The role of Helicobacter pylori in pathogenesis: the spectrum of clinical outcomes.
Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. Most patients continue through life with a chronic superficial gastritis while some develop either duodenal or gastric ulcer. In a very small proportion the lymphoid reaction to H. pylori infection appears to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma, while in others the evidence suggests that chronic superficial gastritis progresses to atrophy, the loss of gastric acid secretory capacity and the development of gastric cancer. The mechanisms involving H. pylori infection in peptic ulceration are increasingly well understood and H. pylori is now accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 95%. More important is the dramatic reduction in duodenal ulcer recurrence after successful eradication of the organism to about 4% in a year compared to recurrences of up to 80% in those who ulcers have been healed but in whom the infection persists. There is also increasing evidence for the involvement of H. pylori in gastric ulcer, where infection is seen in between 60 and 80%, and there is a similar dramatic reduction in recurrence following cure of H. pylori infection. The progression of H. pylori gastritis from the acute infection to chronic superficial gastritis, predominantly antral gastritis or a pangastritis with increasing atrophy appears to be associated with the differing outcomes seen in this disease. Moreover, there is increasing data on the roles played by bacterial heterogeneity and the virulence of the organism, host factors such as the HLA genotype and immune response, environmental factors and the age of acquisition of infection play in determining these clinical outcomes of the disease.
Hunt
R H
RH
Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, Canada.
D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000378:metabolism; D005756:Gastritis / Q000382:microbiology; D005767:Gastrointestinal Diseases / Q000378:metabolism / Q000382:microbiology*; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000382:microbiology; D013004:Somatostatin / Q000378:metabolism; D013274:Stomach Neoplasms / Q000382:microbiology
D005755:Gastrins; D013004:Somatostatin