The aim of this review is to evaluate the underlying pathophysiology, diagnostic challenges, and current therapeutic strategies for nasal hyperreactivity (NHR) across different upper airway inflammatory phenotypes. A comprehensive narrative literature review was conducted utilizing established scientific databases, including PubMed/Medline, Scopus, Web of Science, and Embase, covering articles published up to 2026. A structured search strategy was applied using keywords such as “nasal hyperreactivity,” “neurogenic inflammation,” “cold dry air provocation,” and “transient receptor potential (TRP) channels.” Peer-reviewed clinical trials, mechanistic studies, and authoritative guidelines were included to synthesize the current evidence regarding the diagnosis and management of NHR. Nasal hyperreactivity affects up to two-thirds of rhinitis patients, independent of their atopic status. Its pathophysiology is heavily driven by neurogenic inflammation and the upregulation of TRP channels, specifically TRPV1 and TRPM8, on afferent sensory nerves. While subjective symptom history is commonly utilized in clinical settings, the cold dry air provocation test remains the most reliable objective diagnostic tool, though it is currently underutilized in routine practice. Traditional pharmacotherapies often yield suboptimal results, making targeted neuromodulatory interventions, such as “nasal capsaicin treatment,” highly promising, despite some practical administration challenges. Nasal hyperreactivity represents a distinct and burdensome clinical phenotype requiring a targeted, mechanism-driven therapeutic approach. Establishing standardized objective diagnostic biomarkers and enhancing the accessibility of neuromodulatory therapies are essential steps to optimize patient care and alleviate the significant clinical burden associated with this condition.
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Nuray Bayar Muluk (2026) studied this question.
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