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ISSN: 2161-069X

Journal of Gastrointestinal & Digestive System
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Role of vitamin D deficiency, C- reactive protein and adhesion molecules in severity of ulcerative colitis

7th Global Congress on Gastroenterology & Endoscopy

Romany Helmy Thabet, Abdullah Zidane Al-Shammari and Youssef Nasif Al-Shammari

Northern Borders University, Saudi Arabia

Posters & Accepted Abstracts: J Gastrointest Dig Syst

DOI:

Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD). The hallmark of UC lesions is infiltration of the intestine by mononuclear cells, predominantly lymphocytes. There is growing epidemiological evidence that suggest implication of vitamin D deficiency in the development of IBD and also its influence on disease severity. C-reactive protein (CRP) levels are often used in the follow-up of patients with IBD. Adhesion molecules such as intercellular adhesion molecule (ICAM) and E-selectin are cell surface-expressed glycoproteins that play a prominent role in leukocyte recruitment and proliferation in the inflamed colon. The aim of the present descriptive study is to investigate the role of vitamin D, CRP and the adhesion molecules ICAM and E-selectin in prediction of severity of UC. Samples of blood were taken from 24 diagnosed cases of UC for measurement of serum levels of vitamin D, CRP, ICAM and E-Selectin by enzyme-linked immunosorbent assay (ELISA). Severity index for UC cases and its correlation with the aforementioned measures was determined. Comparing to control groups formed by individuals without clinical and/or laboratory signs of UC, UC patients showed significant increased levels (p<0.001) of sICAM-1, E-selectin and CRP in serum samples. On the contrary, vitamin D levels were significantly decreased in UC patients. Strong correlation was statically determined between vitamin D deficiency, CRP, adhesion molecules and UCEIS. In conclusion, the present work confirmed the role of vitamin D deficiency, adhesion molecules notably ICAM and E-selectin and the acute phase biomarker CRP in pathogenesis of UC.
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