Title : Nasal polyposis and its pulmonary repercussions: A unified airway perspective on type 2 inflammation
Abstract:
Background: Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) is a chronic inflammatory disease of the upper airway, most often driven by type 2 inflammation. Because the nasal and bronchial mucosa share epithelial features and inflammatory pathways, nasal polyposis is rarely a purely local disease: It is closely associated with lower airway involvement, notably asthma, which is frequently late-onset, severe and difficult to control in these patients.
Objective: To provide an expert overview of the pulmonary repercussions of nasal polyposis and to discuss their implications for diagnosis and management in pulmonology practice.
Pathophysiological basis: According to the unified airway concept, epithelial barrier dysfunction and the release of alarmins (TSLP, IL-33, IL-25) activate type 2 innate lymphoid cells and Th2 lymphocytes. The resulting production of IL-4, IL-5 and IL-13 sustains eosinophilic infiltration, local IgE production and mucus hypersecretion in both the nose and the bronchi.
Clinical impact: A substantial proportion of patients with CRSwNP have asthma, and conversely many patients with severe eosinophilic asthma present sinonasal disease. Their coexistence is associated with more frequent exacerbations, greater exposure to systemic corticosteroids, more marked airflow obstruction and a poorer quality of life. Nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (polyposis, asthma and NSAID hypersensitivity) represents a particularly severe, relapsing phenotype. When polyps coexist with lung disease, other conditions such as eosinophilic granulomatosis with polyangiitis, allergic bronchopulmonary aspergillosis, cystic fibrosis or primary ciliary dyskinesia should also be considered.
Assessment: Systematic evaluation of the upper airway (symptom scores, nasal endoscopy, sinus imaging when indicated) is advisable in patients with asthma, while spirometry, fractional exhaled nitric oxide and blood eosinophil count should be considered in patients with nasal polyps, even when respiratory symptoms are mild.
Management: Saline nasal irrigation, intranasal corticosteroids, short courses of oral corticosteroids and endoscopic sinus surgery remain first-line options, but recurrence is common. Biologics targeting the type 2 pathway (such as dupilumab, omalizumab and mepolizumab) can reduce polyp burden and improve asthma control at the same time, supporting a combined, patient-centred strategy.
Conclusion: Nasal polyposis should be regarded as a marker of lower airway risk. Close collaboration between pulmonologists and otorhinolaryngologists, within a multidisciplinary approach, allows earlier detection of lung involvement, better phenotyping and more effective, personalised treatment of the whole airway.
