Type 2-high airway inflammation in childhood asthma distinguishes a more severe phenotype

Abstract

<b>Rationale:</b> There is a limited number of biomarkers to identify different phenotypes in childhood asthma, most reflecting type 2-inflammation. It is largely unknown whether such phenotyping can distinguish disease persistency and trajectories. <b>Method:</b> We included 338 children from the COPSAC₂₀₀₀ at-risk mother-child cohort. Asthma was diagnosed continuously during the whole follow-up period. Specific airway resistance (sRaw) was measured at every visit from age 3. T2-high vs. T2-low asthma was defined at age 7 as asthma with vs. without aeroallergen sensitization (≥ 0.35 kU_A/L) and/or fractional exhaled nitric oxide ≥ 20 ppb and/or blood eosinophil count ≥ 0.5 x 10⁹/L. Differences in lung function trajectories and persistent asthma by age 18 was analysed using linear mixed models and odds-ratio. <b>Results:</b> At age 7, 50 children had asthma including 26 children with T2-high and 24 with T2-low asthma. Of children with T2-high asthma, 12 (46.2 %) had persistent asthma as compared to 4 (16.7 %) with T2-low; OR=4.29 [1.14–16.1]; p=0.031. For T2-high vs. T2-low asthma, the median age of onset was 3.6 and 1.8 respectively (p=0.004) and mean duration of asthma was 9.91 vs. 5.86 years respectively (p=0.07). sRaw was 18 % higher through childhood in children with T2-high compared to T2-low asthma, Figure 1. <b>Conclusion:</b> The T2-high pediatric asthma phenotype has higher persistency and worse long-term lung function compared to T2-low.