Body mass index and phenotype in subjects with mild-to-moderate persistent asthma

Received 9 February 2009; received in revised form 19 March 2009; accepted 1 April 2009.

Background

Although obesity has been hypothesized to worsen asthma, data from studies of subjects with well-characterized asthma are lacking.

Objective

We sought to evaluate the relationship between body mass index (BMI), asthma impairment, and response to therapy.

Methods

BMI (in kilograms per meter squared) and asthma phenotypic and treatment response data were extracted from Asthma Clinical Research Network studies. The cross-sectional relationship between BMI and asthma impairment was analyzed, as was the longitudinal relationship between BMI and response to asthma controller therapies.

Results

One thousand two hundred sixty-five subjects with mild-to-moderate persistent asthma were evaluated. Analyses of lean versus overweight/obese asthmatic subjects demonstrated small differences in FEV1 (3.05 vs 2.91 L, P = .001), FEV1/forced vital capacity ratio (mean, 83.5% vs 82.4%; P = .01), rescue albuterol use (1.1 vs 1.2 puffs per day, P = .03), and asthma-related quality of life (5.77 vs 5.59, P = .0004). Overweight/obese asthmatic subjects demonstrated a smaller improvement in exhaled nitric oxide levels with inhaled corticosteroid (ICS) treatment than did lean asthmatic subjects (3.6 vs 6.5 ppb, P = .04). With ICS/long-acting β-agonist treatment, overweight/obese asthmatic subjects demonstrated smaller improvements in lung function than lean asthmatic subjects, with an 80 mL (P = .04) and 1.7% (P = .02) lesser improvement in FEV1 and FEV1/forced vital capacity ratio, respectively. Significant differences in therapeutic response to leukotriene modifiers between BMI categories were not observed.

Conclusions

Increased BMI is not associated with clinically significant worsening of impairment in subjects with mild-to-moderate persistent asthma. There is a modest association between increased BMI and reduced therapeutic effect of ICS-containing regimens in this patient population. Prospective studies evaluating the effect of being overweight or obese on treatment response in asthma are warranted.

Key words: Asthma, obesity, treatment, severity

Abbreviations used: ACRN, Asthma Clinical Research Network, BAGS, The Addition of Regular-use to Intermittent Rescue β-Agonist for Patients with Mild Asthma, BARGE, β-Agonist Response by Genotype, BMI, Body mass index, DICE, Dose of Inhaled Corticosteroids with Equisystemic Effects, Feno, Fraction of exhaled nitric oxide, FEV1, Forced expiratory volume in one second, FVC, Forced vital capacity, ICS, Inhaled corticosteroid, IMPACT, Improving Asthma Control Trial, LABA, Long-acting β-agonist, MICE, Measuring Inhaled Corticosteroid Efficacy, PRICE, Predicting Responses for Inhaled Corticosteroid Efficacy, SLIC, Salmeterol with and without Inhaled Corticosteroids, SLIMSIT, Salmeterol and Leukotriene Modifiers Versus Salmeterol and ICS Treatment, SMOG, Smoking Modulates Outcomes of Glucocorticoid Therapy in Asthma, SOCS, Salmeterol off Corticosteroids

a National Jewish Health, Denver, Colo

b University of Colorado, Denver, Colo

c Department of Health Evaluation Sciences, Pennsylvania State University, Hershey, Pa

d Section of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Wisconsin Sleep Institute, University of Wisconsin School of Medicine and Public Health, Madison, Wis

e Medical Service and The Sleep Center, William S. Middleton Memorial Veteran's Hospital, Madison, Wis

f Brigham and Women's Hospital, Boston, Mass

g Harvard Medical School, Boston, Mass

Reprint requests: E. Rand Sutherland, MD, MPH, National Jewish Health, 1400 Jackson St, J-201, Denver, CO 80206.

Supported by National Institutes of Health grants (U10) HL51831, HL51845, HL51823, HL51843, HL56443, HL51834, HL51810, HL74227, HL74231, HL074204, HL74212, HL74073, HL074206, HL074208, HL74225, and HL74218.

Disclosure of potential conflict of interest: E. R. Sutherland is on advisory boards for GlaxoSmithKline, and Dey; is a Data and Safety Monitoring Board member for Schering-Plough; and received grant support from the National Institutes of Health, Novartis and Dey. M. Teodorescu received grant support from the University of Wisconsin School of Medicine and Public Health. M. E. Wechsler is a consultant for AstraZeneca, Schering-Plough, Novartis, GlaxoSmithKline, Merck, and Genentech; is on the advisory board for AstraZeneca, Schering-Plough, Novartis, GlaxoSmithKline, Merck, and Genentech; is on the speakers' bureau for AstraZeneca, Novartis, GlaxoSmithKline, Merck, and Genentech; and receives grant support from Asthmatx, GlaxoSmithKline, and the National Institutes of Health. The rest of the authors have declared that they have no conflict of interest.

∗ A list of participating Asthma Clinical Research Network investigators is available in Appendix E1 in this article's Online Repository at www.jacionline.org.

PII: S0091-6749(09)00557-0

doi:10.1016/j.jaci.2009.04.005

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