Childhood asthma phenotypes and endotypes: a glance into the mosaic

Molecular and Cellular Pediatrics

Table 1 Overview of clinical phenotypes in asthmatic children associated with cluster analyses and inflammatory endotypes

Analyzed asthmapopulation	Clinical phenotypes using hypothesis-driven methods	Clinical phenotypes based on clustering methods	Inflammatory endotypes
Severe asthmatics (poor response to ICS)	Severe treatment-resistant asthma (STRA): Poor ICS response independent of modifiable factors [15]	SARP cohort: Four clusters (three atopic, one non-atopic) with differences in asthma onset and lung function [8] TENOR cohort: Five clusters (four atopic, one non-atopic) with differences in gender, ethnicity, and lung function [49]	T2-high (eosinophilic) [56] Eosinophilic non-T2-high [57, 58] Neutrophilic [59, 60] Paucigranulocytic [61] Mixed granulocytic [62]
Severe asthmatics (poor response to ICS)	Difficult-to-treat asthma: Poor response to ICS due to modifiable factors [15]
Mild, intermediate, and severe asthmatics	Allergic asthma: Presence of atopy and T2 biomarkers (e.g., FeNO) [40]	APIC cohort: Five clusters (three atopic and two non-atopic) with differences in lung function [14] CAMP trial: Five clusters (three atopic and two non-atopic) with differences in exacerbation rates, lung function, and response to treatment [10] KAS study: Four clusters (three atopic and one non-atopic) [54]	T2-high (eosinophilic) [63,64,65] Only eosinophilic (based on data from blood) [63] Paucigranulocytic (based on data from blood) [63]
Mild, intermediate, and severe asthmatics	Nonallergic asthma: Not associated with atopy [11]