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)