Background Allergic bronchopulmonary aspergillosis (ABPA) is a severe type 2 inflammatory airway disease caused by hypersensitivity to Aspergillus fumigatus . Although omalizumab has been used as an adjunctive therapy for ABPA, longitudinal changes in type 2 inflammatory and Aspergillus -specific biomarkers during treatment remain incompletely characterized. Objective To evaluate clinical outcomes and longitudinal biomarker changes during omalizumab therapy in patients with ABPA. Methods We retrospectively studied 15 adults with ABPA treated with omalizumab 600 mg every 4 weeks and followed for 36 weeks. Clinical outcomes, including pulmonary function, fractional exhaled nitric oxide (FeNO), blood eosinophil counts, and oral corticosteroid (OCS) use, were assessed at baseline, week 12, and week 36. Serial measurements of total IgE, A. fumigatus -specific IgE and IgG4, thymus and activation-regulated chemokine (TARC/CCL17), IL-4, IL-5, and IL-13 were performed. Longitudinal changes were analyzed using the Friedman test, with false discovery rate (FDR)-adjusted q values calculated for multiple testing. Results Omalizumab treatment was associated with reductions in OCS dose, FeNO, blood eosinophils, TARC, IL-4, IL-5, and IL-13 (all overall P<0.001, FDR q<0.001). Median OCS dose decreased from 15.0 to 0 mg/day, FeNO from 43.0 to 22.0 ppb, and eosinophils from 0.58 to 0.06 ×10 9 /L by week 36. Individual trajectories were predominantly downward, with monotonic declines in 80.0%–100% of participants depending on the marker. PEF increased significantly, whereas the increase in FEV1 was not statistically significant. A. fumigatus -specific IgE and IgG4 declined, while total IgE showed no sustained decrease. No significant associations were detected between total IgE and TARC or the measured cytokines (all nominal P≥0.062; all FDR q≥0.482). No serious treatment-related adverse events were observed. Conclusion In this real-world ABPA cohort, omalizumab therapy was associated with corticosteroid reduction and parallel declines in several type 2-associated biomarkers over 36 weeks. These longitudinal clinical and biomarker profiles provide a more detailed picture of treatment-associated changes and a basis for prospective evaluation of their clinical relevance.
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