Rationale: One-quarter to one-third of individuals with asthma smoke, which may affect response to therapy and contribute to poor asthma control. Objectives: To determine if the response to an inhaled corticosteroid or a leukotriene receptor antagonist is attenuated in individuals with asthma who smoke. Methods: In a multicenter, placebo-controlled, double-blind, doubledummy, crossover trial, 44 nonsmokers and 39 light smokers with mild asthma were assigned randomly to treatment twice daily with inhaled beclomethasone and once daily with oral montelukast. Measurements and Main Results: Primary outcome was change in prebronchodilator FEV 1 in smokers versus nonsmokers. Secondary outcomes included peak flow, PC 20 methacholine, symptoms, quality of life, and markers of airway inflammation. Despite similar FEV 1 , bronchodilator response, and sensitivity to methacholine at baseline, subjects with asthma who smoked had significantly more symptoms, worse quality of life, and lower daily peak flow than nonsmokers. Adherence to therapy did not differ significantly between smokers and nonsmokers, or between treatment arms. Beclomethasone significantly reduced sputum eosinophils and eosinophil cationic protein (ECP) in both smokers and nonsmokers, but increased FEV 1 (170 ml, p ϭ 0.0003) only in nonsmokers. Montelukast significantly increased A.M. peak flow in smokers (12.6 L/min, p ϭ 0.002), but not in nonsmokers. Conclusions: In subjects with mild asthma who smoke, the response to inhaled corticosteroids is attenuated, suggesting that adjustments to standard therapy may be required to attain asthma control. The greater improvement seen in some outcomes in smokers treated with montelukast suggests that leukotrienes may be important in this setting. Larger prospective studies are required to determine whether leukotriene modifiers can be recommended for managing asthma in patients who smoke.

It may be possible to treat mild persistent asthma with short, intermittent courses of inhaled or oral corticosteroids taken when symptoms worsen. Further studies are required to determine whether this novel approach to treatment should be recommended.

Rationale: Several studies suggest that patients with asthma who are homozygous for arginine at the 16th position of the ␤ 2 -adrenergic receptor may not benefit from short-acting ␤-agonists. Objectives: We investigated whether such genotype-specific effects occur when patients are treated with long-acting ␤-agonists and whether such effects are modified by concurrent inhaled corticosteroid (ICS) use. Methods: We compared salmeterol response in patients with asthma homozygous for arginine at B16 (B16Arg/Arg) with those homozygous for glycine at B16 (B16Gly/Gly) in two separate cohorts. In the first, subjects were randomized to regular therapy with salmeterol while simultaneously discontinuing ICS therapy. In the second, subjects were randomized to regular therapy with salmeterol while continuing concomitant ICS. Results: In both trials, B16Arg/Arg subjects did not benefit compared with B16Gly/Gly subjects after salmeterol was initiated. In the first cohort, compared with placebo, the addition of salmeterol was associated with a 51.4 L/min lower A.M. peak expiratory flow (PEF; p ϭ 0.005) in B16Arg/Arg subjects(salmeterol, n ϭ 12; placebo, n ϭ 5) as compared with B16Gly/Gly subjects (salmeterol, n ϭ 13; placebo, n ϭ 13). In the second cohort, B16Arg/Arg subjects treated with salmeterol and ICS concurrently (n ϭ 8

Background-Although guidelines recommend anti-inflammatory therapy for persistent asthma, recent studies suggest that 25-35% of asthmatics may not improve lung function with inhaled corticosteroids.

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