Defective triggering of secondary peristalsis in patients with non-erosive reflux disease

Abstract

The definitive version is available at www.blackwell-synergy.com Copyright © 2006 The Authors, Journal compilation © 2007 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty LtdBackground and Aim: The pathophysiology of non-erosive reflux disease is poorly understood. Triggering of secondary peristalsis is impaired in patients with erosive esophagitis but data in patients with non-erosive reflux disease are lacking. The aim of this study was to evaluate the difference in esophageal motility between patients with non-erosive reflux disease and healthy subjects. Methods: Twenty patients with non-erosive reflux disease, with reflux symptoms occurring more than twice per week, and 20 healthy subjects of comparable age and sex underwent esophageal manometry. Primary peristalsis was tested with 10 swallows of a 5-mL water bolus. Secondary peristalsis was triggered by esophageal distention using a 20-mL air bolus, which was injected rapidly into the mid-esophagus. After 20 s, each stimulus was followed by a dry swallow to clear any residual air and then each stimulus was repeated five times. Results: Basal lower esophageal sphincter pressure, pressure wave amplitude in the upper, middle and lower esophagus, wave velocity and the rates of successful primary peristalsis were similar in non-erosive reflux disease patients and controls. The rate of triggering of secondary peristalsis in patients with non-erosive reflux disease (median 20%, interquartile range 0–40%) was significantly lower (P < 0.0001) than that in healthy subjects (90%, 70–100%). When secondary peristalsis occurred in patients with non-erosive reflux disease, however, there were no differences in the amplitude and velocity of secondary peristalsis between the groups. Conclusions: Triggering of secondary peristalsis is defective in non-erosive reflux disease. This could lead to prolongation of the contact time between refluxed gastric acid and esophageal mucosa thereby leading to symptoms.Katsuhiko Iwakiri, Yoshinori Hayashi, Makoto Kotoyori, Yuriko Tanaka, Noriyuki Kawami, Hirohito Sano, Kaiyo Takubo, Choitsu Sakamoto and Richard H Hollowa