Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sucralfate, which binds to the matrix of the ulcer bed, is theoretically advantageous for duodenal ulcer therapy, but has not fulfilled its promise clinically. We examined the effects of sucralfate and related compounds in a human intestinal epithelial (Caco-2) cell culture model of restitution on sheet migration across and adhesion to collagen I. Migration was quantitated across a collagen I matrix treated with sucralfate or related compounds and correlated with cell adhesion. Caco-2 motility was significantly and dose-responsively inhibited by sucralfate at therapeutic luminal concentrations. Sucrose octaacetate, the sucralfate backbone, and lactose octaacetate exhibited similar effects while the beta-bonded disaccharide maltose octaacetate had little effect. Sucrose itself slightly stimulated motility. Adhesion effects paralleled motility. Thus, sucralfate may inhibit intestinal epithelial motility by sterically interfering with adhesion to collagen I. A sucralfate analog with a lactose octaacetate backbone might retain growth factor binding without inhibiting enterocyte motility, perhaps improving its clinical efficacy.
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PMID:Sucralfate impedes intestinal epithelial sheet migration in a Caco-2 cell culture model. 901 8

Duodenocolic fistula (DCF) is a rare disorder defined by the presence of an internal fistula between the duodenum and colon. Colon cancer, Crohn's disease, diverticulum and duodenal ulcer are common causes of DCF, and vomiting and diarrhea are its main symptoms. We report a 14-year-old boy with DCF who had been treated for a functional gastrointestinal disorder (FGID). The boy had often experienced episodes of vomiting and diarrhea since infancy, and had been diagnosed with FGID. He was referred to our hospital because of a 2-month exacerbation of persistent vomiting and diarrhea. Upper gastrointestinal contrast revealed no abnormalities. Eventually, esophagogastroduodenoscopy detected a duodenal fistula, and DCF was diagnosed by endoscopic fistulography. Colonoscopy showed a diverticulum in the ascending colon near the fistula. In addition, a C13 urea breath test for Helicobacter pylori infection was positive. One hypothetical pathogenesis of his DCF was perforated colonic diverticulitis. Adhesion between the fistula wall and colonic diverticulum near the fistula strongly suggested a relationship between the fistula and the diverticulum. However, he never presented with symptoms of colonic diverticulitis. Thus, a congenital origin was also suspected. After confirming temporary relief from the symptoms by endoscopic closure, surgical closure was performed.
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PMID:A boy with duodenocolic fistula mimicking functional gastrointestinal disorder. 3095 64