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Human gastric carcinomas were examined for<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell differentiation because tumours found in rodents after dosing with inhibitors of acid secretion were reclassified to be of<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell origin. The gastrin receptor is localized to the<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell only, where gastrin stimulates the function and growth. Drug\u2010induced hypo\u2010acidity induces hypergastrinaemia and<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell hyperplasia responsible for rebound acid hypersecretion. Every condition with long\u2010term hypergastrinaemia disposes to<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell neoplasia. In man, both atrophic gastritis and gastrinoma lead to<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell carcinoids. Proton pump inhibitors induce hypergastrinaemia with<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell hyperplasia and<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell carcinoids that disappear when stopping treatment. The gastrin antagonist netazepide induces regression of<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell carcinoids due to atrophic gastritis. Human gastric carcinomas of diffuse type, particularly the signet\u2010ring subtype, show<jats:styled-content style=\"fixed-case\">ECL<\/jats:styled-content>cell differentiation, suggesting involvement of gastrin in the carcinogenesis.<jats:italic>Helicobacter pylori<\/jats:italic>(Hp) causes gastritis and peptic ulcer, and when infecting the antrum only gives a slight hypergastrinaemia with acid hypersecretion predisposing to duodenal ulcer, but protecting from gastric cancer. When Hp infection spreads to oxyntic mucosa, it induces atrophy, reduced acid secretion and marked hypergastrinaemia and cancer.It is remarkable that the interaction between Hp and gastrin may explain the pathogenesis of most diseases in the upper gastrointestinal tract.<\/jats:p>","DOI":"10.1111\/apha.12208","type":"journal-article","created":{"date-parts":[[2013,11,26]],"date-time":"2013-11-26T16:05:07Z","timestamp":1385481907000},"page":"239-256","source":"Crossref","is-referenced-by-count":66,"title":["The regulation of gastric acid secretion \u2013 clinical perspectives"],"prefix":"10.1111","volume":"210","author":[{"given":"H. 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