Abstract
Duodenal ulceration is presumed to be induced and maintained by imbalance between aggressive and defensive factors. Development of drugs for correction of this imbalance has recently concentrated on maximum inhibition of acid secretion e.g. via H2-receptor antagonists but has led to re-evaluation of antacids and antimuscarinics. It has been shown that about the same percentage of ulcers can be healed using low antacid doses or antimuscarinics (e.g. pirenzepine) or doses of H2-receptor antagonists which do not inhibit acid secretion maximally as can be healed using higher doses of H2-receptor antagonists. Avoidance of the intragastric bacterial overgrowth and its consequences and the disturbance of the acid-gastrin feedback mechanism which may follow maximum gastric acid suppression could provide a rationale for use of anti-ulcer therapy based on moderate reduction of gastric acid secretion.
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