Pepsin and pharyngeal reflux

2021/11/17

Pepsin enters the mucosal epithelial cells of the throat through receptor-mediated endocytosis. However, studies have shown that pepsin in the throat epithelial cells can also cause the loss of two protective proteins (CA-Ⅲ and Sep70) in the throat, thereby causing damage to the laryngeal mucosa.

Bardha believes that pepsin causes damage to the throat mucosa through a series of reactions: unactivated pepsin enters the cell through endocytosis and is activated in the cell, resulting in cell damage, which induces oxidative stress and oxygen-free radical accumulation, and then damages mitochondria and leads to cell death. In conclusion, pepsin plays a significant pathogenic role in pharyngeal reflux.

As a macromolecule, pepsin can enter and stay in the epithelial cells of the throat for a long time after reaching the throat through reflux. Therefore, it is easier to detect after the occurrence of gastric acid reflux. These features make pepsin a better diagnostic marker for LPR. A study saw pepsin in children’s airway aspirates and performed laryngoscopy and bronchoscopy at the same time. The results found that the macroscopic changes under laryngoscopy and bronchoscopy were significantly related to pepsin positive, suggesting that pepsin can be used as An indicator of extraesophageal reflux disease. OCAK et al. also tested the pepsin level in the saliva of 20 patients with suspected throat reflux, collected the saliva of the patients with the most severe symptoms, and found that the sensitivity and specificity of the method were 33 % And 100%.

Pepsin is the main component of the disease for throat reflux, and salivary pepsin is an ideal diagnostic marker.

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