Pathological acid secretion not due to gastrinoma.
There are few detailed studies of patients with pathological hypergastrinaemia of antral origin. We have identified four patients with severe acid hypersecretion associated with peptic ulcer disease and in whom no evidence for gastrinoma or isolated retained antrum could be found. Three of these patients also had hypergastrinaemia. In two patients, one with gastric ulcers and one with duodenal ulcer disease, the hypergastrinaemia appeared to be due to antral gastrin cell hyperfunction and there was also evidence for mild antral gastrin cell hyperplasia. In the other hypergastrinaemic patient, a primary intestinal gastrin cell hyperfunction syndrome was suspected, but a hidden gastrinoma could not be excluded. The remaining patient had nearly fatal hypersecretory ulcer disease and cimetidine failed to control the hypersecretory state. In this patient the hypersecretion responded to a more potent H2 antagonist with resolution of a metabolic encephalopathy. No general pathophysiological mechanism could be identified in these patients or in larger groups of patients with gastric or duodenal ulcer disease.
D000328:Adult; D000368:Aged; D004381:Duodenal Ulcer / Q000503:physiopathology; D004386:Duodenum / Q000503:physiopathology; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000097:blood; D006801:Humans; D008297:Male; D010437:Peptic Ulcer / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D011706:Pyloric Antrum / Q000503:physiopathology; D013276:Stomach Ulcer / Q000503:physiopathology; D015043:Zollinger-Ellison Syndrome / Q000503:physiopathology*
D005755:Gastrins