title: Peptic ulcer diseases. Perspectives on pathophysiology and therapy.
abstract: Increased acid secretion characterizes only about one-third of ulcer patients. However acid/peptic activity is a critical factor in all peptic ulcers. When adequate inhibition of acid secretion is achieved even the most refractory ulcer heal, although rapid recurrence upon cessation of therapy belies the non-curative nature of the therapy. Despite the critical necessity for acid and the association with increased acid secretion in some patients, ulcers reflect a focal disturbance in mucosal defense. Once a discrete ulcer has formed, the disruption of mucosal architecture by the ulcer and the presence of an intense surrounding inflammatory response will impair locally the ability of the mucosa to defend itself against injury. Several of the mechanisms hypothesized to be involved in mucosal defense are responsive to prostaglandins (e.g., mucus and bicarbonate secretion, and blood flow). However, these mechanisms may not be critical variables to the healing of ordinary peptic ulcers because synthetic prostaglandins which stimulate these defensive mechanisms, heal ordinary peptic ulcers with an effectiveness predicted from their antisecretory potential. Although one could therefore hypothesize that prostaglandin modulation of mucosal defense is not a relevant concept in humans, it is possible that prostaglandins fail to enhance the healing of peptic ulcers because the targets for their effects on mucosal defense (e.g., epithelial cells and normal mucosal vasculature) are disrupted in the vicinity of the ulcer. Mucosal defense may be impaired by the inhibition of prostaglandin production via nonsteroidal anti-inflammatory drugs or may be secondary to the gastroduodenitis found with Campylobacter pylori infection, although causal relationships in the latter instance remain controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Center for Ulcer Research and Education, VA Wadsworth Hospital Center, Los Angeles, CA 90073.
authors: A H
authors: AH
authors: Soll
mesh_terms: D000818:Animals; D004381:Duodenal Ulcer / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000503:physiopathology; D006801:Humans; D010437:Peptic Ulcer / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy