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The patho physiology of gastric and duodenal ulcer from the viewpoint of gastric acid secretion and gastric emptying


The patho physiology of gastric and duodenal ulcer from the viewpoint of gastric acid secretion and gastric emptying



Stomach and Intestine 17(7): 757-764



ISSN/ISBN: 0536-2180

Previous reports have suggested certain differences between a gastric ulcer and a duodenal ulcer in the etiology and the pathophysiology of the ulcer. Therefore, the pathophysiology of ulcers was investigated from the standpoint of gastric acid secretion and gastric emptying using the acetaminophen method. Gastric acid secretion in gastric ulcer patients varied from normosecretion to hyposecretion on BOA (basal acid output) and MAO (maximal acid output) stimulated by tetragastrin. The progressive atrophic change of the gastric mucosa seen in aging seems to reduce the gastric acid secretion. The gastric emptying in gastric ulcer was delayed more than normal controls and duodenal ulcers, and was unrelated to the difference in gastric acid secretion. However, ulcers located on the M portion, including the angle, had a much more delayed gastric emptying than other locations. In duodenal ulcer patients with gastric hypersecretion (BAO and MAO), atrophy of the gastric mucosa and a reduction of gastric acid secretion were noted and found. Gastric emptying was more rapid than normal controls and gastric ulcers. Gastric emptying in duodenal ulcer with acid hypersecretion (MAO > 20 meq/h) was much more rapid than in normal normosecretory patients (MAO .ltoreq. 20). Patients with recurrent gastric ulcers had a more delayed gastric emptying, and, in those with recurrent duodenal ulcers, a more rapid gastric emptying than those without proven recurrence. The pathophysiology of gastric ulcers may be considered important in the damage of mucosal resistance which follows various gastritis and gastric atrophy due to delayed gastric emptying, in spite of hyposecretion. On the other hand, the pathophysiology of duodenal ulcers may involve both the hypersecretion in gastric acid output and rapid gastric emptying in addition to increased vagal stimulation, a disturbance in the negative feedback (duodenal brake) may be one of the important factors.

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Accession: 006731554

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