Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of goblet cells in the adaptive response of the intestine to jejunoileal bypass was studied in rats submitted to an 85% end-to-side jejunoileal bypass or sham bypass. At 36 weeks the length and wet weight of the duodenum and large bowel was 13-48% greater in animals with jejunoileal bypass. Measurements of villous height and crypt depth confirmed mucosal hyperplasia in the residual functioning small bowel and the distal colon. Histochemical studies in both groups of rats showed an overall predominance of sulphomucins throughout the intestinal tract, but jejunoileal bypass caused a disproportionate increase in the number of sialomucin containing goblet cells in functioning segments of small bowel and distal colon. An abundance of sialomucin cells at the site of anastomosis after jejunoileal bypass may have been a protective response to local mechanical trauma. Goblet cell hyperplasia is a feature of compensatory growth of the intestinal tract after surgical shortening. The changes in colonic mucin seen after jejunoileal bypass resemble those observed in ulcerative colitis and mucosal dysplasia.
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PMID:Goblet cell hyperplasia is a feature of the adaptive response to jejunoileal bypass in rats. 669 Mar 74

When rectal biopsies from 65 patients with ulcerative colitis and 20 patients with Crohn's disease was stained for mucins, an abnormal pattern (excess of sialomucins) was seen in about half of them. This is in contrast with 65 cases of non-specific proctitis where the mucin pattern of rectal biopsies was normal in all except one case. The abnormal mucin secretion in patients with ulcerative colitis was apparently related to the activity, duration, and extent of the disease. All biopsies with dysplasia showed predominant sialomucin staining except one. All biopsies showing sialomucins during remission also had dysplasia, while during active disease a number of biopsies had increased sialomucins without the evidence of dysplasia. It is not known if such cases will subsequently develop morphological atypia.
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PMID:Mucin secretion in inflammatory bowel disease: correlation with disease activity and dysplasia. 707 23

Patients with ulcerative colitis are at increased risk of developing adenocarcinoma of the colon. The authors describe a patient whose colonic neoplasm demonstrated histologic characteristics of both an adenocarcinoma and a carcinoid tumor and which was pathologically identical to a appendiceal adenocarcinoid. Because individual tumor cells stained positively for both mucin and argentaffin granules, the histologic picture is unique among the malignancies seen in patients with ulcerative colitis and cannot be explained as a composite of two independent neoplasms that have grown together. Since the tumor discussed seems to have originated from a single cell line, the theory that carcinoids develop from neural crest cells which have migrated to embryonic gut endoderm must be regarded with considerable doubt.
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PMID:Adenocarcinoid tumor of the colon arising in preexisting ulcerative colitis. 724 10

A variety of premalignant lesions, including Barrett's esophagus, colonic polyps, ulcerative colitis, primary sclerosing cholangitis, intraductal mucin secreting papillomatosis are now well recognized and accessible to direct endoscopic assessment and biopsy or brushing. This review emphasizes the potential usefulness of genetic markers, in particular Ki-ras oncogene and p53 tumor suppressor gene mutations, in the endoscopic surveillance of these premalignant conditions. The adjunction of Ki-ras and p53 assays in material collected during endoscopic procedures may help the clinician detect earlier and with a higher accuracy neoplastic progression.
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PMID:Use of genetic markers during endoscopic screening and follow-up of gastrointestinal precancerous lesions. 757 78

Previous studies have shown the presence in faeces of sulphatases, sialidases, glycosidases, and proteases relevant to mucus degradation, but the relative role of these enzymes in the degradation of colonic mucus has been unclear. A total mucinase assay using 14C threonine biologically labelled human colonic mucin as substrate was therefore developed in this study. Faecal mucinase activity of a pooled normal faecal filtrate was capable of removing 80% of the 14C threonine label from mucin within eight hours incubation, but 20% remained intact despite prolonged incubation. The pH profile of mucinase activity is broad (pH 4.5-9.5) suggesting contribution from multiple enzymes. Mucinase activity was reduced by preincubation with 100 micrograms/ml chymostatin (82.8%), 0.5 mg/ml EDTA (91.6%), and 4 g/l bismuth subsalicylate (72.0%). All 55 faecal samples studied contained detectable mucinase activity, measured as dpm release/micrograms protein/hour, which was greater in samples from patients with ulcerative colitis (n = 17, median 52.7, interquartile range 32.9-66.9), than controls (n = 26, 34.4, 26.8-40.4, p < 0.02) or patients with Crohn's disease (n = 12, 35.5, 17.5-55.7, p < 0.05). There was, however, no significant difference in faecal mucinase activity between inactive and active ulcerative colitis. These results suggest that faecal mucinase activity is one factor contributing to the thin mucus layer in ulcerative colitis and represents a potential target for drug treatment.
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PMID:Faecal mucinase activity assessed in inflammatory bowel disease using 14C threonine labelled mucin substrate. 767 82

Colonic mucin is heavily sulphated and it has been shown that enzymatic desulphation by faecal bacterial sulphatases greatly increases its susceptibility to degradation by faecal glycosidases. A possible role for faecal mucin sulphatase in the pathogenesis of inflammatory bowel disease has therefore been explored. Faecal mucin sulphatase activity assayed using 35S mucin as substrate was increased in ulcerative colitis (median 80.2 units/g pellet weight (range 6.9-1063; 95% confidence intervals (CI): 45.2 to 293.8, n = 22) compared with 11.3 units/g (range 3.0-53.5; 95% CI: 8.7 to 29.8, n = 17) in healthy controls (p < 0.01), where one unit released 1000 dpm free sulphate/hour from 35S mucin (1680 dpm/microgram). Patients with active ulcerative colitis had higher sulphatase activity (median 146; 95% CI: 98 to 253 units/g, n = 10) than those with inactive ulcerative colitis (median 42.2; CI: 22.5 to 81.6 units/g, n = 12) (p < 0.05). Longitudinal studies in patients with ulcerative colitis show fluctuations of faecal mucin sulphatase activity corresponding to clinical disease activity in six of seven patients. Faecal mucin sulphatase activity was not significantly increased in Crohn's disease (median 36.6, range 5.7-106.6; 95% CI: 22.9 to 65.3 units/g, n = 14). The bismuth salts, bismuth subcitrate and bismuth subsalicylate were found to inhibit faecal mucin sulphatase activity at concentrations achievable therapeutically. The increased faecal mucin sulphatase activity in ulcerative colitis could be the result of greater intraluminal substrate (mucin) availability leading to bacterial enzyme induction, but would probably result in more rapid degradation of secreted mucin and represents a potential target for treatment.
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PMID:Increased faecal mucin sulphatase activity in ulcerative colitis: a potential target for treatment. 773 66

It is clinically important to distinguish idiopathic inflammatory bowel disease (IBD) from other colitides, and ulcerative colitis (UC) from Crohn's disease (CD); however only a few histological criteria based on colonic biopsies have been established. We investigated 209 consecutive series of biopsies taken from 38 patients with UC, 12 with CD, and 105 with other colitides, to evaluate whether combinations of histological features, selected on the basis of our experience, and listed below, could be useful criteria for the differential diagnosis of IBD, and, more specifically, of UC: (A) chronic inflammation with a predominant increase of plasma cells, (B) crypt distortion, (C) crypt atrophy, (D) diffuse chronic inflammation within a biopsy and between biopsies, and (E) diffuse mucin depletion within a biopsy and between biopsies. Findings that fulfilled all or two of A-C distinguished IBD from the other colitides with high sensitivity (94.3%) and specificity (95.8%). When the findings fulfilled the additional criteria of D and/or E, UC was differentiated from CD or the other colitides with high sensitivity (86.4%) and specificity (99.3%).
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PMID:A study of the histological criteria for ulcerative colitis: retrospective evaluation of multiple colonic biopsies. 777 49

South Asians in Britain have a high incidence of ulcerative colitis and a low incidence of colorectal cancer. The pattern of mucus production in 12 South Asian and 16 European colitics and a control group of 19 South Asians was studied. Three types of mucin were identified after organ culture of colonic biopsy specimens with a dual label of [3H]-glucosamine and sodium [35S]-sulphate: type A had a high [35S]:[3H] ratio and high incorporation ([3H] dpm/micrograms DNA > 500); type B had a low ratio and high incorporation; and type C had low incorporation but with either high (C1) or low (C2) ratios. European colitic mucins show a significant reduction in the level of sulphation detected by mucin histochemistry with high iron diamine/Alcian blue staining, together with predominantly type B or C2 mucins (low sulphation). South Asian colitics showed histochemically normal patterns of high sulphation and largely type A and C1 mucins (high sulphation). There was no correlation of mucin type with disease activity index in either ethnic group. The appearance of apparently normal mucin in patients with ulcerative colitis may be a useful marker for the identification of a subgroup at low risk of colorectal cancer.
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PMID:South Asian and European colitics show characteristic differences in colonic mucus glycoprotein type and turnover. 779 19

The effect of the inflammatory mediator bradykinin on glycoprotein synthesis and mucin secretion in the human colonic adenocarcinoma cell line HT29-18N2 was examined. Bradykinin, at a threshold of 0.01 microM, accelerated the rate of mucin discharge as assessed by a mucin-specific ELISA. Using immunofluorescence microscopy, a thick meshwork of extracellular mucus was observed over bradykinin-treated monolayers but not mock-treated controls. Morphometric analysis of bradykinin-treated monolayers revealed no decreases in intracellular mucin stores or any other easily discernable morphological alteration. The ability of the cyclooxygenase inhibitors indomethacin and naproxen to decrease the response to bradykinin by approximately 68% indicates the effect is mediated, at least partially, through the generation of prostaglandins. Bradykinin did not alter the rate of incorporation of 3H-glucosamine into newly synthesized glycoproteins. Bradykinin-accelerated mucin secretion may be linked to the depletion of intracellular mucin stores in the inflammatory bowel disease ulcerative colitis.
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PMID:Bradykinin modulates mucin secretion but not synthesis from an intestinal goblet cell line. 787 99

Sialylation of mucus glycoproteins confers charge and increased resistance to enzymatic degradation. The hypothesis that mucus sialylation might be altered in ulcerative colitis has been studied using in vitro culture of mucosal biopsies for 24 h with 3H N-acetyl mannosamine as a specific sialic acid precursor. Rectal biopsies were obtained at colonoscopy from patients with clinically inactive ulcerative colitis (n = 9) and controls (n = 12) who were patients found to have a normal colonoscopy performed for iron deficiency anaemia or altered bowel habit. The incorporation of 3H N-acetyl mannosamine into mucin was increased in ulcerative colitis (n = 9; 150; 113.3-393.2 dpm/micrograms mucin, median and interquartile ranges), compared with controls (n = 12; 33.6; 19.7-68.4 dpm/micrograms; p < 0.01). The ratio of incorporation into mucin of 3H N-acetyl mannosamine/14C N-acetyl galactosamine was also increased in ulcerative colitis (3.27; 1.93-4.98 dpm/dpm), compared with controls (1.35; 1.24-1.7 dpm/dpm; p < 0.001) suggesting that the increased incorporation of N-acetyl mannosamine probably reflects an increase in the average extent of sialylation per mucin oligosaccharide chain rather than an increase in the number of oligosaccharide chains. This increase in mucin sialylation seems unlikely to have a pathogenic role in the development of colitis but provides further evidence for the similarity between the alterations that occur in ulcerative colitis, colonic polyposis and malignancy.
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PMID:Increased rate of sialylation of colonic mucin by cultured ulcerative colitis mucosal explants. 789 33


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