Disease relevance of Colonic Diseases

• Factors associated with conversion were internal fistula as an indication for surgery, smoking, steroid administration, extracecal colonic disease, and preoperative malnutrition [1].
• In vitro bromodeoxyuridine immunohistochemical technique was used to assess the effect of daily oral supplementation with vitamin E (160 mg), vitamin C (750 mg), or beta-carotene (9 mg) on the colonic crypt cell proliferation in patients with adenomatous polyps (n = 40) compared with normal subjects with no colonic disease (n = 20) [2].
• Expression of binding of plasminogen, thrombospondin, vitronectin, and fibrinogen, and adhesive properties by Escherichia coli strains isolated from patients with colonic diseases [3].
• Traditional risk factors include long disease duration and greater extent of colonic disease, but newer factors such as associated primary sclerosing cholangitis, folate deficiency, and family history of colon cancer may help to refine risk stratification [4].
• CONCLUSIONS: Neutrophil migration to the gut lumen in Crohn's disease is a feature of colonic disease irrespective of associated ileal lesions [5].

High impact information on Colonic Diseases

• CONCLUSIONS: Butyrate has dual effects in markedly reducing colonic epithelial urokinase activity, and these may have important implications to understanding colonic epithelial physiology and the pathogenesis and treatment of colonic diseases [6].
• This high level expression of PPARgamma in colon warrants further study in view of the well established role of fatty acid and arachidonic acid derivatives in colonic disease [7].
• Thus severe colonic disease noted during the course of DBA/2----B6D2F1 murine GVHD was found to have significant histopathologic similarities to both human GVHD enteropathy and other inflammatory diseases of the human colon [8].
• However, the consistent association of the deletion at codon 1309 with more severe colonic disease than that observed in patients with mutations at codons 1061 and 1068, supports a correlation between mutation site and penetrance of FAP [9].
• In conclusion, a fish oil diet prevents the increase in thromboxane in the chronic state of inflammation and shortens the course of the colonic disease by diminishing both the severity of the lesions and their progression to chronicity [10].

Chemical compound and disease context of Colonic Diseases

• A significant correlation was found between 24 and 48 h faecal Indium-111 excretion for small bowel (r = 0.708, p less than 0.0001) and colonic disease (r = 0.994, p less than 0.0001) [11].
• Determination of prostaglandin synthetase activity in rectal biopsy material and its significance in colonic disease [12].
• Of those patients who had colonic gallium activity that did not change in location or intensity during the study, 9 had proved colonic disease [13].
• Because colonic disease activity and treatment with sulfasalazine have been found to be of independent importance for development of colonic carcinoma in UC, this study aims to determine if differences exist concerning colonic disease activity in UC patients with and without PSC [14].
• Development of a chronic colonic intubation model in rats for the study of luminal factors in colonic diseases [15].

Gene context of Colonic Diseases

• An association between nonsynonymous variants in the TLR1, -2, and -6 genes and extensive colonic disease in UC and CD was found [16].
• Expression of hormone receptors, cathepsin D, and HER-2/neu oncoprotein in normal colon and colonic disease [17].
• These results further demonstrate that IL-2 plays a significant role in normal immune responses in the body and that plasma SAA levels both reflect colonic disease severity and may indicate subclinical disease in both IL-2(-/-)and IL-2(+/-)mice [18].
• In 14 patients with a variety of benign colonic diseases the mean faecal CEA was 7.12 +/- 1.39 micrograms/g which was not significantly different from the mean pre-operative value in the cancer patients [19].
• The carriage of allele 2 may favour steroid-dependent disease and to a lesser extent fistulizing and colonic disease, possibly secondary to a more intense TNF-alpha-driven inflammatory reaction at the mucosal level [20].

References