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PepsinPepsin as a Biomarker: A Silent Biomarker for Reflux Aspiration or an Active Player in Extra-Esophageal Mucosal Injury?

Peter J. Kahrilas, MD; Leila Kia, MD
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From the Department of Medicine, Northwestern University, Feinberg School of Medicine.

CORRESPONDENCE TO: Peter J. Kahrilas, MD, Northwestern University, Feinberg School of Medicine, Department of Medicine, 676 St. Clair St, 14th Floor, Chicago, IL; e-mail:p-kahrilas@northwestern.edu


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following conflicts of interest: Dr Kahrilas has consulted for Reckitt Benckiser Group plc, AstraZeneca plc, and Pfizer Inc. Dr Kia has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(2):300-301. doi:10.1378/chest.15-0506
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The interactions among pepsin, acid, and mucosal injury have been a subject of interest since studies in the 1960s implicated pepsin as a major determinant of reflux injury at low pH.1 In its enzymatically active form, pepsin is the primary proteolytic enzyme of the digestive tract and key to the pathogenesis of “peptic” esophagitis in gastroesophageal reflux disease (GERD). Synthesized primarily by chief cells of the gastric fundus as the zymogen pepsinogen, pepsin requires an acidic environment before it can be converted to its active form. Its pH activity curve peaks at pH 2, falls off rapidly above pH 4.5, and is negligible above pH 5.5.2 As a biomarker for reflux, it is easily detected and uniformly found in gastric refluxate.3 Consequently, the presence of pepsin in the oropharynx or the tracheobronchial tree is indicative of regurgitation with or without aspiration. However, its presence in and of itself does not establish a causal relationship to epithelial damage and/or symptom generation from supraesophageal reflux. There must be a mechanism for activation as well. One such proposed mechanism in patients who are thought to have proton pump inhibitor-refractory supraesophageal GERD pathology is that inactive (but not denatured) pepsin is sufficiently reactivated by subsequent weakly acidic refluxate to cause laryngeal mucosal injury. Evidence substantiating that hypothesis is the demonstration of pepsin-induced depletion of laryngeal protective proteins (carbonic anhydrase isoenzyme III and squamous epithelial stress protein) in patients with laryngopharyngeal reflux.4-6

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