Introduction
Laryngopharyngeal reflux (LPR) is defined as extra-esophageal reflux of gastroduodenal content to the laryngopharynx, affecting the upper aerodigestive tract.1 LPR is similar to gastroesophageal reflux disease (GERD), in which gastric acid rises up the esophagus. Because of their similarities, gastroenterologists manage LPR patients as a subtype of GERD.2 However, otolaryngologists consider LPR as a new disease entity because many patients with LPR-related symptoms have no GERD-associated symptoms.3 Moreover, non-acid reflux or even gas reflux can be a disease etiology of LPR, owing to its multifactorial nature.4
The gastroesophageal junction consists of a lower esophageal sphincter (LES), diaphragm, and phrenoesophageal ligament.5 The primary LES function is to allow food transit during swallowing and prevents the reflux of gastroduodenal contents back into the esophagus. Transient lower esophageal sphincter relaxation (TLESR) is defined as spontaneous LES relaxation without swallowing. The TLESR exists physiologically to prevent the swallowing of air. However, TLESR also allows gastroesophageal reflux to occur.6 TLESR can be triggered by gastric distension after meals.7 Since TLESR mainly occurs after meals, it has been considered as a major cause of post-prandial GERD-related symptoms.8 A meta‐analysis reported that baclofen, which inhibits TLESR, decreases the number of reflux episodes in GERD patients.9
‘Laryngopharyngeal Reflux Study Group of Young Otolaryngologists of the International Federation of Otorhinolaryngological Societies’ indicated that 24‐hour multichannel intraluminal impedance‐pH (24hr MII‐pH) monitoring is the best way to diagnose LPR based on hypopharyngeal-esophageal reflux episodes (HREs).10However, to the best of our knowledge, there has been no study specifically showing whether HREs occurring in LPR actually occur frequently after meals, as shown in the TLESR phenomenon in GERD. Therefore, in this study, we tried to investigate the antecedent relationship between diet and HREs in LPR patients through diachronic analysis of 24hr MII-pH monitoring.