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Clinical Trial Summary

Syndecan-1 is a protein on the surface intestinal cells. previous studies proved low levels of mucosal syndecan-1 levels on the surface of intestinal cells is patients with acute and chronic inflammation due to inflammatory bowel disease.

this protein might shed from cell surface to the serum. The investigators wish to prove that elevated serum levels of syndecan-1 may be predictive of disease presence, extent and severity, that buy taking a simple blood sample from patients diagnosed with inflammatory bowel disease and comparing to normal subjects and to other markers.


Clinical Trial Description

One of the main hypothesis for the etiology of Inflammatory bowel disease (IBD) is an inappropriate and ongoing activation of the mucosal immune system in response to the presence of normal luminal flora. This aberrant response is most likely facilitated by defects in both the barrier function and the mucosal immune system of the intestinal epithelium. Syndecans are a class proteoglycans that take part in both cell adhesion and growth factor binding. Of the four known syndecan core proteins, syndecan-1 (CD138) and one of the best studied of this group and is also the relevant to the this study as it is expressed on the basolateral surface of columnar epithelial cells of the colon. Syndecan-1 functions as an integral membrane protein that participates in cell proliferation, cell migration and cell matrix interactions in the GI tract. Evidence for a reduction of syndecan-1 expression in the regenerating epithelium that overlies inflamed tissue was reported in both acute and chronic inflammation. This protein that is lost from the inflamed mucosal membrane might shed to the serum. Elevated serum levels of syndecan-1 may be predictive of disease presence and extent. ;


Study Design

Observational Model: Cohort, Time Perspective: Cross-Sectional


Related Conditions & MeSH terms


NCT number NCT01430039
Study type Observational
Source Meir Medical Center
Contact
Status Completed
Phase N/A
Start date October 2011
Completion date April 2015

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