Esophageal Infusion of Menthol Does Not Affect Esophageal Motility in Patients with Gastroesophageal Reflux Disease.

Menthol is thought to trigger gastroesophageal reflux disease (GERD) symptoms by influencing esophageal peristalsis and lower esophageal sphincter (LES) function. We evaluated the effect of esophageal menthol infusion on esophageal motility and the LES in healthy volunteers and in patients with GERD. High resolution manometry (HRM) catheter with attached thin tube for menthol infusion was placed transnasally. Protocol which included baseline recording, 16 water swallows (5 ml, 10 ml, and 15 ml) and the multiple rapid swallows was performed before and after esophageal infusion of menthol (3 mM, 20 min, 8 ml/min). We evaluated the effect of this infusion on the HRM parameters of esophageal peristalsis (distal contractile integral, distal latency, contractile front velocity) and the lower esophageal sphincter (LES) barrier function (integrated relaxation pressure and the inspiratory augmentation of the LES). Simultaneously we evaluated the quality and intensity of the symptoms during the menthol infusion. Esophageal infusion of menthol did not appreciably affect HRM measurements characterizing esophageal peristalsis and LES pressure in healthy subjects (N = 13) or GERD patients (N = 11). The magnitude of the distal contractile integral (5 ml) was changed neither in the healthy volunteers' group, (735 ± 127 vs. 814 ± 117 mmHg, p = 0.5), nor in the GERD patients (295 ± 78 vs. 338 ± 96 mmHg, p = 0.99). In healthy volunteers menthol did not change the inspiratory augmentation of the LES (8.67 ± 1.09 vs. 7.69 ± 0.96 mmHg, p = 0.15) and neither did for GERD patients (8.8 ± 1.18 vs. 8.22 ± 0.91 mmHg, p = 0.43). We observed no significant difference in any HRM parameter following menthol infusion, except for distal latency in 10 ml swallows. By contrast, menthol infusion induced significantly more intense discomfort in GERD patient than in healthy volunteers. Our results suggest no significant temporal effect of menthol on the esophageal motility or LES function, neither in healthy volunteers, nor in GERD. Arguably, other mechanisms are responsible for menthol-related heartburn.