Role of gastrin supersensitivity in the pathogenesis of lower esophageal sphincter hypertension in achalasia

Sidney Cohen; William Lipshutz; William Hughes

doi:10.1172/JCI106601

¹Gastrointestinal Section, Department of Medicine of the University of Pennsylvania at the Hospital of the University of Pennsylvania and Veterans Administration Hospital, Philadelphia, Pennsylvania 19104

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Published in Volume 50, Issue 6 on June 1, 1971
J Clin Invest. 1971;50(6):1241–1247. https://doi.org/10.1172/JCI106601.
© 1971 The American Society for Clinical Investigation

Published June 1, 1971 - Version history

Intraluminal manometric studies were carried out in 19 patients with untreated achalasia and in 20 normals. Lower esophageal sphincter (LES) pressure was 50.5 ±4.6 mm Hg in patients with achalasia as compared with 19.4 ±1.3 mm Hg in the normal group. In both groups, the LES pressure was lowered when exogenous 0.1 N HCl was placed into the stomach. Although the nadir of pressure attained with acid suppression was the same, the per cent inhibition was significantly greater in patients with achalasia. Serum gastrin levels were the same in the two groups studied. The patients with achalasia, pre- and postpneumatic dilatation, showed a supersensitivity to exogenous intravenous gastrin I, as compared with normals. These data suggest that high, acid-suppressible levels of LES pressure, in patients with achalasia, are due to supersensitivity to endogenous gastrin.