• O Nyrén.
• Dept. of Surgery, University Hospital, Uppsala, Sweden.
• Scand. J. Gastroenterol. Suppl. 1991 Jan 1; 182: 25-8.

AbstractDuring the past 30 years much interest has been focused on gastric acid as a possible causative factor in functional dyspepsia. The similarities to duodenal ulcer with regard to the symptoms, previous reports of a high risk of subsequent ulcer development, and a growing number of clinical therapeutic trials showing a significant advantage for acid-reducing drugs over placebo--although challenged by many investigators--have all contributed to a common notion that the gastric acid may play an equally important pathogenic role in functional dyspepsia as in peptic ulcer disease. However, recent studies in patients with well-defined functional dyspepsia indicate quite clearly that hypersecretion of hydrochloric acid is a rare finding. Available data also contradict the hypothesis that patients with functional dyspepsia are abnormally sensitive to their gastric acid. Those dyspeptic individuals who benefit from antacids purchased over the counter usually do not have functional dyspepsia but rather organic diseases such as esophagitis or peptic ulcer. The association or pathophysiologic parallelism between functional dyspepsia and peptic ulcer implied by the results of some studies of functional dyspepsia in the past might be explained by unintended inclusion of overlooked or subclinical cases of peptic ulcer disease in those studies.

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