D1.145 - Clinical Impact of Type 2 Phenotype in Severe Asthma Patients with Exacerbations During Biologic Treatment

Poster abstract

Background

Biologic therapies in severe asthma aim to improve disease control and reduce exacerbations by targeting Type 2 inflammation. However, despite biologic treatment, asthma exacerbations may persist in a subset of patients. In this patient group, whether Type 2 inflammation persists may be a key determinant for re-evaluating treatment strategies. Biologic therapies in severe asthma aim to improve disease control and reduce exacerbations by targeting Type 2 inflammation. However, despite biologic treatment, asthma exacerbations may persist in a subset of patients. In this patient group, whether Type 2 inflammation persists may be a key determinant for re-evaluating treatment strategies.

Method

Patients with severe asthma who were receiving biologic therapy and had experienced at least one asthma exacerbation within the previous 12 months were retrospectively evaluated. Patients were divided into two groups according to post-treatment peripheral blood eosinophil levels: those without a Type 2 phenotype (eosinophils < 150/µL) and those with persistent Type 2 phenotype (eosinophils ≥ 150/µL). Demographic characteristics, comorbidities, laboratory parameters, pulmonary function test results, and Asthma Control Test (ACT) scores were compared between the groups. Continuous variables were analyzed using the independent samples t-test or Mann–Whitney U test, depending on data distribution, while categorical variables were analyzed using the chi-square test or Fisher’s exact test.

Results

Among patients receiving biologic therapy for severe asthma (n = 139), 51 patients who experienced at least one asthma exacerbation within the past year were included in the study (Type 2–negative phenotype, n = 34; persistent Type 2 phenotype, n = 17). No significant differences were observed between the two groups with regard to age, sex, body mass index (BMI), smoking history, rhinitis, gastroesophageal reflux disease, nasal polyps, or aspirin/NSAID hypersensitivity. Pre-treatment eosinophil levels were higher in the persistent Type 2 phenotype group (p = 0.022). Post-treatment eosinophil levels remained significantly higher in this group (240 [205–310] vs 82.5 [10–100] cells/µL, p < 0.001). There were no significant differences between the groups in pulmonary function test parameters (FEV₁ and FEF₂₅–₇₅) or in pre- and post-treatment Asthma Control Test (ACT) scores. Changes in ACT scores and reductions in exacerbation frequency were similar in both groups.

Conclusion

As a result of our study, in patients with severe asthma experiencing exacerbations under biologic therapy, the persistence of the Type 2 phenotype was not associated with additional differences in clinical control, pulmonary function, or Asthma Control Test (ACT) scores. In contrast, persistently elevated peripheral blood eosinophil levels despite biologic therapy were notable in patients with a persistent Type 2 phenotype. These findings suggest that Type 2 inflammation may not be fully suppressed in patients who develop exacerbations while receiving biologic therapy and indicate that additional biomarkers should be considered in the evaluation of this patient population.