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At least 307 records · Page 17Linked to original sources
PubMed2004

Modern imaging using computer tomography and magnetic resonance imaging for inflammatory bowel disease (IBD) AU1.

Radiologic imaging--especially of the small bowel--plays an important role in the diagnosis and management of patients with inflammatory bowel disease. The radiographic examination of the small intestine with barium either as enteroclysis or as small bowel follow through are still the mainstays in small bowel imaging. However, abdominal CT or MRI, which has the advantage of not utilizing ionizing radiation, or the techniques of CT- or MR-enteroclysis, are overall comparable with regard to the sensitivity and specificity in detecting intestinal pathologies and have already replaced the conventional techniques in centers dedicated to the management of inflammatory bowel disease. Additionally, these cross-sectional imaging techniques provide, in a sense, a "one stop abdominal imaging workup," the diagnosis of extraluminal disease manifestations or complications. Future developments of CT- or MR-based virtual colonography and endoscopy in patients with inflammatory bowel disease are currently being investigated, but should momentarily be considered as purely experimental approaches.

Colonoscopy↗
PubMed2006

Role of the NFKB1 -94ins/delATTG promoter polymorphism in IBD and potential interactions with polymorphisms in the CARD15/NOD2, IKBL, and IL-1RN genes.

BACKGROUND: Recently, an association of the NFKB1 polymorphism -94ins/delATTG with ulcerative colitis (UC) has been reported. This 4-bp insertion/deletion polymorphism is localized in the promoter region of the NFKB1 gene and appears to be functionally relevant. The aim of the present study was to confirm the association of the -94ins/delATTG (W/D) NFKB1 promoter polymorphism with UC in a population of German origin and to test for a potential association with Crohn's disease (CD). Furthermore, potential interactions of the -94ins/delATTG polymorphism with the IKBL and the IL-1RN genes should be determined. MATERIALS AND METHODS: The study population comprised 630 patients with CD, 365 patients with UC, and 974 healthy controls. Genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism analysis. For statistical evaluation, the chi-square test and the Fisher exact test were used. RESULTS: No significant association of the W/D NFKB1 polymorphism with CD or UC was detected. In addition, no significant interactions between the -94ins/delATTG NFKB1 polymorphism and polymorphisms within the IKBL and the IL-1RN genes, respectively, were found in CD or UC. Also, no significant interactions of the NFKB1 polymorphism with mutations of the CARD15/NOD2 gene and with clinical phenotypes were detected in CD. Moreover, no associations of the NFKB1 polymorphism were found in UC depending on disease localization. CONCLUSIONS: The present study could not confirm the reported association of the -94ins/delATTG NFKB1 polymorphism with UC and also found no evidence for a role of this polymorphism in CD. The results do not give evidence for a role of this NFKB1 polymorphism in the pathogenesis of UC and CD.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Past and current theories of etiology of IBD: toothpaste, worms, and refrigerators.

While tremendous advances have improved the understanding of inflammatory bowel disease, with regard to environmental risk factors as well as the biochemical nature of the inflammatory process, a determination of primary etiology remains elusive. Numerous theories have been proposed in the past century concerning the cause of Crohn's disease and ulcerative colitis with implications for specific therapies. On further study, most of these ideas and therapies have failed to be accurate in theory or therapeutic approach. Others remain untested or are the focus of current investigation and controversy. This paper reviews the dominant theories of primary etiology. These hypotheses include infectious causes such as Mycobacteria paratuberculosis and measles. Allergic and nutritionally related causes have been the focus of considerable research. Microparticles, which is part of the concept behind toothpaste as a cause, have been suggested more broadly to be the principal factor initiating Crohn's disease. Several of these concepts rely on the idea that there is an increased intestinal permeability that is the central defect leading to Crohn's disease. Rather than being an excessive T cell driven process, Crohn's has been suggested to be an innate immune deficiency, leading to the use of colony stimulating factors to augment the intestinal barrier function and innate immunity. A variety of changes in the gut flora, ranging from a basic dysbiosis to the absence of helminths, have been proposed as the root cause of inflammatory bowel disease.

Colitis, Ulcerative↗
PubMed2006

Segmental colitis associated with diverticular disease and other IBD look-alikes.

Segmental colitis associated with diverticular disease is an inflammatory disorder that bears close clinical and histopathologic similarities to idiopathic inflammatory bowel disease. Comparison with other inflammatory bowel disease-like disorders, such as blind-ended pouches in ulcerative colitis, chronic granulomatous appendicitis, and delayed-surgery appendicitis, affords intriguing analogies and potential clues to its pathogenesis.

Colitis↗