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Role of gastrin supersensitivity in the pathogenesis of lower esophageal sphincter hypertension in achalasia
Sidney Cohen, … , William Lipshutz, William Hughes
Sidney Cohen, … , William Lipshutz, William Hughes
Published June 1, 1971
Citation Information: J Clin Invest. 1971;50(6):1241-1247. https://doi.org/10.1172/JCI106601.
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Research Article

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

Abstract

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.

Authors

Sidney Cohen, William Lipshutz, William Hughes

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