Journal Article

<i>Helicobacter pylori</i> Gastritis, Peptic Ulcer, and Gastric Cancer: Clinical and Molecular Aspects

C. Stewart Goodwin

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 25, issue 5, pages 1017-1019
Published in print November 1997 | ISSN: 1058-4838
Published online November 1997 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/516077
Helicobacter pylori Gastritis, Peptic Ulcer, and Gastric Cancer: Clinical and Molecular Aspects

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Helicobacter pylori causes specific ultrastructural changes to the gastric mucosa. In developing countries a high percentage of infants acquire this infection, which initially causes a transient drop in stomach acid and thus allows transit of lower bowel pathogens, with consequent diarrhea and malnutrition. When infection occurs at an early age, the acid-producing cells of the stomach are involved in the inflammation, and the lifelong reduced acid output means a duodenal ulcer rarely develops. However, lifelong gastric inflammation leads in due course to atrophy, and in the presence of other factors gastric cancer may develop. People infected with H. pylori on average are of shorter stature than uninfected people. Adherence of H. pylori to the gastric mucosa is a prerequisite for infection, and a new binary model of adherence has been shown recently. Chaperonins of H. pylori induce macrophages to secrete cytokines, which leads to an immunologic cascade and inflammation.

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Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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