الفهرس 
Primary Nephrotic SyndromeOnly 14 pages are availabe for public view
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Abstract
ABSTRACT
Background: Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract, including ulcerative colitis (UC) and Crohn’s disease (CD). The pathophysiology of IBD involves various factors such as intestinal microbiota, aberrant immune responses, environmental variables, and genetic predisposition. Immunological dysregulation characterized by inflammation and immune cell infiltration contributes to the development of IBD. Proinflammatory cytokines, including TNF, IL-1, IFN-, and cytokines of the IL-23/Th17 pathway, are produced in large quantities, leading to inflammation and tissue damage. Adipose tissue, particularly visceral adipose tissue, produces adipokines that can exacerbate inflammation in IBD.
Aim of the Work: to evaluate the role of visfatin, an adipokine, in the diagnosis, disease activity, and correlation with clinical findings in newly diagnosed IBD patients. This study was a Case Control study that was conducted in gastroenterology outpatient clinic, Alex fever hospital and Ain Shams University over 60 studied subjects divided into two groups.
Patients and Methods: Demographic data, clinical parameters, inflammatory markers, and serum visfatin levels were analyzed in IBD patients and healthy controls. The severity and activity of the disease were assessed using various diagnostic procedures, including endoscopy, blood testing, stool analysis, and imaging examinations.
Results: There were no statistically significant differences in demographic data between the IBD patients and healthy controls. However, significant differences were observed in clinical parameters, inflammatory markers, and serum visfatin levels among the studied groups. IBD patients showed abnormal findings in CBC, lipid profile, HbA1C, inflammatory tests, and fecal calprotectin compared to healthy controls. Serum visfatin levels were significantly higher in IBD patients than in the control group, indicating its potential role in IBD pathogenesis. Previous studies have suggested that adipokines, including visfatin, can modulate inflammation in IBD. Elevated visfatin levels have been associated with bowel inflammation and have been proposed as a marker for disease activity and severity. However, the correlation between serum visfatin levels and disease activity remains inconclusive. Some studies have reported higher visfatin levels in CD compared to UC, while others have found no significant difference between the two subtypes.
Conclusion: The serum visfatin level was significantly higher in newly diagnosed patients with IBD than in controls. Serum visfatin might be a novel noninvasive marker to detect activity in IBD patients and can be used as a predictor of disease extension in patients with UC. Further studies on big sample sizes and on different populations are recommended to confirm these results.