Abstract

The prevention and therapy of gastric and duodenal ulcers, until recently, have been virtually restricted to neutralization of intraluminal acid or reduction of HC1 secretion. The introduction of the concept of gastric cytoprotection in the late 1970s and 1980s promised a new approach, but the results were mainly disappointing since gastro protection only referred to the prevention of acute hemorrhagic gastric erosions and had nothing to do with the treatment of chronic gastric and duodenal ulcers. Nevertheless, the existing alternatives to the acid-oriented approach were reviewed in the late 1980s [1] and were exemplified by the efficacy of locally acting antiulcer drugs such as sucralfate and colloidal bismuth, which brought about rapid duodenal ulcer healing without suppression of gastric acidity [2–4]. Recent studies have also suggested that the ulcer relapse rate was lower after treatment with sucralfate than following the healing achieved with antisecretory drugs [5].

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