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| Year : 1998 | Volume
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| Issue : 3 | Page : 137 |
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| The pathogenic role of helicobacter pylori in peptic ulcer disease and non-ulcer dyspepsia |
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Richard V Heatley1, Keith Bodger2
1 Consultant Physician & Gastroenterologist, St. James's University Hospital, Leeds, United Kingdom
2 Clinical research fellow, St. James's University Hospital, Leeds, United Kingdom
Click here for correspondence address and email
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How to cite this article:
Heatley RV, Bodger K. The pathogenic role of helicobacter pylori in peptic ulcer disease and non-ulcer dyspepsia. Saudi J Gastroenterol 1998;4:137 |
< Helicobacter pylori  present in the stomach in nearly all those with duodenal ulcer, the majority of those with gastric ulceration and in more with nonulcer dyspepsia than age-matched controls. This organism undoubtedly plays a major role in the pathogenesis of peptic ulcer disease since eradication dramatically reduces the risks of ulcer recurrence. Its role in non-ulcer dyspepsia is, however, less clear since eradication definitely reduces the degree of associated gastritis but has yet to be shown to have major effects on symptoms.
H. pylori infection of the stomach and duodenum stimulates inflammatory change particularly in active disease with polymorph infiltration. This is in part perpetuated by release of cytokines and other soluble mediators. Gastric inflammation appears a necessary precursor for peptic ulceration, gastric ulcers developing possibly as a result of the interaction of ingested NSAIDs, the reflux of bile salts or smoking on the ensuing atrophic gastric mucosa. A necessary precursor for duodenal ulcer disease is the development of gastric metaplasia within the duodenum, a known acid-related phenomenon. In this situation, duodenal colonization and subsequent inflammation can occur if an individual develops an H. pylori positive gastritis[1]
H. pylori infection of the stomach appears to stimulate both cellular and humoral defenses, yet expulsion of the organism does not occur in all individuals. It is apparent some strains of H. pylori are particularly pathogenic, cagA positive for instance being particularly associated with duodenal ulceration. Apart from the release of proinflammatory cytokines, recent evidence has revealed that the counter inflammatory IL-10 is also present in increased amounts in the gastric mucosa of H. pylori infection individuals[2]. It is possible that this helps to explain why persistent H. pylori infection occurs in up to one half of the world's population.
 References | |  |
| 1. | Wyatt JI, Rathbone BJ, Dixon MF, et al. Campylobacter pyloridis and acid-induced gastric metaplasia in the pathogenesis of duodenitis. J Clin Path 1987;40:841-8.  [PUBMED] [FULLTEXT] |
| 2. | Bodger K, Wyatt JI, Heatley RV. Gastric mucosal secretion of interleukin-10: relations to histopathology, Helicobacter pylori status, and tumor necrosis factor-,α secretion. Gut 1997;40:739-44. [PUBMED] [FULLTEXT] |
Correspondence Address:
Richard V Heatley
Consultant Physician & Gastroenterologist, St. James's University Hospital, Leeds
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 19864761 
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