CHRONIC RHINOSINUSITIS AND ASTHMA: CLINICAL AND INFLAMMATORY RELATIONSHIP
Keywords:
chronic rhinosinusitis; asthma; type 2 inflammation; eosinophils; nasal polyps; unified airway; PRISMAAbstract
DOI: https://doi.org/10.46296/yc.v10i19.0981
Abstract
Introduction: Chronic rhinosinusitis (CRS) and asthma frequently coexist and share inflammatory mechanisms that underpin the concept of the unified airway. However, the magnitude of their clinical association and the concordance between upper and lower airway biomarkers vary according to the CRS phenotype and inflammatory endotype. Objective: To synthesize evidence regarding the clinical and inflammatory relationship between CRS and asthma, focusing on symptom control, exacerbations, lung function, asthma onset, and type 2 (T2) inflammation markers. Methods: A systematic review was conducted following PRISMA 2020 guidelines. The primary search was performed in PubMed (January 1, 2015, to May 30, 2026) using MeSH terms and free-text terms for CRS, asthma, inflammation, eosinophils, T2 inflammation, and clinical outcomes. Original studies in humans that directly evaluated the coexistence or association between CRS and asthma and reported clinical or inflammatory outcomes were included. The heterogeneity of study designs and measurements warranted a qualitative synthesis. Results: A total of 216 records were identified; 61 were sought for retrieval, 57 were assessed for eligibility, and 27 were included in the final synthesis. Evidence consistently showed that CRS—particularly CRS with nasal polyps and eosinophilic phenotypes—is associated with a higher asthma burden, poorer control, increased use of systemic corticosteroids, and a higher risk of exacerbations. Recent longitudinal studies also support a temporal relationship between sinonasal inflammation and the subsequent onset of asthma. Regarding inflammation, convergence was observed in blood and tissue eosinophilia, elevated FeNO, periostin levels, and activation of IL-4/IL-13/IL-5 pathways, although some studies described T2/T3 overlap and heterogeneity outside the polypoid phenotype. Conclusion: CRS and asthma should be considered interrelated manifestations of airway disease, with a particularly strong association in the context of T2/eosinophilic inflammation. Joint assessment of clinical severity and biomarkers can improve risk stratification and facilitate integrated therapeutic decisions.
Keywords: chronic rhinosinusitis; asthma; type 2 inflammation; eosinophils; nasal polyps; unified airway; PRISMA.
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