Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets - PubMed (original) (raw)

Review

. 2022 Jun;279(6):2743-2752.

doi: 10.1007/s00405-021-07201-w. Epub 2021 Dec 3.

Gaofan Xu 1, Bingduo Zhou 2, Yishuang Tang 1, Xiaowen Liu 1, Yue Wu 1, Yi Wang 1, Jing Kong 1, Tingting Xu 1, Cong He 1, Shengliang Zhu 1, Xiaosu Wang 1, Jianning Zhang 1

Affiliations

Review

Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets

Yading Li et al. Eur Arch Otorhinolaryngol. 2022 Jun.

Abstract

Purpose: Laryngopharyngeal reflux disease (LPRD) is a general term for the reflux of gastroduodenal contents into the laryngopharynx, oropharynx and even the nasopharynx, causing a series of symptoms and signs. Currently, little is known regarding the physiopathology of LPRD, and proton pump inhibitors (PPIs) are the drugs of choice for treatment. Although acid reflux plays a critical role in LPRD, PPIs fail to relieve symptoms in up to 40% of patients with LPRD. The influence of other reflux substances on LPRD, including pepsin, bile acid, and trypsin, has received increasing attention. Clarification of the substances involved in LPRD is the basis for LPRD treatment.

Methods: A review of the effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases was conducted in PubMed.

Results: Different reflux substances have different effects on LPRD, which will cause various symptoms, inflammatory diseases and neoplastic diseases of the laryngopharynx. For LPRD caused by different reflux substances, 24-h multichannel intraluminal impedance combined with pH-metry (MII-pH), salivary pepsin, bile acid and other tests should be established so that different drugs and treatment courses can be used to provide patients with more personalized treatment plans.

Conclusion: This article summarizes the research progress of different reflux substances on the pathogenesis, detection index and treatment of LPRD and lays a theoretical foundation to develop target drugs and clinical diagnosis and treatment.

Keywords: Laryngopharyngeal reflux; Mechanistic studies; Precancerous conditions; Reflux substance; Therapeutic target.

© 2021. The Author(s).

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Fig. 1

Fig. 1

Potential mechanisms of reflux material in LPRD patients (details are provided in the text). Arrows terminating with → represent activation, while those terminating with ┴ represent inhibition/deterioration. CA III carbonic anhydrase III, IL interleukin, CXCR 2 CXC chemokine receptor 2, Sep squamous epithelium stress proteins, NF-κB nuclear factor kappa-B, STAT3 signal transducer and activator of transcription factor 3, EGFR epidermal growth factor receptor, mTOR mammalian target of rapamycin, TNF-α tumor necrosis factor-α, BCL-2 B cell lymphoma 2, TRAIL tumor necrosis factor-related apoptosis inducing ligand, 8-OHdG 8-hydroxy-2'-deoxyguanosine, LRP1 lipoprotein receptor-related 1, α-2M alpha-2 macroglobulin, EMT epithelial–mesenchymal transition, TGF-β1 transforming growth factor-β1, MMP-9 matrix metalloproteinase-9, miR microRNA, PAR-2 proteinase-activated receptor-2, TRPV transient receptor potential vanilloid type, SP substance P, ROK Rho-associated protein kinase, NKR 1/2 natural killer receptors 1/2, p38 MAPK p38 mitogen-activated protein kinase, ERK 1/2 extracellular signal-regulated protein kinase 1/2, LES lower esophageal sphincter

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