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Lookup NU author(s): Dr David Bulmer,
Professor Jeffrey Pearson
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This is the second annual report of an international collaborative research group that is examining the cellular impact of laryngopharyngeal reflux (LPR) on laryngeal epithelium. The results of clinical and experimental studies are presented. Carbonic anhydrase (CA), E-cadherin, and MUC gene expression were analyzed in patients with LPR, in controls, and in an in vitro model. In patients with LPR, we found decreased levels of CAIII in vocal fold epithelium and increased levels in posterior commissure epithelium. The experimental studies confirm that laryngeal CAIII is depleted in response to reflux. Also, cell damage does occur well above pH 4.0. In addition, E-cadherin (transmembrane cell surface molecules, which have a key function in epithelial cell adhesion) was not present in 37% of the LPR laryngeal specimens. In conclusion, the laryngeal epithelium lacks defenses comparable to those in esophageal epithelium, and these differences may contribute to the increased susceptibility of laryngeal epithelium to reflux-related injury.
Author(s): Bulmer D, Ross PE, Axford SE, Johnston N, Gill GA, Pearson JP, Dettmar PW, Panetti M, Pignatelli M, Koufman JA
Publication type: Article
Publication status: Published
Journal: Annals of Otology, Rhinology and Laryngology
ISSN (print): 0003-4894
ISSN (electronic): 1943-572X
Publisher: Annals Publishing
PubMed id: 12834114