Heterogeneous origin of hyperacidity in duodenal ulcer.
Recent advances in the medical therapy of duodenal ulcer support the long held concept that acid hypersecretion is an important pathophysiological abnormality in the majority of patients with duodenal ulcer. The origin of acid hypersecretion is heterogeneous (Table 1). Certain specific physiologic abnormalities that lead to acid hypersecretion may have a genetic basis. The various physiologic abnormalities, alone or in combination, may lead to two final common pathways: abnormally large meal-stimulated and nocturnal acid secretion. Indeed, the success of medical therapy aimed at the control of postprandial acid secretion alone or that of nocturnal acid secretion alone strongly support the significance of these two final acid hypersecretory pathways.
D002940:Circadian Rhythm; D004381:Duodenal Ulcer / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D004435:Eating; D004759:Enterochromaffin Cells / Q000473:pathology; D005006:Ethnicity; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000494:pharmacology; D005769:Gastrointestinal Motility; D006801:Humans; D006984:Hypertrophy; D010295:Parietal Cells, Gastric / Q000378:metabolism / Q000473:pathology; D011706:Pyloric Antrum / Q000473:pathology; D012636:Secretory Rate / Q000187:drug effects; D014630:Vagus Nerve / Q000503:physiopathology; D015043:Zollinger-Ellison Syndrome / Q000235:genetics / Q000503:physiopathology
D005755:Gastrins