Abstract
β2-Agonists are the most commonly prescribed asthma medication, and the β2-adrenergic receptor gene has been studied extensively. A single-nucleotide polymorphism causing the substitution of arginine (Arg) for glycine (Gly) at position 16 (Gly16Arg) of the β2-adrenergic receptor affects the response to β2-agonists. Regular exposure to β2-agonists results in down-regulation and uncoupling of β2-adrenoreceptors with associated subsensitivity or tachyphylaxis of response.1 Retrospective studies have reported an impaired therapeutic response in terms of peak expiratory flow in adults treated with long-acting β2-agonists (LABAs).
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