Consequences of gastric acid inhibition in man

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Abstract

For more than 100 years it has been known that gastric acid secretion is not the only but an essential causative factor in the pathogenesis of acid-related diseases. Thus reduction of acid secretion became a major therapeutic goal. For most of this century, effective acid reduction could be achieved only by surgery (gastric resection and vagotomy). The introduction of potent inhibitors of acid secretion, that is the H2-receptor blocking agent cimetidine and its analogues in the late seventies and the even more potent proton pump inhibitor (PPI) omeprazole and its analogues in the late eighties have revolutionized therapy. Surgery became superfluous for benign oesophagogastric diseases, except in case of perforation or haemorrhage. However, soon after the introduction of the H2-receptor blockers concern was expressed about the risk of hypochlorhydria or achlorhydria. This concern originates in the conviction that gastric acid is needed for normal life and that achlorhydria will cause serious problems. But do we really know how much gastric acid we need?