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Chronic Inflammatory Bowel Disease (chronic + inflammatory_bowel_disease)
Selected AbstractsSECOND LOOK COLONOSCOPY: INDICATION AND REQUIREMENTSDIGESTIVE ENDOSCOPY, Issue 2009Jean-Francois Rey Background:, There are circumstances when a colonoscopy should be repeated after a short interval following the first endoscopic procedure which has not completely fulfilled its objective. Review of the literature:, A second look colonoscopy is proposed when there remains a doubt about missed neoplastic lesions, either because the intestinal preparation was poor or because the video-endoscope did not achieved a complete course in the colon. The second look colonoscopy is also proposed at a short interval when it is suspected that the endoscopic removal of a single or of multiple neoplastic lesions was incomplete and that a complement of treatment is required. When the initial endoscopic procedure has completely fulfilled its objective, a second look colonoscopy can be proposed at longer intervals in surveillance programs. The intervals in surveillance after polypectomy are now adapted to the initial findings according to established guidelines. This also applies to the surveillance of incident focal cancer in patients suffering from a chronic inflammatory bowel disease. Conclusion:, Finally, in most developed countries, a priority is attributed to screening of colorectal cancer and focus is given on quality assurance of colonoscopy which is considered as the gold standard procedure in the secondary prevention of colorectal cancer. [source] Acute experimental colitis and human chronic inflammatory diseases share expression of inflammation-related genes with conserved Ets2 binding sitesINFLAMMATORY BOWEL DISEASES, Issue 2 2009Tineke C.T.M. van der Pouw Kraan PhD Abstract Background: Ulcerative colitis (UC) and Crohn's disease (CD) are characterized by chronic inflammation of the gastrointestinal tract, with overlapping clinical characteristics and unknown etiology. We reasoned that in intestinal inflammation the initial activation of the innate immune response fails to resolve, finally resulting in uncontrolled chronic inflammatory bowel disease. Methods: To identify the early inflammatory events in colitis that remain active in human chronic colitis, we analyzed the changes of the colonic transcriptome during acute experimental colitis and compared the outcome with previously published profiles of affected tissues from patients with UC and CD, and as a control for intestinal inflammation in general, tissues from celiac disease patients. Rheumatoid arthritis synovial tissues were included as a nonintestinal inflammatory disease. The expression profiles of each disease were analyzed separately, in which diseased tissues were compared to unaffected tissues from the same anatomical location. Results: Gene ontology analysis of significantly regulated genes revealed a marked activation of immunity and defense processes in all diseases, except celiac disease, where immune activation is less prominent. The control region of upregulated genes contained an increase in Ets2 binding sites in experimental colitis, UC, and rheumatoid arthritis, and were associated with upregulated immune activity. In contrast, upregulated genes in celiac disease harbored the transcription factor binding site GLI, which binds to the Gli family of transcription factors involved in hedgehog signaling, affecting development and morphogenesis. Conclusion: Ets2 may be an important transcription factor driving inflammation in acute as well as chronic inflammatory disease. (Inflamm Bowel Dis 2008) [source] Endoscopic factors in the diagnosis of colorectal dysplasia in chronic inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 5 2005Murat Toruner MD Abstract Background: Surveillance colonoscopy in inflammatory bowel diseases (IBDs) is advocated for early diagnosis of neoplasia but is imperfect because some patients develop cancer despite surveillance. We sought to determine if any endoscopic factors during surveillance colonoscopy were associated with the diagnosis of colorectal dysplasia before the development of cancer. Methods: We reviewed the Mayo Clinic endoscopic database and medical records of patients with IBD who underwent surveillance colonoscopy between January 2002 and November 2003. Associations were sought between endoscopic factors and the diagnosis of dysplasia. Among 635 IBD patients, 24 (3.8%) had flat dysplasia and 12 (1.9%) had IBD-related polypoid dysplasia. In 28 patients (4.4%), sporadic tubular adenoma was identified. Colonoscopies in which flat dysplasia was identified varied in duration from 7 to 81 minutes (median, 24.5 min) compared with 3 to 70 minutes (median, 22 min) for those in which dysplasia was not found. Results: Using logistic regression analysis, we found that every additional minute in total colonoscopy time increased the flat dysplasia diagnosis rate by 3.5% (P = 0.0157). There was a significant correlation between median surveillance colonoscopy duration per endoscopist and flat dysplasia diagnosis rate (P = 0.0066). The number of biopsies taken during the procedures with flat dysplasia ranged from 6 to 36 (median, 28) compared with 2 to 54 (median, 25) in those without flat dysplasia. There was no significant effect of biopsy number of dysplasia diagnosis. Conclusions: Our results show that the practice of surveillance colonoscopy varies greatly among endoscopists, and longer procedure duration is significantly associated with the likelihood of dysplasia diagnosis. [source] Signal transducers and activators of transcription 3 signaling pathway.INFLAMMATORY BOWEL DISEASES, Issue 2 2005An Essential Mediator of Inflammatory Bowel Disease, Other Forms of Intestinal Inflammation Abstract Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of chronic inflammatory bowel disease (IBD), are characterized by mucosal immune cell activation that is driven by a cytokine imbalance. Several cytokines involved in IBD act through the activation of the signal transducers and activators of transcription (STAT) family. We investigated the activation of STAT3 in the mucosa of CD and UC patients, and evaluated whether this event is specific for IBD patients. Using immunofluorescence and immunoblotting, total and phosphorylated STAT3 levels were assessed in biopsy specimens, isolated lamina propria mononuclear cells, and peripheral blood mononuclear cells from patients with CD, UC, other forms of intestinal inflammation, and control subjects. Immunoblotting revealed phosphorylated STAT3 in mucosal biopsy specimens from patients with CD, UC, celiac disease, and acute self-limited colitis, but not in the normal mucosa of control subjects. In IBD patients, STAT3 activation was confined to actively inflamed areas. Accordingly, activated STAT3 was detected in isolated lamina propria mononuclear cells from inflamed IBD tissues, but not in peripheral blood mononuclear cells from control subjects or IBD patients. Immunofluorescence demonstrated that the sources of activated STAT3 were macrophages and T lymphocytes, but not neutrophils. STAT3 activation also was detected in T cells infiltrating the duodenal mucosa of celiac disease patients. We conclude that STAT3 signaling occurs in both CD and UC, where it is strictly confined to areas of active inflammation and is limited to infiltrating macrophages and T cells. The occurrence of STAT3 signaling in other acute and chronic intestinal inflammatory conditions suggests that, rather than a specific feature of IBD, it represents a fundamental signaling pathway that is shared by multiple forms of gut inflammation. [source] Attenuation of a rocuronium-induced neuromuscular block in patients receiving prednisoloneACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2009S. SOLTÉSZ Background: This study tested the influence of continuous medication (more than 4 weeks) with prednisolone on a rocuronium-induced neuromuscular block. Methods: The time course of a rocuronium-induced neuromuscular blockade (0.3 mg/kg) was investigated in 40 patients with chronic inflammatory bowel disease undergoing elective abdominal surgery. The primary end point was the time from the start of injection of rocuronium until recovery of the TOF ratio to 0.9. Twenty patients received continuous medication with prednisolone (group A), and 20 were without glucocorticoid medication (group B). Additionally, another 20 patients without inflammatory bowel disease and without glucocorticoid medication served as control (group C). Results: The onset time was prolonged in group A [253 (51.2) s] compared with group B [187 (61.3) s]. Twitch height at the onset of the block was higher in group A [16.5 (0,61)%] than that in group B [5.0 (0,33)%]. The duration to 25% twitch height was shorter in group A [12.6 (0,20.7) min] compared with group B [16.7 (0,25.3) min] and group C [16.9 (0,29.3) min]. The recovery to a train-of-four ratio of 0.9 was reduced in group A [25.7 (23,34.3) min] compared with group B [34.7 (32.7,44.2) min] and group C [36.5 (31.7,42.3) min]. Conclusions: Prednisolone treatment in patients with inflammatory bowel disease is associated with a delayed onset and a shorter duration of action of rocuronium. The presence of an inflammatory bowel disease did not influence the neuromuscular block. [source] Population-Specific Susceptibility to Crohn's Disease and Ulcerative Colitis; Dominant and Recessive Relative Risks in the Japanese PopulationANNALS OF HUMAN GENETICS, Issue 2 2010Shigeki Nakagome Summary Crohn's disease (CD), a type of chronic inflammatory bowel disease (IBD), is commonly found in European and East Asian countries. The calculated heritability of CD appears to be higher than that of ulcerative colitis (UC), another type of IBD. Recent genome-wide association studies (GWAS) have identified more than thirty CD-associated genes/regions in the European population. In the East Asian population, however, a clear association between CD and an associated gene has only been detected with TNFSF15. In order to determine if CD susceptibility differs geographically, nine SNPs from seven of the European CD-associated genomic regions were selected for analysis. The genotype frequencies for these SNPs were compared among the 380 collected Japanese samples, which consisted of 212 IBD cases and 168 controls. We detected a significant association of both CD and UC with only the TNFSF15 gene. Analysis by the modified genotype relative risk test (mGRR) indicated that the risk allele of TNFSF15 is dominant for CD, but is recessive for UC. These results suggest that CD and UC susceptibility differs between the Japanese and European populations. Furthermore, it is also likely that CD and UC share a causative factor which exhibits a different dominant/recessive relative risk in the Japanese population. [source] Abrogation of IFN-, mediated epithelial barrier disruption by serine protease inhibitionCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2005L. E. M. Willemsen Summary The intestinal barrier function is often impaired in a variety of diseases including chronic inflammatory bowel disease. Increased intestinal permeability during episodes of active disease correlates with destruction or rearrangement of the tight junction protein complex. IFN-, has been widely studied for its effect on barrier function and tight junction structures but its mode of action remains unclear. Since the claudin family of tight junction proteins is proposed to be involved in barrier maintenance we studied the effect of IFN-, on claudin expression in relation to epithelial barrier function. Cycloheximide and protease inhibitors were used to study mechanisms of IFN-, mediated barrier disruption. Intestinal epithelial cells were exposed to IFN-, and permeability was evaluated by horse radish peroxidase (HRP) and 4 kD FITC-dextran fluxes. Occludin and claudin-1, -2, -3, and -4 tight junction protein expression was determined by Western blotting. Occludin and claudin-2 protein expression was dramatically reduced after IFN-, exposure, which correlated with increased permeability for HRP and FITC-dextran. Interestingly, cleavage of claudin-2 was observed after incubation with IFN-,. Serine protease inhibitor AEBSF completely abrogated IFN-, mediated barrier disruption which was associated with preservation of claudin-2 expression. Moreover, IFN-, induced loss of barrier integrity was found to affect claudin-2 and occludin expression through different mechanisms. Since inhibition of serine protease activity abrogates IFN-, mediated barrier disruption this may be an important target for therapeutic intervention. [source] The genetics of inflammatory bowel diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2001T. Ahmad Recent epidemiological, clinical and molecular studies have provided strong evidence that inherited predisposition is important in the pathogenesis of chronic inflammatory bowel diseases. The model most consistent with the epidemiological data suggests that Crohn's disease and ulcerative colitis are related polygenic diseases, sharing some but not all susceptibility genes. Investigators throughout the world have applied the complementary techniques of genome-wide scanning and candidate gene analysis. Four areas of linkage have been widely replicated on chromosomes 16 (IBD1), 12 (IBD2), 6 (IBD3,the HLA region), and most recently on chromosome 14. Fine mapping of these regions is underway. Of the ,positional' candidate genes, most attention has centred on the genes of the major histocompatibility complex. Genes within this region may determine disease susceptibility, behaviour, complications and response to therapy. Hope continues that studies of inflammatory bowel disease genetics will provide fresh insight into disease pathogenesis and soon deliver clinical applications. [source] | ||||||||||