Aetiology of peptic ulcer.
Peptic ulcer should no longer be regarded as a single disease entity but as a group of heterogeneous conditions, as evident epidemiologically, genetically, clinically and pathophysiologically. In duodenal ulceration, "hyperacidity" must be the major culprit since specific therapeutic reduction of gastric acidity results in ulcer healing in about 70% of patients. However when the physiologic abnormalities leading to hyperacidity are analysed, it is obvious that each abnormality occurs usually in about a third of the patients only. Each of these abnormalities, however, can theoretically lead to an abnormal postprandial acid output or abnormal nocturnal acid output, and may explain why the majority of patients appear to have "hyperacidity". Indeed, controlling the meal-stimulated acid secretion alone and controlling the nocturnal acid secretion alone have been shown to heal duodenal ulcer. Corpus gastric ulcers, prepyloric ulcers, and gastric ulcers associated with duodenal ulcers appear physiologically distinct, and often behave differently on clinical grounds. This may explain why therapeutic reduction of acid secretion is less successful in healing gastric ulcer than duodenal ulcer.
D000328:Adult; D001655:Bile Reflux / Q000503:physiopathology; D004381:Duodenal Ulcer / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005746:Gastric Emptying; D005796:Genes; D006723:Hong Kong; D006801:Humans; D008297:Male; D008875:Middle Aged; D010439:Peptic Ulcer Perforation / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D013276:Stomach Ulcer / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D006113:United Kingdom; D014481:United States