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.