الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of IBD remains unknown, the most accepted hypothesis of IBD pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host.
IBD are 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 IBD 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 IBD, 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 IBD patients. Therapeutic advances in the management of IBD have led to a paradigm shift in the assessment of IBD 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 IBD exist, each of which has its merits, although none is perfect. These disease activity indices depend on clinical, endoscopic, radiological and histological assessment of IBD patients.
Calprotectin is a small calcium-binding protein and it contribute to ~60% of the protein content of the cytosol in neutrophils. In the presence of active intestinal inflammation, neutrophils migrate to the intestinal lumen resulting in leakage of neutrophils, and hence, calprotectin, into the lumen and its subsequent excretion in feces. Mesuring of FC includes the traditional ELISA method and the rapid POCT. Initial studies of FC focused on its ability to distinguish between IBS and IBD. In other studies, FC has been shown to differentiate between active and inactive IBD and therefore, it correlates well with disease activity indices.
Neopterin, a pyrazino-[2,3-d]-pyrimidine compound, is a metabolite of cyclic guanosine monophosphate that is released by activated T lymphocytes and macrophages after induction by interferon γ. In humans, the accuracy of neopterin measured in blood or in urine has been previously investigated for monitoring disease activity in various immune-mediated and chronic inflammatory disorders.
In IBD, Relationships between serum or urinary neopterin and disease activity have been previously investigated. In contrast to calprotectin that reflects indirectly the degree of granulocytes influx into the intestinal lumen, fecal neopterin whose secretion by macrophages, in response to inflammation represents a reliable indicator of Tcell-mediated immune activation. Neopterin release from activated macrophages may provide, at least theoretically by its intrinsic mechanism of release, an advantage over calprotectin which is not secreted and represents a neutrophil-derived protein.
The study aimed to determine the value of fNeo concentration in patients with IBD both active and inactive groups and to correlate them with clinical and endoscopic disease activity scores in comparison to FC.
The study was conducted on sixty patients and twenty healthy volunteers representing group III. The sixty patients were divided into four groups. group Ia included fifteen patients with active UC, group Ib included fifteen patients with inactive UC, group IIa included fifteen patients with active CD and group IIb included fifteen patients with inactive CD. Disease activity was assessed by SCCAI in UC patients and CDAI in CD patients. Patients with diseases known to increase the neopterin level as GUT malignancies, recent gastrointestinal surgeries, colonic polyposis and diverticulosis and indeterminate colitis were excluded.
All candidates in the study were subjected to full history taking, thorough clinical examination and laboratory investigations including CBC, ESR, CRP, albumin, FC and fNeo by ELISA. All candidates were also subjected to ileocolonoscopy and CTE. Clinical disease activity was assessed by SCCAI in UC patients and CDAI in CD patients. Endoscopic disease activity was assessed by UCEIS in UC patients and SES-CD in CD patients.
There was statistically significant higher Hb level, PLT count, ESR and CRP in group IA than in group IB. Also haemoglobin, PLT count, ESR and CRP were statistically significant higher in group IIA than in group IIB. However there were no statistically significant differences in between group IA and IIA and between group IB and IIB.
Patients in group IA have statistically significant higher WBCs than patients in group IB. Unlike hemoglobin and platelets patients in group IIA have no statistically significant higher WBCs than patients in group IIB. Moreover, there was no statistically significant difference between group IA and IIA, and group IB and IIB.
Patients in group IA have statistically significant lower albumin than patients in group IB. Also patients in group IIA have statistically significant lower albumin than patients in group IIB. However, there was no statistically significant difference between group IA and IIA, and group IB and IIB.
Regarding the stool calprotectin, there were statistically significant differences between group IA, IB, IIA and the control group. While there was no statistically significant differences between group IIB and the control group. There was also statistically significant difference in stool calprotectin level between active and inactive UC groups and between active and inactive CD groups. FC was also found to be statistically significant higher in UC groups over CD groups.
Like stool calprotectin, there were statistically significant differences in stool neopterin level between group IA, IB, IIA and the control while there was no statistically significant differences between group IIB and the control group. Comparing group IA (active UC) and IB (inactive UC) there was no statistically significant difference in stool neopterin level but there was a statistically significant difference between group IIA (active CD) and group IIB (inactive CD). Stool neopterin level showed no statistically significant