الفهرس 
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Abstract
Chronic gastritis is a histopathologic entity characterized by chronic inflammation of the gastric mucosa. Gastritis can be classified on the basis of the underlying cause (e.g. Helicobacter pylori, bile reflux, non steroidal anti-inflammatory drugs, autoimmunity or allergic responses) or on the basis of histopathological pattern which may reflect the severity of the disease and suggest the cause (e.g. H. pylori-associated multifocal atrophic gastritis). H. pylori gastritis is the most frequent cause of chronic gastritis.
Until the 1980s, research into gastritis was sparse and not particularly attractive. Before discovery of Helicobacter pylori by Warren and Marshall in 1983, gastritis was considered a more or less useful histological finding but not a disease. In 1990, a new system for classification of gastritis was presented at the World Congress of Gastroenterology held in Sydney. This Sydney system was largely based on aetiology, topography and morphology of gastritis.
Helicobacter pylori is a helix shaped Gram-negative, microaerophilic bacterium found in the stomach. It was identified in 1982 by Barry Marshall and Robin Warren, in patients with chronic gastritis and gastric ulcers. It is also linked to the development of duodenal ulcers and stomach cancer.
More than 50% of the world’s population harbor H. pylori in their upper gastrointestinal tract. However, the majority of those individuals are asymptomatic. Infection is more prevalent in developing countries compared to Western societies.
Two related mechanisms by which H. pylori could promote cancer. One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other proposed mechanism has been called a ”perigenetic pathway” and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins, such as adhesion proteins. H. pylori is able to induce inflammation and locally high levels of TNF-α and/or interleukin 6 (IL-6).
P53 is a tumor suppressor protein that in humans is encoded by the TP53 gene. P53 is crucial in organisms, where it regulates the cell cycle and thus, functions as a tumor suppressor molecule that is involved in preventing cancer. As such, P53has been described as ”the guardian of the genome” because of its role in conserving stability by preventing genome mutation.
This study was designed to detect any mutation and/or over expression of P53 in cases of non-neoplastic, non-dysplastic chronic gastritis. We selected 55 cases with non-dysplastic, non-neoplastic chronic gastritis. Then we commented on the five parameters described in Sydney system (gastric atrophy, intestinal metaplasia, chronicity, activity and Helicobacter pylori). We compared each parameter of Sydney system with P53 expression to detect any association. There were positive association between P53 and both Helicobacter pylori-induced chronic gastritis and neutrophilic infiltrate. But not with any other parameters (gastric atrophy, intestinal metaplasia and chronicity).
17 patients out of the 18 ones who were P53 positive were also Helicobacter pylori positive and only one was negative for Helicobacter pylori infection.
Conclusion:
- P53 which is a tumor suppressor gene may be affected in chronic inflammatory conditions as chronic gastritis even before passing into stages of dysplasia or neoplasia.
- Over expression of P53 is greatly enhanced in active rather than inactive chronic gastritis.
Recommendations:
- In order to comment on a gastric biopsy as advised in Sydney, five gastric biopsies taken by the upper GIT endoscopy should be placed in three different containers. Each of the two corporal and two antral biopsies should be put in two separate containers, a third one for incisura angularis biopsy.
- Any case of gastritis must not be considered as negative for Helicobacter pylori unless stained immunohistochemically by anti H. pylori antibodies or geimsa staining.
- In cases of Helicobacter pylori-induced chronic gastritis especially with neutrophilic infiltrate, immunohistochemical detection of P53 should be done before and after successful eradication of the bacteria. Any positive expression should be taken seriously to guard against cancer development.