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

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 3α‐hydroxysteroid dehydrogenase–based 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 10–10010) μM and pepsin activity of 408 (range 27–3892)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 10–100μM. 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 2.0–6.0. 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