Meta Description: Asthma treatment is effective in many children, there is large variability in the response as evidenced by improved symptom control, reduced exacerbations and lung function improvement.
Asthma treatment is effective in many children, there is large variability in the response as evidenced by improved symptom control, reduced exacerbations and lung function improvement. One mechanism for heterogeneity in treatment response seems likely to be due to genetic variations within the asthma population. These genetic variants may be due to either innate difference in underlying disease subtype all manifesting clinically as asthma or to pharmacokinetic or pharmacodynamics influences on drug level or target.
Candidate gene approaches to a lesser extent, whole-genome association studies have identified several genetic loci associated with poor treatment response or severe asthma, including FCER2 (coding for a low-affinity immunoglobin E (IgE) receptor, also known as CD23), the 17q21 locus, and GLCCI1 (encoding glucocorticoid-induced transcript 1 protein). This might have implications for the treatment of asthma and suggests that we should move to a personalized (or stratified) approach guided by both clinical and genetic cues (i.e. pharmacogenetics) to benefit children with asthma. The benefits would be in terms of improvement of both drug efficacy and also drug safety of existing drugs.
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