الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Inflammatory bowel disease (IBD) is a group of chronic, autoimmune and inflammatory disorder of the large and small intestine. The major types of IBD are Ulcerative colitis (UC) and Crohn’s disease (CD).
The etiology of inflammatory bowel disease (IBD) involves complex interactions among susceptibility genes, the environment, and the immune system. IBD has been long recognized as a systemic inflammatory entity and as such it is anticipated to induce changes exceeding bowel mucosa, being reflected in a broader spectrum of tissues, including blood. Examples of such changes are the fluctuations in the levels of C-reactive protein (CRP), Serum amyloid A (SAA), tumor necrosis factor-alpha (TNF- alpha), Interleukins , S100 Proteins, metalloproteinases, angiogenins.
As intestinal symptoms are a frequent cause of referrals to gastroenterologists, and mainly due to subtle or atypical presentation that in some cases the discrimination of Crohn’s disease (CD) or ulcerative colitis (UC), from other diseases of the alimentary tract, especially from irritable bowel syndrome (IBS), becomes rather problematic. (10)
The diagnosis of IBD is established with laboratory, endoscopic, radiological and pathological tests. Currently available biochemical tests have several limitations.
There are several reasons why laboratory markers have been studied in IBD in the past decades: firstly, to gain an objective measurement of disease activity as symptoms are often subjective; and secondly, to avoid invasive (endoscopic) procedures which are often a burden to the patient. An ideal marker should have many qualities. It should be easy and rapid to perform, cheap, and reproducible between patients and laboratories. The ideal laboratory marker should furthermore be able to identify individuals at risk for the disease and should be disease specific; it should be able to detect disease activity and monitor the effect of treatment; and finally it should have a prognostic value towards relapse or recurrence of the disease.
An important mechanism in the initiation and perturbation of inflammation in IBD is the activation of innate immune mechanisms. Among the factors released by infiltrating neutrophils are proteins of the S100 family.
The S100A12, also known as calgranulin C, is a member of the S100 protein family. S100A12, like S100A8/A9 (calprotectin), is considered phagocyte-specific, exhibits proinflammatory properties and has already been linked to many different diseases of inflammatory origin, including IBD.
The aim of the work is to evaluate the utility of serum S100A12 levels in discriminating inflammatory bowel disease (IBD) from irritable bowel syndrome (IBS), while at the same time examining serum S100A12 titres with respect to the two disease types of IBD: ulcerative colitis and Crohn’s disease (UC and CD), traditional markers of inflammation C-reactive proteins (CRP) and serum amyloid A (SAA), patients characteristics and treatment modalities.
The present study was carried out on eighty patients and divided them into three groups:
Chron’s disease group: twenty CD patients.
Ulcerative colitis group: twenty UC patients.
Irritable bowel syndrome group: fourty outpatients diagnosed after full work-up as having IBS.
The diagnosis of IBD was established upon the co-evaluation of findings originating from clinical and endoscopic procedures, imaging studies, histopathology and laboratory analyses.
The results showed that serum S100A12 showed a significant high level in IBD group compared to IBS group. (p<0.001)
The median value of serum S100A12 in IBD patients was 68pg/ml and the median value of serum S100A12 was 24.80 pg/ml in IBS group. The mean serum S100A12 level for IBD patients was 70.99 ± 27.61pg/ml, and the mean level for IBD patients 63.63± 25.76 pg/ml.
There was a significant high level of serum S100A12 in CD group and UC group compared to IBS group. The median value of serum S100A12 in CD patients was 75.15pg/ml (range 34.30-132.0 pg/ml), in UC patients was 54.65pg/ml (range 41.40 – 132.0) pg/ml, and 24.80 pg/ml (range 15.90-44.10 pg/ml) in IBS group. The mean serum S100A12 level for CD patients was 78± 28.05 pg/ml, the mean level for UC patients was 63.63± 25.76 pg/ml, finally the mean level for IBS group was 26.10±7.45 pg/ml. (p<0.001, p value between CD and UC= 0.060, p value between CD and IBS<0.001, p value between UC and IBS<0.001).
Significant positive correlations were found between CRP,SAA and serum S100A12.
A significant positive correlation was found between ESR, fecal calprotectin and serum level of S100A12 in UC but no correlation was found between ESR, fecal calprotectin and serum level of S100A12 in CD.
A significant positive correlation was detected between the activity of UC using CAI and the serum level of S100A12but no correlation detected between the serum level of S100A12 and the activity of CD using CDAI in the studied cases of CD.
There was no statistically significant difference between male and female gender smokers and non smokers, and the presence of extraintestinal manifestations in IBD groups and serum level of S100A12. There was no statistically significant difference between the effect of 5ASA and steroids as a treatment on the serum level of S100A12 in both IBD groups. There was no statistical significance between disease location in CD, disease extent in UC and serum level of S100 A12.
It was concluded from the current study that there is an increase in serum S100A12 in IBD compared to IBS. The increase in serum S100A12 is correlated with the classical markers of inflammation CRP and SAA. No correlation was found between serum S100A12 levels and IBD patient’s characteristics as regard sex, smoking history and presence of extraintestinal manifestations. Finally In spite of that the increase in serum S100A12 is correlated with the classical markers of inflammation CRP and SAA, there is an absence of a similar association with IBD activity determined by conventional inflammatory indices