Helicobacter pylori and ulcerogenesis.
The dictum "no acid-no ulcer" had, in the past, summarized the thinking concerning the pathogenesis of peptic ulcer disease. It is now recognized that infection with Helicobacter pylori is the major causal factor leading to both duodenal and gastric ulceration. Infection is associated with many of the acid secretory abnormalities that have traditionally characterized peptic ulcer disease; indeed, acid secretory physiology returns to normal following bacterial eradication. Since not all individuals infected with H. pylori develop ulcers, host susceptibility, bacterial virulence, and/or specific environmental factors must determine the response to infection and the ultimate clinical outcome. The relative importance of these factors and their complex interactions remain to be determined. H. pylori infection produces tissue damage indirectly because the organism does not directly invade gastroduodenal tissue. A variety of bacterial enzymes, toxins, and inflammatory mediators produced in response to bacterial colonization challenge the integrity of host mucosal defenses. In a susceptible host, breached defenses render epithelium more vulnerable to acid injury and ulcer development. Eradication of H. pylori leads to rapid ulcer healing and reversal of tissue injury, thereby obviating ulcer recurrence.
Peura
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Department of Medicine, Division of Gastroenterology, University of Virgina Health Sciences Center, Charlottesville 22908, USA.
D004381:Duodenal Ulcer / Q000382:microbiology / Q000503:physiopathology; D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000097:blood; D005756:Gastritis / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D010437:Peptic Ulcer / Q000235:genetics / Q000382:microbiology* / Q000503:physiopathology*; D013276:Stomach Ulcer / Q000382:microbiology / Q000503:physiopathology
D005755:Gastrins