Chronic rhinosinusitis is a risk factor for interstitial lung disease in Sjogren’s syndrome

Résumé fourni par la source

Interstitial lung disease (ILD) is a leading cause of morbidity and mortality in Sjögren’s syndrome (SS), but its risk factors remain unclear. Although SS affects both the upper and lower respiratory epithelium, it is unknown whether this occurs simultaneously or separately. In other autoimmune conditions—such as eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis—upper airway disease precedes lower lung involvement by months or even years. We hypothesized that chronic rhinosinusitis (CRS), as an upper airway disease, may be a risk factor for ILD in SS. We analyzed the TriNetX Research Network database to compare incident ILD in SS patients with or without CRS. Patients with pre-existing ILD or CRS were excluded, and all participants were being treated with Sjögren’s related immunosuppression or sicca therapies. Incident ILD and risk ratios (RR) were calculated at 5 and 10 years after adjusting for important confounding variables, such as age, gender, race, comorbid conditions, and other risk factors. In matched cohorts, overall risk for developing ILD was significantly higher in patients with CRS. At 5 years, incidence of ILD was 2.56% in patients with CRS versus 1.66% in those without CRS (adjusted RR 1.57, p = 0.01, 95% CI: 1.09–2.27). Likewise, at 10 years, the ILD incidence was 3.01% in patients with CRS versus 1.96% in those without CRS (adjusted RR 1.53, p = 0.01, 95% CI: 1.09–2.13). Our results suggest SS patients with CRS are at higher risk for developing ILD, indicating a possible need for more intensive screening in this population. 1. Patients with Sjögren’s syndrome (SS) who develop chronic rhinosinusitis (CRS) have a nearly 50% higher risk of interstitial lung disease (ILD) compared to those without CRS. 2. CRS may precede and predict the onset of lower respiratory tract diseases like ILD in SS patients, highlighting upper airway involvement as a potential early indicator. 3. The association between CRS and ILD in SS may stem from shared pathogenic mechanisms—such as glandular dysfunction, impaired mucociliary clearance, and altered mucosal immunity—warranting further research. 4. Recognizing CRS as a risk factor for ILD emphasizes the need for early respiratory evaluation and monitoring in SS patients, which could lead to timely interventions and improved long-term pulmonary outcomes.

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