Copyright ©The Author(s) 2015.
World J Clin Pediatr. May 8, 2015; 4(2): 13-18
Published online May 8, 2015. doi: 10.5409/wjcp.v4.i2.13
Table 1 Examples of proposed clinical phenotypes
Clinical levelClinical characteristicsBiological levelMolecular levelTherapeutic level
Xie et al[2]Exercise induced asthmaMild asthma and reactive bronchospasm in response to sustained exerciseMast-cell activation; Th2 cytokines; cysteinyl leukotrienesResponsive to cysteinyl leukotriene modifiers, beta agonists and antibody to IL-9
Obesity asthma phenotypeAdult onset Mostly females Severe symptomsLack of Th2 biomarkers; oxidative stress ADMAResponsive to weight loss, antioxidants and possibly to hormonal therapy
Early-onset Allergic asthma> 3 episodes per year Mild, moderate, or severe Family history of asthmaSpecific IgE; Th2 cytokines; thick SBM17q12; Th2-related genesCorticosteroid-responsive; Th2-targeted
Late-onset Eosinophic asthmaAdult onset Often severe Sinus diseaseIncreased both peripheral eosinophils and IL-5Responsive to antibody to IL-5 and cysteinyl leukotriene modifiers; corticosteroid-refractory
Zedan et al[8]Shortness of breath phenotype> 10 yr No sex predominance Longer disease duration Negative family history of asthmaIncreased total serum IgEHigher prevalence of TT genotype of SNP IL-4C 590T (Zedan et al[18])Responsive to fluticasone alone
Cough phenotype< 10 yr Female predominance Shorter disease duration Positive family history of asthmaIncreased both peripheral eosinophis and sECPResponsive to montelukast alone
Wheezy phenotypeIncrease in peripheral eosinophilis and sECPResponsive to both fluticasone and montelukast