BACKGROUND: Atrophic gastritis is defined as a loss of the glandular structures and a collapse of the reticulin skeleton of the stomach mucosa. It is often accompanied by intestinal metaplasia. Both conditions result from long-term persistent chronic active gastritis and significantly increase the risk for gastric cancer. METHODS: Review of the role of Helicobacter pylori in the pathogenesis of atrophic gastritis. Specific attention is given to the classifications and histologic features of atrophic gastritis, the frequency with which atrophic gastritis occurs in H. pylori-infected subjects, the factors that influence the process of development of atrophic gastritis in the presence of infection, and the various mechanisms by which this bacterial infection may induce atrophic gastritis. In addition, the possible role of H. pylori in the etiology of auto-immune atrophic gastritis and pernicious anemia is discussed. CONCLUSIONS: H. pylori infection eventually causes atrophic gastritis in a considerable number of infected subjects. In different populations, the prevalence of atrophic gastritis increases by 1 to 3% per annum. Factors that may increase the risk for atrophy are infection at an early age, cytotoxin production by the infecting strain, and lowering of acid output. The association between H. pylori infection and the development of atrophic gastritis significantly supports the role of this infection in gastric carcinogenesis.
BACKGROUND:Atrophic gastritis is defined as a loss of the glandular structures and a collapse of the reticulin skeleton of the stomach mucosa. It is often accompanied by intestinal metaplasia. Both conditions result from long-term persistent chronic active gastritis and significantly increase the risk for gastric cancer. METHODS: Review of the role of Helicobacter pylori in the pathogenesis of atrophic gastritis. Specific attention is given to the classifications and histologic features of atrophic gastritis, the frequency with which atrophic gastritis occurs in H. pylori-infected subjects, the factors that influence the process of development of atrophic gastritis in the presence of infection, and the various mechanisms by which this bacterial infection may induce atrophic gastritis. In addition, the possible role of H. pylori in the etiology of auto-immune atrophic gastritis and pernicious anemia is discussed. CONCLUSIONS:H. pyloriinfection eventually causes atrophic gastritis in a considerable number of infected subjects. In different populations, the prevalence of atrophic gastritis increases by 1 to 3% per annum. Factors that may increase the risk for atrophy are infection at an early age, cytotoxin production by the infecting strain, and lowering of acid output. The association between H. pyloriinfection and the development of atrophic gastritis significantly supports the role of this infection in gastric carcinogenesis.
Authors: P Malfertheiner; F Megraud; C O'Morain; F Bazzoli; E El-Omar; D Graham; R Hunt; T Rokkas; N Vakil; E J Kuipers Journal: Gut Date: 2006-12-14 Impact factor: 23.059
Authors: Y Maor-Kendler; G Gabay; J Bernheim; T Naftali; I Lesin; G Leichtman; I Pomeranz; B Novis Journal: Dig Dis Sci Date: 1999-04 Impact factor: 3.199
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Authors: Hashem B El-Serag; John Y Kao; Fasiha Kanwal; Mark Gilger; Frank LoVecchio; Steven F Moss; Sheila E Crowe; Adam Elfant; Thomas Haas; Ronald J Hapke; David Y Graham Journal: Clin Gastroenterol Hepatol Date: 2018-03-17 Impact factor: 11.382