Optimizing NSAID-exacerbated respiratory disease treatment: Biologics, ATAD and phenotype-based care

What is the optimal treatment for N-ERD? New EAACI 2026 data compare biologics and ATAD, exploring responses across distinct clinical phenotypes.

Treatment options for NSAID-Exacerbated Respiratory Disease (N-ERD) have expanded considerably in recent years, with biologic therapies joining established approaches such as aspirin therapy after desensitization (ATAD). Nevertheless, disease control remains challenging for many patients, underscoring the need to optimize treatment selection and long-term management.

In this interview, Dr Melek Cihanbeylerden (Ağrı Research and Training Hospital, Ağrı, Turkey) spoke with touchRESPIRATORY about the current treatment landscape for N-ERD, including the recent addition of biologic therapies. Dr Cihanbeylerden also outlined the aims, design and key findings from her retrospective, phenotype-based comparative study assessing the efficacy of biologics in N-ERD.

Abstract: Clinical Efficacy of Biologics and ATAD in NSAID-Exacerbated Respiratory Disease: A Phenotype-Based Comparative Study. EAACI 2026, June 12–5, Istanbul, Turkey.

touchRESPIRATORY coverage of EAACI 2026

Could you describe the current treatment landscape for NSAID-exacerbated respiratory disease?

NSAID-exacerbated respiratory disease (N-ERD) is a heterogeneous inflammatory airway disease involving both the upper and lower airways. Traditionally, management has included avoidance of triggering NSAIDs, standard asthma and chronic rhinosinusitis treatment, endoscopic sinus surgery when needed, and aspirin therapy after desensitization (ATAD).

More recently, biologic therapies targeting type 2 inflammation, such as omalizumab, mepolizumab, and benralizumab, have become important options, particularly in patients with severe asthma, recurrent nasal polyposis, eosinophilic inflammation, or high corticosteroid burden. However, as N-ERD is clinically heterogeneous, selecting the most appropriate treatment for each patient remains challenging.

What were the aims and design of your retrospective study?

The aim of our study was to compare the clinical efficacy of omalizumab, mepolizumab, benralizumab, ATAD, and ATAD–biologic combination therapy in patients with N-ERD. We also aimed to evaluate whether treatment responses differed according to clinical phenotypes and to propose a phenotype-based treatment approach.

This was a retrospective study including 70 adult patients with N-ERD who had received treatment for at least 6 months. We assessed asthma control, sinonasal symptoms, smell/taste scores, blood eosinophil levels, oral corticosteroid use, and emergency department visits before and after treatment. In addition, hierarchical clustering analysis was used to identify different clinical phenotype groups.

What were the comparative efficacy findings between therapies?

All treatment groups showed clinical improvements, but the pattern of benefit differed between therapies. The ATAD plus biologic combination group showed the most comprehensive improvement across several outcomes, including sinonasal symptoms, eosinophil levels, asthma control, oral corticosteroid use, smell/taste scores, and emergency department visits.

Among biologic therapies, benralizumab was associated with the greatest reduction in eosinophil levels and emergency department visits. Omalizumab showed strong effects on asthma control, sinonasal symptoms, and reduction in oral corticosteroid use. Mepolizumab was associated with the greatest improvement in smell/taste scores.

What therapies were associated with better outcomes in the different phenotype groups?

We identified three clinical phenotype groups:

• Cluster 1 represented a more severe phenotype, including older patients with higher BMI, longer disease duration, lower FEV1/FVC, multiple previous sinus surgeries, smoking history, and atopy. This group appeared to benefit most from ATAD plus biologic combination therapy.
• Cluster 2 represented a moderate phenotype, with comorbidities, atopy, intermediate disease duration, and moderate airflow limitation. In this group, biologic monotherapy was associated with clinical improvement.
• Cluster 3 represented a milder phenotype, with female predominance, lower BMI, shorter disease duration, preserved lung function, and no smoking history. This group appeared to respond well to ATAD monotherapy.

How could these findings be used to optimize treatment strategies in N-ERD?

Our findings support a personalized, phenotype-guided approach to N-ERD treatment. Rather than applying a single treatment strategy to all patients, clinical characteristics such as disease severity, lung function, eosinophilic inflammation, sinonasal disease burden, previous sinus surgeries, atopy, smoking history, and corticosteroid requirement may help guide treatment selection.

In mild phenotypes, ATAD may be a suitable option. In moderate phenotypes, biologic therapy may be preferred. In severe or treatment-resistant phenotypes, especially when both upper and lower airway disease are prominent, combination therapy with ATAD and a biologic may provide broader clinical benefit. These findings may help clinicians optimize treatment decisions and reduce unnecessary delays in selecting the most appropriate therapy.