الفهرس 
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Abstract
Human trefoil factor 3 (TF3), also known as intestinal trefoil factor, belongs to a small group of mucin-associated peptides. Being extremely resistant towards acids, proteolytical cleavage or heat degradation, TF3 is expressed mainly in the mucous cells of the small and large intestines, where it maintains the integrity of mucous layer and in cooperation with mucins protects the intestinal epithelial cells against various injurious agents.
The secretion of TF3 is triggered by the presence of certain inflammatory mediators and neurotransmitters. Over expression of TF3 occurs at the site of damage of the gastrointestinal tract, being upregulated and secreted in an autocrine fashion in response to gastrointestinal injury, acting as a motogen to facilitate cell migration into the lesion, thus forming a protective barrier.
Helicobacter pylori (H.pylori) is a gram-negative microaerophilic bacterium that infects the gastric mucosa. At least half the world populations are infected by the bacterium, making it the most widespread infection in the world. People infected with H.pylori at an early age are likely to develop more intense inflammation (atrophic gastritis) with a higher risk of developing gastric ulcer, gastric cancer or both. Acquisition at an older age brings different gastric changes more likely to lead to duodenal ulcer.
In view of the role of TF3 in gastric mucosal repair following injury elicited by several stimuli and as H. pylori is now recognized as one of the most important infective sources of gastric irritation, it was noteworthy to study serum TF3 level in H. pylori infected patients.
The present work aimed at evaluating the possible association of serum TF3 with H.pylori infection in patients presenting with gastric or duodenal ulcer.
The present study was conducted on eighty individuals divided into two groups; group (A) consisted of 40 patients (20 males and 20 females) with H. pylori induced gastritis, and group (B) consisted of 40 patients (18 males and 22 females) with H. pylori induced gastric ulcers. H.pylori infection was documented in all patients using the stool antigen test, and the rapid urease test done on gastric biopsies obtained by endoscopy.
To all patients, complete blood count (CBC), and serum levels of fasting serum glucose, creatinine, albumin, iron, total iron binding capacity (TIBC), and ferritin as well as activities of aminotransferases (AST / ALT) and alkaline phosphatase (ALP), Serodetection of hepatitis-C viral antibodies and hepatitis-B virus surface antigen was also done. ,were determined. Serum TF3 level was determined using an enzyme immunoassay technique.
The main results revealed in this study were:
1. A hypochromic microcytic anemia prevailed in most H. pylori infected patients included in our study.
2. A significantly higher serum TF3 median value was noted in the H. pylori infected cases without gastric ulcers compared to those with gastric ulcers.
3. Based on a receiver operating characteristic curve generated cut off value for serum TF3 of 2.4 ng/mL, the diagnostic performance of serum TF3 as a non-invasive biomarker revealed a low specificity of 42.50%, moderate sensitivity of 67.50 %, positive and negative predictive values of 54% and 56.67% respectively, and an overall accuracy of 55 %.
from this study the following could be concluded:
1. A potential protective role for the upregulated gastric TF3 expression against the development of gastric ulcers in H. pylori infected patients; reflected on its high serum level in gastritis patients compared to those with ulcers.
2. A potential biomarker role for serum TF3 in prediction of gastric ulcer development in H. pylori infected patients, being moderately sensitive rather than specific in the development of H. pylori induced gastric ulcer.