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Bile acids in laryngopharyngeal refluxate: Will they enhance or attenuate the action of pepsin?

Lookup NU author(s): M Shamsher Ali, Dr Shruti Parikh, Dr Peter Chater, Professor Jeffrey Pearson

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Abstract

Objectives/Hypothesis: To assess if, as previously reported in the literature, bile acids inhibit pepsin activity, resulting in pepsin having a less important role in laryngopharyngeal damage in reflux disease. Study Design: Prospective translational research study. Methods: A total of 78 patient's fasting gastric juice samples were obtained from routine endoscopy. The total bile acid (TBA) content and pepsin activity were measured using a 3-hydroxysteroid dehydrogenasebased kit for bile acids; and pepsin activity was measured using succinyl albumin/dimethylhaemoglobin as a substrate and the development of new N-terminals. The ability of bile acids to effect pepsin activity was assessed with three primary bile acids, two unconjugated and one taurine conjugated, using the above N-terminal assay. Results: Gastric juice contained median TBA of 40 (range 1010010) M and pepsin activity of 408 (range 273892)ug/ml. We used this data to inform the relative levels of pepsin and bile acids that might occur in a reflux event, and we used concentrations of bile acids between 10100M. Pepsin activity was pH dependent, but 28% of the activity was retained at pH 5.5. None of the bile acids showed any significant effect on pepsin activity across the pH range 2.06.0. Conclusions: At the levels and pH that pepsin and bile acids might occur in an LPR event, bile acids do not attenuate pepsin activity. Pepsin could be considered a damaging factor even at high pH, and it will aggravate further any damaging effects of bile acids in the refluxate. Laryngoscope, 2012


Publication metadata

Author(s): Ali MS, Parikh S, Chater P, Pearson JP

Publication type: Article

Publication status: Published

Journal: The Laryngoscope

Year: 2013

Volume: 123

Issue: 2

Pages: 434-439

Print publication date: 01/02/2013

ISSN (print): 0023-852X

ISSN (electronic): 1531-4995

Publisher: John Wiley & Sons, Inc.

URL: http://dx.doi.org/10.1002/lary.23619

DOI: 10.1002/lary.23619


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