Abstract Rationale The role of type 2 inflammation in bronchiectasis remains incompletely understood. Serum immunoglobulin E (IgE) and blood eosinophils are often considered overlapping biomarkers, yet their independent prognostic significance has not been delineated. We aimed to determine whether IgE represents a distinct inflammatory pathway with clinical implications that differ according to eosinophil status. Methods A multicenter retrospective cohort study was conducted at 16 centers in Taiwan between January 2017 and October 2020, enrolling patients with bronchiectasis. Individuals with allergic bronchopulmonary aspergillosis were excluded. The cohort was stratified by IgE thresholds of 100 and 500 IU/mL within both eosinophilic and non-eosinophilic populations. The primary outcome was severe acute exacerbation requiring hospitalization within one year. Secondary outcomes included sputum pathogen profiles, pulmonary function parameters, and radiographic characteristics. Multivariable logistic regression models adjusting for age, sex, body mass index, smoking status, asthma, chronic obstructive pulmonary diseas, and absolute eosinophil count, in conjunction with sensitivity analyses in clinically relevant subgroups, were performed to evaluate the independent association of IgE with clinical outcomes. Results Among 579 patients (mean age 63.1 years, 45.3% female), 86 individuals (14.9%) demonstrated eosinophilia. Klebsiella pneumoniae was isolated more frequently in eosinophilic patients when IgE exceeded 500 IU/mL (P=0.002), whereas pathogen distribution remained unchanged across IgE levels in non-eosinophilic patients. IgE concentration was not associated with lobar involvement or radiographic severity scores at either threshold in both eosinophilic and non-eosinophilic subgroups. Pulmonary function parameters were comparable across groups as well. However, among non-eosinophilic patients, IgE levels exceeding 500 IU/mL were associated with substantially higher rates of severe exacerbations (9.8%) compared with IgE levels of 100 IU/mL or less (2.3%) or 100 to 500 IU/mL (0.9%) (P=0.009; adjusted odds ratio 2.30). Conversely, no significant association was observed in the eosinophilic subgroup. Multivariable logistic regression pinpointed that IgE 500 IU/mL remained the strongest independent predictor or primary endpoint after adjusting potential confounders (odds ratio 8.283, P0.001). Sensitivity analyses further demonstrated that the effect of elevated IgE was more pronounced among women (odds ratio 4.58), with asthma (odds ratio 4.79) or chronic obstructive pulmonary disease (odds ratio 4.65), and in the presence of tree-in-bud (odds ratio 33.64). Conclusions Serum IgE levels exceeding 500 IU/mL independently predicted severe exacerbations requiring hospitalization in non-eosinophilic bronchiectasis, revealing a distinct IgE-mediated pathway that operates independently of eosinophilic inflammation. These findings exemplified biomarker-guided risk stratification and suggested potential implications for anti-IgE therapeutics. This abstract is funded by: None
Kao et al. (Fri,) studied this question.