Clinical asthma phenotyping: A trial for bridging gaps in asthma management

Table 1 Examples of proposed clinical phenotypes

	Clinical level	Clinical characteristics	Biological level	Molecular level	Therapeutic level
Xie et al[2]	Exercise induced asthma	Mild asthma and reactive bronchospasm in response to sustained exercise	Mast-cell activation; Th2 cytokines; cysteinyl leukotrienes		Responsive to cysteinyl leukotriene modifiers, beta agonists and antibody to IL-9
	Obesity asthma phenotype	Adult onset Mostly females Severe symptoms	Lack of Th2 biomarkers; oxidative stress ADMA		Responsive to weight loss, antioxidants and possibly to hormonal therapy
	Early-onset Allergic asthma	> 3 episodes per year Mild, moderate, or severe Family history of asthma	Specific IgE; Th2 cytokines; thick SBM	17q12; Th2-related genes	Corticosteroid-responsive; Th2-targeted
	Late-onset Eosinophic asthma	Adult onset Often severe Sinus disease	Increased both peripheral eosinophils and IL-5		Responsive 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 asthma	Increased total serum IgE	Higher 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 asthma	Increased both peripheral eosinophis and sECP		Responsive to montelukast alone
	Wheezy phenotype		Increase in peripheral eosinophilis and sECP		Responsive to both fluticasone and montelukast

ADMA: Asymmetric dimethyl arginine; SBM: Subepithelial basement membrane; SNP: Single nucleotide polymorphism; sECP: Serum eosinophilic cationic protein; IL: Interleukin; Th2: T helper type 2.