title: Geographic factors probably modulating alternative pathways in Helicobacter pylori-associated gastroduodenal pathology: a hypothesis.
abstract: It is hypothesized that probable geographic factors of nutritional type, nonrelated to development or socioeconomic level, may modulate the conversion of Helicobacter pylori-associated active chronic gastritis from its early stages to chronic atrophic gastritis (CAG). The factors could be diets low in antioxidant vitamins and other micronutrients such as selenium. In regions of the world where these modulating factors are not present, active chronic gastritis tends to stay in its early stages and to predispose individuals to duodenal ulcer. On the contrary, in regions where the modulating factors are present, the frequency of CAG increases markedly. When CAG becomes severe and extensive, hypochlorhydria ensues. Hypochlorhydria decreases the predisposition to duodenal ulcer, while CAG, a precancerous lesion, predisposes individuals to gastric cancer of the intestinal type. The hypothesis could be tested in a multicenter, multiregional study to (1) determine endoscopically and histologically the prevalence rates of duodenal ulcer, gastric ulcer, gastric cancer, and H. pylori-associated CAG in large series of dyspeptic patients and (2) correlate these prevalence rates with blood levels of micronutrients in these patients.
authors.affiliation: Gastrointestinal Physiology Working Group of the Cayetano Heredia Peruvian University, Lima.
authors.forename: R
authors.initials: R
authors.lastname: León-Barúa
authors.forename: R
authors.initials: R
authors.lastname: Berendson-Seminario
authors.forename: S
authors.initials: S
authors.lastname: Recavarren-Arce
authors.forename: R H
authors.initials: RH
authors.lastname: Gilman
mesh_terms: D018450:Disease Progression; D005757:Gastritis, Atrophic / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016481:Helicobacter Infections / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008954:Models, Biological; D010437:Peptic Ulcer / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology