Clinical Asthma Phenotypes and Therapeutic Responses

Asthma is a heterogeneous disease that means not all asthmatics respond to the same treatment. We hypothesize an approach to characterize asthma phenotypes based on symptomatology (shortness of breath (SOB), cough, and wheezy phenotypes) in correlation with airway inflammatory biomarkers and FEV1. We aimed to detect whether those clinical phenotypes have an impact on the response to asthma medications. Two hundred three asthmatic children were allocated randomly to receive either montelukast (5？mg at bed time) or fluticasone propionate (100？ug twice daily) for 8 consecutive weeks. Serum concentrations of IL-2Rs, ICAM-1, VCAM-1, total IgE, eosinophilic %, eosinophil cationic protein (ECP), and FEV1 were done before and after treatment to patients and once to controls. Children who have SOB were found to have higher levels of total sIgE, older age, and longer disease duration, and they responded to fluticasone alone. Cough group was found to have higher levels of eosinophilic % and sECP, younger age, shorter disease duration and responded to montelukast alone. Wheezy group showed mixed pattern and responded to both medications. Conclusion. Although there is variability in response to ICS and LTRAs, we did identify characteristics of patient that should guide the clinician in the choice of asthma medications. 1. Introduction Evidence is increasing that asthma is a heterogeneous disease constituted by overlapping separate syndromes with probably different, but yet undefined, causes and natural histories. There is a need to identify each of these groups of patients (the so-called asthma phenotypes), whose clinical and prognostic characteristics and responses to treatment may be heterogeneous between groups and homogeneous within each group [1]. All asthmatics, by definition, share a common physiologic abnormalities of reversible airflow obstruction detected by spirometry, airway hyperreactivity, and symptoms that can include shortness of breath, wheezes, and cough. Despite these shared features, a great heterogeneity was noticed in the severity of airway obstruction, clinical phenotypes, degree of reversibility, and the amount of improvement in response to asthma medicines [2]. These phenotypes include allergic and nonallergic asthma. Other phenotypes defined by clinical or physiological categories (i.e., severity, age at onset, and chronic airway obstruction), by asthma triggers (i.e., viral, exercise, occupational allergens, or irritants), by their pathobiology (i.e., eosinophilic, neutrophilic, and paucigranulocytic asthma), or by their course (i.e.,