Abstract
This study aimed to learn the incidence of Helicobacter pylori infection in patients with various gastroduodenal endoscopic lesions and the frequency of virulence H.pylori associated genes CagA and VacA in these patients. One hundred seventy six patients (96 males and 80 females) attending endoscopy units for various dyspeptic symptoms were studied. Antral biopsies were obtained to detect H.pylori by rapid urease test, culturing and histopathologic examination. Twenty five patients with positive H.pylori isolates who were found to be mannose resistant, were tested for cytotoxic associated (CagA) and vacuolating cytotoxin A (VacA) genes. Among studied patients, positive H.pylori detected by rapid urease test, culturing and histopathologic examination (from 50 patients only) were 113 (63%), 127 (71%) and 25 (50%) respectively. Out of 25 patients with positive H.pylori isolates who were found to be mannose resistant, positive genes of either CagA or VacA were detected in 18 (72%) patients with positive isolates, while positivity of both genes were detected in 13(52%) patients with positive isolates. Five (45.4%) and 5 (45.4%) out of patients with duodenal ulcers and gastritis respectively were positive for both (CagA) and (VacA) genes. In conclusion, the highest detection rate of H.pylori infection was by bacterial culture. A correlation between CagA and VacA genes and endoscopic lesions of duodenal ulcers and gastritis was found.
Highlights
H.pylori is a human specific pathogen lives deep beneath the mucus layer closely attached to the gastric epithelium[1]
The highest detection of H. pylori isolates was recorded in the age group more than 60 years 22/35 (62.8%), while the lowest detection rate was recorded in the age group below 20 years 2/7 (28.5%), the differences were statistically not significant (p>0.05)
The highest detection rates of bacteria were recorded in the age group more than 60 year (62.8%), while the lowest detection rates were recorded in the age group below 20 year( 28.5%)This result was nearly similar to other study[30]
Summary
H.pylori is a human specific pathogen lives deep beneath the mucus layer closely attached to the gastric epithelium[1]. Host dependent noxious substances lead to progressive damage to the gastric mucosa, deregulation of acid production, induction of gastric metaplasia and development of chronic gastritis. These H. pylori virulence factors and host noxious substances include cytotoxin associated gene A (CagA), vacuolating cytotoxin A (VacA), ammonia, lipopolysaccharide (endotoxin), platelet activating factors, nitric oxide and interleukin–8 8,9. Infection with vacuolating cytotoxin positive strains is reported to be associated with peptic ulcer disease. Infection with H. pylori strain expressing cytotoxin associated Cag A protein is more virulent and is associated with increased risk of development gastric cancer[16]. Cag A positive H. pylori strains have been shown to be associated with interleukin–8 (IL.8) induction in gastric epithelium, neutrophilic infiltration and be related to gastric inflammation and gastroduoderal diseases[18,19]
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