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Updated: Jan 15, 2026

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
Divergent Risk Patterns of Upper Airway Inflammation in Autoimmune Diseases: A Nationwide Retrospective Analysis
Jessan A Jishu1, Cameron Galic1, Abdelrahman Shata2
1Tulane University School of Medicine, New Orleans, Louisiana.
Abstract:
ObjectivesWhile autoimmune diseases (ADs) are known for systemic inflammation, their specific association with upper airway inflammation (UAI) has not been extensively characterized. We aim to investigate the associations between various ADs and subsequent UAI development in a large, national cohort.MethodsThis retrospective cohort study utilized de-identified electronic health records from TriNetX, a national collaborative database. Adolescent and adult patients with a diagnosis of 1 or more ADs were identified. A 12 month washout period was implemented to exclude preexisting UAI. The primary outcome was the incidence of UAI (chronic rhinosinusitis, allergic rhinitis, nonallergic rhinitis, chronic laryngitis, obstructive sleep apnea) following AD diagnosis. Hazard ratios and relative risks (RRs) with 95% confidence intervals (CIs) were calculated.ResultsAfter propensity matching, 1 327 186 patients with ADs and 1 327 186 controls were included. Patients with ADs exhibited a significantly lower overall incidence of UAI compared to controls (9.11% vs 13.81%; RR 0.71, 95% CI 0.70-0.71). This reduced risk was notable for allergic rhinitis (RR 0.64, 95% CI 0.64-0.65) and chronic sinusitis (RR 0.88, 95% CI 0.87-0.89). Juvenile idiopathic arthritis and type 1 diabetes demonstrated the most pronounced reductions in UAI risk. However, granulomatosis with polyangiitis and eosinophilic granulomatosis with polyangiitis were associated with a significantly increased risk of UAI.ConclusionMost ADs were associated with a reduced overall risk of subsequent UAI. However, certain vasculitides significantly increased UAI risk, highlighting disease-specific pathophysiological mechanisms. These findings suggest a complex interplay between systemic autoimmunity and localized airway inflammation, warranting further investigation into underlying mechanisms and the impact of AD treatments.
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