T2-low asthma and its reflection on clinical burden

<bold>Background:</bold> The main inflammatory pathway in asthma is type-2 inflammation (T2-high asthma). However, a less studied T2-low asthma phenotype also exists. <bold>Aims and objectives:</bold> We conducted this study to determine the proportion and clinical features of T2-low asthma in a general asthma population. <bold>Methods:</bold> Participants with physician-diagnosed current asthma (n=896) in the population-based West Sweden Asthma Study were included. T2-high asthma was defined as either blood eosinophils ≥150 cell/µL or fractional exhaled nitric oxide ≥20 ppb or allergen-driven disease based on GINA 2023. If none of these were present, participants were classified as T2-low asthma. <bold>Results:</bold> In total, 14.3% (n=128) had T2-low asthma, characterized by female and later asthma onset dominancy compared to T2-high asthma. Surprisingly, there was no difference in obesity, smoking status, or dyspnea between the T2-low and T2-high asthma groups. Participants with T2-high asthma had lower FEV₁/FVC with higher reversibility, whereas the T2-low asthma group was more prone to exacerbations and activity limitation <bold>(Table 1)</bold>. <bold>Conclusions:</bold> Our data suggest that T2-inflammatory status could identify clinically meaningful profiles with different disease burden in asthma from the population-based perspective. T2-high asthma was more obstructive with higher reversibility, whereas T2-low inflammatory profile was more prone to daily life limitation and exacerbations. <fig><object-id>erj;64/suppl_68/PA1257/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>