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.