Could chronic peptic ulcers be localised areas of acid susceptibility generated by autoimmunity?
It is argued that all chronic gastroduodenal peptic ulcers result from localised increase in mucosal susceptibility to acid attack at the interface between a segment of gastroduodenitis and gastric fundus or duodenal mucosa. The site is predetermined by the background mucosal pattern. Changes can occur in the differentiated gastroduodenal mucosa that closely resemble cell population transformations described in embryology and regeneration biology. A second pathological process, gastroduodenitis, may develop that does not of itself predispose to ulceration, but the combination of factors can produce a zone of increased acid susceptibility. These complex changes could be generated by immunologically activated gastroduodenitis. Destructive or stimulatory immune reactions, analogous to those seen in the thyroid gland, could affect the gastrin-secreting G cells and other paracrine cells. The resulting tropic and inflammatory reactions would provide the background for peptic ulceration.
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D001323:Autoantibodies / Q000276:immunology*; D002908:Chronic Disease; D004382:Duodenitis / Q000276:immunology / Q000473:pathology; D004386:Duodenum / Q000473:pathology; D005748:Gastric Fundus / Q000378:metabolism; D005750:Gastric Juice / Q000378:metabolism; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000502:physiology*; D005756:Gastritis / Q000276:immunology / Q000473:pathology; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D010295:Parietal Cells, Gastric / Q000276:immunology; D010437:Peptic Ulcer / Q000276:immunology* / Q000473:pathology; D015043:Zollinger-Ellison Syndrome / Q000276:immunology
D001323:Autoantibodies; D005755:Gastrins