C39-26 Elevated Serum Ige and Clinical Outcomes in Idiopathic Pulmonary Fibrosis: A Real World Propensity Matched Analysis

Abstract Background Immunoglobulin E (IgE) is a key antibody mediating type I hypersensitivity. Upon allergen exposure, IgE bound to mast cells triggers degranulation, releasing inflammatory mediators that drive acute allergic reactions. Mast cells, through the release of tryptase and transforming growth factor-β (TGF-β), may contribute to fibrogenesis. Experimental models have identified Th2 cell infiltration and IgE-producing B cells within fibrotic lesions, suggesting that IgE-driven inflammation could promote fibrosis. Beyond its well-established roles in asthma, allergic bronchopulmonary aspergillosis (ABPA), cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD), IgE’s contribution to interstitial lung disease (ILD) remains largely uncharacterized. Our study aims to examine the role of elevated IGE in clinical outcomes of patients with IPF. Methods Utilizing Trinetx global health research, the multi-health care organization de-identified the electronic health record (EHR) database, and 5-year outcomes, including all-cause mortality, were compared between two sets of cohorts comprising IPF patients with IgE ≥100 IU/mL and IgE ≥500 IU/mL, with their 1:1 propensity-matched control cohort with normal IgE levels. Mortality outcome was calculated using Kaplan-Meier curves. Results After propensity score matching for baseline characteristics and confounders such as Asthma 1,056 per group), mortality was higher among patients with elevated IgE compared to normal IgE levels (33.6% vs 29.8%), though this did not reach statistical significance (HR 1.14, 95% CI 0.98-1.32, p = 0.33). Other outcomes, including rates of respiratory failure, pneumonia, pulmonary hypertension, mechanical ventilation, and antifibrotic use, were similar between groups. Corticosteroid use was higher in patients with elevated IgE (82.2% vs 78.5%, p = 0.03). In the IgE ≥500 IU/mL analysis (730 patients; 365 per group), elevated IgE was associated with significantly higher mortality (37.3% vs 28.8%; p = 0.015). Other respiratory outcomes, including acute hypoxic respiratory failure, steroid use, and transplant rates, were comparable. Conclusion In our study, serum IgE elevation correlated with increased mortality in patients with IPF. Prospective investigations that integrate mechanistic and therapeutic assessments are needed to determine whether IgE serves only as a prognostic biomarker or actively contributes to the pathogenesis of Interstitial Lung Disease. This abstract is funded by: none