梅尼埃病与咽喉反流相关性的研究进展
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1.河南科技大学临床医学院;2.河南科技大学第一附属医院

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R764.33

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河南省医学科技攻关计划联合共建项目(LHGJ20220680)


Research Progress on the Correlation between Ménière‘s Disease and Laryngopharyngeal Reflux
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The First Affiliated Hospital,and College of Clinical Medicine of Henan University of Science and Technology,Luoyang,China

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    摘要:

    梅尼埃病(MD)是以膜迷路积水为核心病理特征的内耳疾病,表现为发作性眩晕、波动性听力下降、耳鸣及耳闷胀感。除遗传、免疫、病毒感染等已知因素外,近年来越来越多的研究表明,咽喉反流(LPR)可能参与MD的发生和发展。由于咽喉部与中耳通过咽鼓管直接相通,LPR较胃食管反流(GER)更可能直接影响耳部功能。反流物中的胃酸、胃蛋白酶等可能通过经咽鼓管的直接化学损伤与压力失衡、迷走神经介导的神经源性炎症、靶向内淋巴囊的免疫与全身性炎症以及跨腔室压力传递等多种途径,参与内淋巴积水的形成与加重。目前尚缺乏LPR与MD直接因果关系的证据,现有结论多基于间接研究和机制假说。本文旨在系统综述LPR与MD相关性的研究进展,并阐述其潜在作用机制,以期为未来研究提供方向。

    Abstract:

    Ménière"s disease (MD) is an inner ear disorder characterized pathologically by endolymphatic hydrops, manifesting as episodic vertigo, fluctuating hearing loss, tinnitus and aural fullness. In addition to known factors such as genetics, immunity, and viral infection, a growing number of recent studies have suggested that laryngopharyngeal reflux (LPR) may be involved in the occurrence and development of MD. Due to the direct connection between the pharynx and larynx and the middle ear via the eustachian tube, LPR is more likely to directly affect ear function than gastroesophageal reflux. Gastric acid, pepsin and other components of refluxate may participate in the formation and aggravation of endolymphatic hydrops through various pathways, including direct chemical injury and pressure imbalance via the eustachian tube, vagus nerve-mediated neurogenic inflammation, immune and systemic inflammation targeting the endolymphatic sac, and trans-compartment pressure transmission. Currently, direct evidence for a causal relationship between LPR and MD is lacking, and existing conclusions are mostly based on indirect studies and mechanistic hypotheses. This article aims to systematically review the research progress on the correlation between LPR and MD, and to elaborate its potential mechanisms, so as to provide directions for future research.

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  • 收稿日期:2026-06-25
  • 最后修改日期:2026-08-18
  • 录用日期:2026-08-19
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