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Research Article Free access | 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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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
Find articles by Lipshutz, W. in: JCI | PubMed | Google Scholar
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
Find articles by Hughes, W. in: JCI | PubMed | Google Scholar
Published June 1, 1971 - More info
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.