Extraesophageal reflux up-to-date
Karol Zeleník Orcid.org 1, Pavel Schwarz Orcid.org 1, Ondřej Urban Orcid.org 2,3, Jitka Vydrová Orcid.org 4, Pavel Komínek Orcid.org 5,6
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Summary
Extraesophageal symptoms of gastroesophageal reflux disease (posterior laryngitis, vocal fold granuloma, globus pharyngeus, subglotis and tracheal stenosis, laryngopharyngeal carcinoma, poorly controlled asthma bronchiale, paroxysmal cough and others) have been studied more since the 1990's. It was long believed that extraesophageal reflux causes mucosal damage of the hypopharynx and larynx in the same way as gastroesophageal reflux in the oesophagus. However, this premise did not work in practice (only a few extraesophageal reflux episodes have been proven during pH-metry, poor correlation between symptoms and findings, limited effect of proton pump inhibitors) and this led to scepticism regarding the role of extraesophageal reflux in the pathogenesis of the diseases mentioned above. But research in the last few years has revealed much new information about the pathogenesis of extraesophageal reflux and has completely changed our understanding of this controversial issue. Acidity alone is no longer considered to be the main pathogenetic agent during extraesophageal reflux episodes, while pepsin, which maintains its stability and activity also in weakly acid refluxes, is considered to play an essential role. Furthermore, it has been revealed that mucosa of the hypopharynx, larynx and other parts of the airways is much more sensitive to refluxate than esophageal mucosa. Therefore, treatment is focused not only on cutting down the acidity, but also on reducing reflux episodes and minimizing the negative pepsin effect.
Keywords
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