Laryngopharyngeal Reflux and Gastritis Connection

Pathophysiological Mechanisms

The laryngeal mucosa is more sensitive to refluxate than esophageal tissue, requiring fewer reflux episodes to produce symptoms 1

Laryngoscopic findings alone are unreliable for diagnosing LPR, with sensitivity and specificity less than 50% 2, 3
Reflux monitoring has limited diagnostic value for extraesophageal reflux manifestations, including LPR 2, 3
There is currently no single diagnostic tool that can conclusively identify gastroesophageal reflux as the cause of LPR symptoms 1

A therapeutic trial of proton pump inhibitors (PPIs) is often the most pragmatic approach for suspected reflux-related symptoms, including LPR 3
For patients with suspected extraesophageal manifestations of GERD who fail one trial of PPI therapy, objective testing for pathologic gastroesophageal reflux should be considered 1
A multidisciplinary approach involving gastroenterologists and otolaryngologists is important, since LPR is often multifactorial 1

Symptom improvement of LPR while on PPI therapy may result from mechanisms other than acid suppression and should not be regarded as confirmation of GERD as the underlying cause 1
Laryngeal findings like reflux granuloma, vocal cord edema, and posterior commissure hypertrophy are often attributed to LPR but have poor specificity 2, 3
The presence of erosive reflux disease (ERD) detected by endoscopy is predictive of a good treatment response of LPR symptoms to PPI treatment 3