الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Inflammatory bowel disease (IBD) includes: Crohn’s disease (CD) and ulcerative colitis (UC) characterized by chronic inflammation of the intestine of unknown etiology. It has been assumed that it is a multifactorial disease involving interactions between aberrant immune response, environmental and genetic factors.
The most accepted hypothesis of IBD pathogenesis is that an immune response against the intestinal microbiota that is triggered by environmental factors in a genetically predisposed host.
Ulcerative colitis (UC) is characterized by episodes of relapses and remissions of intestinal and extra-intestinal manifestations. Disease management has to focus on achieving and maintaining remission, preventing complications, improving quality of life (QOF) and minimising hospital admissions.
Diagnosis of UC depends on clinical symptoms, laboratory, radiological and endoscopic investigations.
Non-invasive biomarkers are needed. These biomarkers help to avoid invasive diagnostic tests that may cause patient’s discomfort and complications. The ability to determine the severity, prognosis and response to therapy of IBD, using biomarkers is a goal of clinical researchers but till now still no single biomarker is perfect.
The role of using CBC, CRP, ESR, albumin, ASCA and ANCA were previously investigated in IBD patients. Therapeutic advances in the management of IBD have led to a paradigm shift in the evaluation of IBD disease activity. Beyond clinical remission, objective assessment of inflammation is now critical to guide for subsequent therapy as part of a ’treat to target’ strategy. Multiple domains of disease activity assessment in IBD exist, each of which has its merits, although none is perfect. These disease activity indices depend on clinical, endoscopic and histological assessment of IBD patients.
While there is great expansion of studies for electrolytes dependent immune responses especially sodium, the literature on the association between potassium and inflammatory responses is limited. A recent study found an inverse relationship between dietary potassium intake and risk of CD and UC. This shows that potassium is associated with attenuated gut inflammatory responses.
Potassium enhances the generation of FoxP3+ Treg cells in the presence of TGFβ1 and reinforces the Foxp3 expression in Th17 cells by activating Smad 2/3 and inhibiting Smad 7 expression.
The study aimed to assess the role of urinary potassium concentration as a marker for disease activity in patients with Ulcerative colitis.
The study was conducted on forty patients and twenty healthy volunteers representing group II. The forty patients were divided into two groups. group IA included twenty patients with active UC, group IB included twenty patients with inactive UC. Disease activity was assessed by mayo scoring system in UC patients. Patients on drugs which may influence the urinary potassium (diuretics, ACE inhibitors, ARBs), patients with CKD, diabetes mellitus (DM), hypertension and patie