الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
 |  | from | 79 |  |  |
| | | from | 79 | | |
Abstract
UC is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of UC remains unknown, the most accepted hypothesis of UC pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host.
UC is characterized by episodes of exacerbations and remissions of intestinal and extraintestinal manifestations. Because the course is unpredictable and there is no cure, disease management must focus on achieving and maintaining remission, preventing complications, improving quality of life, and minimizing the impact of comorbid conditions.
Diagnosis of UC is based on clinical symptoms combined with radiological and endoscopic investigations. Determination of the correct diagnosis is important for its implications in selecting treatment and in the timing and type of surgery that may be required.
The employment of non-invasive biomarkers is needed. These biomarkers have the potential to avoid invasive diagnostic tests that may result in discomfort and potential complications. The ability to determine the type, severity, prognosis and response to therapy of UC, using biomarkers has long been a goal of clinical researchers. Unfortunately, no single biomarker is perfect.
The role of using CBC, ESR, CRP, albumin, ASCA and ANCA were extensively previously investigated in UC patients. Therapeutic advances in the management of UC have led to a paradigm shift in the assessment of UC disease activity. Beyond clinical remission, objective assessment of inflammation is now critical to guiding subsequent therapy as part of a ’treat to target’ strategy. Multiple domains of disease activity assessment in UC exist, each of which has its merits, although none is perfect. These disease activity indices depend on clinical, endoscopic, radiological and histological assessment of UC patients.
Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, p19 and p40. IL-23 is involved in differentiation of Th17 cells in a pro-inflammatory context and especially in the presence of tumor growth factor-beta (TGF-β) and interleukin-6 (IL-6). Activated Th17 cells produce interleukin-17A (IL-17A), interleukin-17F (IL-17F), interleukin-6 (IL-6), interleukin-22 (IL-22), tumor necrosis factor alpha (TNF-α), and granulocyte monocyte –colony stimulating factor (GM-CSF). Inflammatory macrophages express interleukin-23R (IL-23R) and are activated by interleukin-23 (IL-23) to produce interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), and
IL-23 itself. These effects identify inteleukin-23 (IL-23) as a central cytokine in autoimmunity and a highly promising treatment target for ulcerative colitis.