Purpose of review
A variety of novel asthma treatments have been developed based on phenotypes, and the clinical trial results show promising responses. This review summarizes the current knowledge of biomarkers for the determination of asthma phenotypes.
Eosinophilic inflammation is the most focused phenotype because most novel asthma treatments have targeted T-helper type 2 (Th2) pathway. Fractional-exhaled nitric oxide (FeNO) is a new method that represents an eosinophilic airway inflammation with a significant correlation with sputum eosinophilia and asthma severity instead of sputum eosinophil count that easily influenced by corticosteroid therapy. However, some reports indicated the discordance between treatment response or adjustment and FeNO levels. Serum periostin is a strong serum biomarker for eosinophilic airway inflammation and an indicator of Th2-targeted therapy (such as lebrikizumab or omalizumab) and airflow limitation. YKL-40 is associated with asthma severity and airway remodeling. In addition, genetic and metabolomic approaches have been made to determine asthma phenotypes and severity.
Biomarkers such as FeNO and serum periostin represent eosinophilic airway inflammation, together with eosinophil-derived neurotoxin and osteopontin (OPN) needed more replication studies. Periostin, YKL-40, OPN and some metabolites (choline, arginine, acetone and protectin D1) are related to asthma severity and airflow limitation.