderate to severe symptoms. Patients with a stricture diameter < 10 mm differed significantly in symptom score (p < 0.05) from those with wider anastomoses. CONCLUSIONS: The study indicated that intestinal resection was as important for symptoms as endoscopically viewed recurrent ileal inflammation. The diameter at which an intestinal stricture produces symptoms is less than previously argued, and the association of small-bowel resection with symptoms underlines the advisability of minimal surgery.

Adult↗
PubMed2001

Review article: Helicobacter pylori, mucosal inflammation and symptom perception--new insights into an old hypothesis.

The role of Helicobacter pylori and the accompanying mucosal inflammatory response in functional dyspepsia is still undefined. Human and animal studies have clearly demonstrated a link between intestinal mucosal inflammation and changes in sensory-motor function. Growing clinical and basic evidence supports the concept that a similar paradigm may occur in H. pylori-related dyspepsia. The infection may both induce gastric dysmotility and trigger neuroplastic changes in the afferent neural pathways leading to visceral hyperalgesia. A reduction of central antinociceptive control systems may also play a pathophysiological role. H. pylori eradication has provided disappointing results in terms of improvement of symptoms. This may reflect the long-term recovery of neuroplastic changes occurring in the afferent nervous system or, alternatively, the incomplete resolution of gastritis and the persistent production of inflammatory mediators by resident cells in the muscularis externa. The identification of these mechanisms may provide a better understanding of the pathophysiology of H. pylori-related dyspepsia and prompt innovative therapeutic approaches.

Animals↗
PubMedDate not supplied

Inguinal hernia incarceration as a form of intestinal tuberculosis.

We report the case of a 41 year-old male who came to the emergency room with a complaint of abdominal pain, and was diagnosed to have an acute obstructive abdomen due to a right inguinal hernia incarceration. During surgery, an intestinal granulomatous inflammation was observed adhered to the hernial sac. The histopathologic study confirmed the diagnosis of tuberculosis. We present a review of the different clinical forms of intestinal tuberculosis and the difficulties encountered in the differential diagnosis of such, emphasizing the uncommon presentation described in our patient.

Abdomen, Acute↗
PubMed1995

Hyperaggregation of platelets in intestinal tuberculosis: role of platelets in chronic inflammation.

Eighty-eight percent (38/43) patients of intestinal tuberculosis showed significant hyperaggregation of platelets (P < 0.001). Serum and plasma from 15 patients when incubated with normal platelets caused hyperaggregation. Gel filtered platelets from 2 patients suspended in normal plasma showed hyperaggregation of platelets with arachidonic acid. Tubercular protein had no effect on platelet aggregation. A role of hyperactive platelets in chronic inflammatory response is discussed.

Adolescent↗
PubMedDate not supplied

Inflammatory cytokine mRNAs in surgical specimens of necrotizing enterocolitis and normal newborn intestine.

Coagulation necrosis, inflammation, and hemorrhage are pathologic hallmarks of necrotizing enterocolitis (NEC). Because cytokines are peptides that mediate inflammatory cell recruitment and amplify the immune response, several of the inflammatory cytokines have been implicated in NEC. We hypothesized that mRNA levels for the interrelated cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), IL-6, and the neutrophil chemotactic factor IL-8 would be increased in NEC and would be associated with the presence of inflammation. In this study, we determined the relative levels and localization of mRNA for these cytokines in surgical pathology archival intestinal tissue from 29 premature infants with acute NEC and 15 control infants with congenital intestinal malformations using a novel quantitative in situ hybridization technique. Compared with controls, there were higher IL-1 beta mRNA levels in full-thickness sections and higher TNF-alpha mRNA levels in full-thickness and mucosa sections of acute NEC samples, suggesting a potential role for these cytokines in the pathogenesis of local inflammation in NEC. IL-6 and IL-8 mRNA levels were similar in samples of control and acute NEC cases. Analysis of covariance including all subjects showed that the presence of acute inflammation was associated with increased IL-1 beta mRNA levels in mucosa (P = .035) and increased IL-8 in full-thickness sections (P = .005) and mucosa (P = .01). In four of five NEC cases in which intestinal specimens were available from reanastomosis surgery, cytokine mRNA levels decreased to low or undetectable levels. These data suggest that the inflammatory cytokines are involved in neutrophil recruitment and augmentation of the inflammatory response in neonatal intestine.

Cytokines↗
PubMed2000

Uncoupling of intestinal mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase are required for the development of NSAID-enteropathy in the rat.

BACKGROUND: The pathogenesis of NSAID-induced gastrointestinal damage is believed to involve a nonprostaglandin dependent effect as well as prostaglandin dependent effects. One suggestion is that the nonprostaglandin mechanism involves uncoupling of mitochondrial oxidative phosphorylation. AIMS: To assess the role of uncoupling of mitochondrial oxidative phosphorylation in the pathogenesis of small intestinal damage in the rat. METHODS: We compared key pathophysiologic events in the small bowel following (i) dinitrophenol, an uncoupling agent (ii) parenteral aspirin, to inhibit cyclooxygenase without causing a 'topical' effect and (iii) the two together, using (iv) indomethacin as a positive control. RESULTS: Dinitrophenol altered intestinal mitochondrial morphology, increased intestinal permeability and caused inflammation without affecting gastric permeability or intestinal prostanoid levels. Parenteral aspirin decreased mucosal prostanoids without affecting intestinal mitochondria in vivo, gastric or intestinal permeability. Aspirin caused no inflammation or ulcers. When dinitrophenol and aspirin were given together the changes in intestinal mitochondrial morphology, permeability, inflammation and prostanoid levels and the macro- and microscopic appearances of intestinal ulcers were similar to indomethacin. CONCLUSIONS: These studies allow dissociation of the contribution and consequences of uncoupling of mitochondrial oxidative phosphorylation and cyclooxygenase inhibition in the pathophysiology of NSAID enteropathy. While uncoupling of enterocyte mitochondrial oxidative phosphorylation leads to increased intestinal permeability and low grade inflammation, concurrent decreases in mucosal prostanoids appear to be important in the development of ulcers.

Animals↗