Background: Sensitization of esophageal chemoreceptors, either directly by intermittent acid exposure or indirectly through esophagitis-associated inflammatory mediators, is likely to be the mechanism underlying the perception of heartburn.
Aims: To compare basal esophageal sensitivity with electrical stimulation and acid, and to compare the degree of acid-induced sensitization in controls and in patient groups across the entire spectrum of gastroesophageal reflux disease: erosive oesophagitis (EO), nonerosive reflux disease (NERD), and functional heartburn (FH).
Methods: Esophageal sensory and pain thresholds to electrical stimulation were measured before, 30, and 60 minutes after an intraesophageal infusion of saline or HCl. Patients received a 30-minute infusion of 0.15 M HCl and controls were randomized to receive either HCl (n=11) or saline (n=10). After electrical sensory threshold testing, participants received another 30-minute infusion of HCl to determine whether sensitivity to acid is increased by prior acid exposure
Results: All patient groups had higher basal sensory thresholds than healthy controls (controls, 13±1.4 mA; FH, 20±5.1 mA; NERD, 21±5.1 mA; EO, 23±5.4 mA; P<0.05). Acute esophageal acid exposure reduced sensory thresholds to electrical stimulation in FH and NERD patients (P<0.05). The level of acid sensitivity during the first HCl infusion was comparable between all patient groups and controls. The secondary infusion caused increased discomfort in all participants (P<0.01). This acid-induced sensitization to HCl was significantly elevated in the patient groups ( P<0.05).
Conclusions: (1) Esophageal acid infusion sensitizes it to subsequent electrical and chemical stimulation. (2) The acid-related sensitization is greater in gastroesophageal reflux disease than in controls and may influence in part symptom perception in this population. (3) Acid-related sensitization within the gastroesophageal reflux disease population is not dependant on mucosal inflammation.
Department of Gastroenterology and Hepatology, St George Hospital and University of NSW, Sydney, NSW, Australia
Supported by NH&MRC Australia, Project Grant ID:222880. The authors declare no conflict of interest.
Reprints: Michal Marcin Szczesniak, PhD, Department of Gastroenterology and Hepatology, St George Hospital, Kogarah, NSW 2217, Australia (e-mail: email@example.com).
Received May 9, 2011
Accepted December 20, 2011