الفهرس 
Aim of the workOnly 14 pages are availabe for public view
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Abstract
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Summary
Helicobacter pylori (H. pylori) is a gram-negative, micro-aerophilic, curved rod that causes a transmissible bacterial infection of the gastric mucosal surface and affect about one half of the world’s population. It induces chronic gastritis in all infected individuals, but only induces clinical diseases in 10-20% of them.
This may be related to differences in genetic susceptibility of the host, environmental factors, and genetic diversity of H. pylori. The well-established H. pylori associated diseases include peptic ulcer disease, non-ulcer dyspepsia, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT)-type lymphoma.
This study was conducted to identify the frequency of the genetic virulence factors (cagA, vacA and babA2) of H. pylori and their possible association with gastroduodenal diseases. It was conducted on 70 adult patients with upper gastrointestinal complaints. Patients who received anti-microbial therapy, H2 receptor blockers, proton pump inhibitors, non-steroidal anti-inflammatory drugs or corticosteroids in the last month were excluded.
All patients were subjected to full history taking, clinical examination, gastroduodenoscopy. Four antral biopsies were taken for genotyping by PCR, histopathological examination and culture.
Results revealed that all the patients (100%) had chronic active H. pylori gastritis by histopathological examination. The most frequent H. pylori genotype was cagA (67.8%) followed by vacA s1a (61%) and
Summary
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vacA m2 (61%), while the least frequent was babA2 (18.6%). CagA was associated with vacA s1a in (83.3%) with statistical significance.
Most patients with cagA positive isolates (77.8%) had no heart burn with statistical significance which may support the protective role of cagA against GERD. There was no significant difference between genotypes distribution as regards culture positive and culture negative H. pylori strains.
CagA, vacA s1a and vacA m2 had the highest prevalence in patients with PUD, gastritis and duodenitis while babA2 had the least prevalence. Although in patients with PUD and NUD the prevalence of cagA was (65.1%, 75%) and vacA s1 was (62.8%, 56.3%) respectively, the association between these H. pylori genotypes and PUD did not reach a level of statistical significance.
None of H. pylori genetic virulence factors individually can accurately predict clinical outcome and one has to recognize the importance of the bacteria-host interaction in the final outcome. It is possible that other some genes of the cag pathogenicity island (PAI) are responsible for pathogenicity and disease outcome.