Protective drugs in the treatment of gastroduodenal ulcer disease.
Reduction of gastric acidity by the inhibition of secretion or neutralization is the therapeutic principle most widely used in peptic ulcer disease. From a pathophysiological standpoint, this does not appear logical, because in a majority of patients gastric acid secretion is not increased. In addition, there is some concern about the consequences of a reduction in gastric acidity, especially in the long term. And finally, all available inhibitors of gastric acid secretion have a systemic action and may thus cause systemic side effects. Carbenoxolone, sucralfate, and tri-potassium dicitrato bismuthate have been shown to accelerate healing of ulcers without appreciable acid inhibition. Despite an apparently different mode of action, the healing rates are similar to those of commonly used acid inhibitors. Several possible mechanisms of action have been claimed for each of these agents, but none has been convincingly demonstrated to be essential in ulcer healing. This may reflect ignorance of the relevant events rather than an action by a combined principle.
D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D002229:Carbenoxolone / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy*; D005744:Gastric Acid / Q000378:metabolism; D006801:Humans; D009942:Organometallic Compounds / Q000627:therapeutic use; D013276:Stomach Ulcer / Q000188:drug therapy*; D013392:Sucralfate / Q000627:therapeutic use
D000897:Anti-Ulcer Agents; D009942:Organometallic Compounds; D013392:Sucralfate; C002791:bismuth tripotassium dicitrate; D002229:Carbenoxolone