Pathogenesis of Lower-Esophageal-Sphincter Incompetence

Abstract

Since patients with symptomatic gastroesophageal reflux have diminished lower-esophagealsphincter pressure, we studied the pathogenesis of this diminished sphincteric pressure. In 23 patients with symptomatic reflux as compared to 20 controls, the lower-esophageal-sphincter response to direct muscle stimulation by a parasympathomimetic drug (beth-anechol chloride) and to the effect of a cholinesterase inhibitor (edrophonium chloride) was identical. Complete dose-response curves of lower-esophagealsphincter pressure to exogenous intravenous pentagastrin were also similar in both groups. The response to endogenous gastrin release was diminished in reflux patients. Pressure (mean ± S.E.) increased in response to gastric deacidification in reflux subjects by 1.5 ± 0.5 mm Hg (70.5 ± 3.6 per cent) and by 10.5 ± 1.5 mm Hg (197.5 ± 11.6 per cent) in the controls (p<0.001). The response to the gastric infusion of glycine was 2.3 ± 0.5 mm Hg (35.7 ± 5.0 per cent) in reflux subjects as compared to 19.4 ± 3.4 mm Hg (118.4 ± 4.8 per cent) in control subjects (p<0.001 ). We suggest that a diminished release of endogenous gastrin may be responsible for sphincteric hypotension in patients with gastroesophageal reflux. (N Engl J Med 289:182–184, 1973)