Abstract
Oral corticosteroids are the cornerstone of management of acute moderate or severe asthma whilst preventive inhaled corticosteroids are the mainstay of the preventive management of children with asthma. Yet, variation in the magnitude of response to corticosteroids has been observed. There is increasing evidence that preschool-aged children with viral-induced asthma may display a certain degree of corticosteroid resistance, requiring higher doses of corticosteroids to overcome it. The identification of determinants of responsiveness is complicated by design issues, including heterogeneous populations of children with asthma and bronchiolitis or of children with viral-induced and multi-trigger asthma phenotypes in published trials. Potential key determinants of responsiveness may include age, trigger, phenotype, tobacco smoke exposure and genotype. The mechanistic pathway for corticoresistance may originate from a gene-environment interaction, leading to non-eosinophilic airway inflammation. The clinician should carefully confirm the diagnosis of asthma and ascertain the phenotype to select appropriate phenotype-specific therapy.