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Laryngopharyngeal reflux disease (LPRD) is a commonly encountered extraesophageal reflux condition in otolaryngology practice. Its prevalence is steadily increasing, with an onset observed in progressively younger populations. The clinical manifestations of LPRD are notably nonspecific, often resulting in misdiagnosis. In its more severe forms, LPRD can lead to a range of complications, and some studies have suggested a possible association with laryngeal cancer, although the evidence remains controversial. The gut microbiota, often referred to as the human “second genome,” plays crucial roles in host metabolism, immune regulation, and the maintenance of mucosal barrier integrity. As a result, gut dysbiosis is closely linked to a wide array of systemic disorders.Recent evidence has demonstrated that patients with LPRD exhibit reduced gut microbial diversity alongside imbalances in the relative abundance of specific bacterial taxa. In parallel, proton pump inhibitors (PPIs), the first-line pharmacotherapy for LPRD, can further exacerbate gut dysbiosis and elevate the risk of small intestinal bacterial overgrowth (SIBO), thereby perpetuating a vicious cycle of reflux deterioration. This review synthesizes the latest advances in the mechanistic pathways through which gut dysbiosis contributes to LPRD, with the aim of elucidating its pathogenesis and inspiring novel therapeutic strategies.
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Zhang et al. (2026) studied this question.
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