The Role of Pepsin in Laryngopharyngeal Reflux.
10.3342/kjorl-hns.2015.58.8.529
- Author:
Sang Hyuk LEE
1
;
Sung Min JIN
;
Nikki JOHNSTON
Author Information
1. Department of Otorhinolaryngology-Head and Neck Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. entlsh@hanmail.net
- Publication Type:Review
- Keywords:
Carcinogenesis;
Diagnosis;
Laryngeal cancer;
Larynopharyngeal reflux;
Pepsin
- MeSH:
Alcohol Drinking;
Carcinogenesis;
Chief Cells, Gastric;
Diagnosis;
Esophagus;
Humans;
Hydrochloric Acid;
Hypopharynx;
Incidence;
Laryngeal Neoplasms;
Laryngopharyngeal Reflux*;
Pepsin A*;
Pepsinogen A;
Prevalence;
Smoke;
Smoking;
Stomach
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2015;58(8):529-533
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Laryngopharyngeal reflux (LPR) is a very prevalent condition with a rising incidence. The diagnosis remains challenging and often controversial because the pathophysiology of LPR is often poorly understood and there is currently no diagnostic gold standard for LPR. Pepsin is produced by gastric chief cells in zymogen form as pepsinogen, and subsequently cleaved by the hydrochloric acid in the stomach, generating active pepsin protein. Pepsin is only produced in the stomach, and thus when detected in the laryngopharynx, it can be used as a specific marker for reflux. The carcinogenic properties of the gastric contents may also lead to cancer in target organs especially considering that they do not have intrinsic protective mechanisms as found in the esophagus. Many studies have demonstrated a high prevalence of LPR in patients with laryngeal cancer, but these studies are confounded by the cofactor such as smoking and alcohol consumption. This review focuses on the current studies about pepsin as a specific marker for LPR and putative relationship between pepsin and laryngeal cancer.
