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International Journal of Otolaryngology
Volume 2012 (2012), Article ID 646901, 13 pages
Review Article

Reflux Revisited: Advancing the Role of Pepsin

1Rotherham General Hospital, Moorgate Road, Rotherham, South Yorkshire S60 2UD, UK
2Technostics Ltd., The Deep Business Centre, Kingston Upon Hull, East Yorkshire HU1 4BG, UK

Received 28 July 2011; Accepted 9 September 2011

Academic Editor: Petros D. Karkos

Copyright © 2012 Karna Dev Bardhan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Gastroesophageal reflux disease is mediated principally by acid. Today, we recognise reflux reaches beyond the esophagus, where pepsin, not acid, causes damage. Extraesophageal reflux occurs both as liquid and probably aerosol, the latter with a further reach. Pepsin is stable up to pH 7 and regains activity after reacidification. The enzyme adheres to laryngeal cells, depletes its defences, and causes further damage internally after its endocytosis. Extraesophageal reflux can today be detected by recognising pharyngeal acidification using a miniaturised pH probe and by the identification of pepsin in saliva and in exhaled breath condensate by a rapid, sensitive, and specific immunoassay. Proton pump inhibitors do not help the majority with extraesophageal reflux but specifically formulated alginates, which sieve pepsin, give benefit. These new insights may lead to the development of novel drugs that dramatically reduce pepsinogen secretion, block the effects of adherent pepsin, and give corresponding clinical benefit.