Effect of increased body mass index on asthma risk, impairment and response to asthma controller therapy in African Americans

Abstract

Objective:

To explore whether obesity alters the risk, impairment and response to treatment in African Americans with asthma.

Methods:

The data used for this secondary analysis are from a 1-year study in African American subjects comparing fluticasone propionate/salmeterol 100/50 µg combination (FSC) and fluticasone propionate 100 µg (FP). Subjects were retrospectively stratified by body mass index (BMI) <20 [underweight], 20–24.9 [normal weight], 25–29.9 [overweight], 30–34.9 [obese I], 35–39.9 [obese II], and ≥40 [obese III] kg/m². Outcomes studied included impairment domains: FEV₁, morning and evening peak expiratory flow (AM and PM PEF), daily albuterol use, daily symptom scores and future risk domain: exacerbations.

Clinical trial registration:

www.clinicaltrials.gov; NCT00102765

Results:

There were 475 subjects evenly distributed between FSC and FP by baseline parameters. There were 207 subjects with a BMI ≥30, including 70 subjects with a BMI ≥40. Baseline BMI ≥40 was associated with numerically lower baseline AM and PM PEF. There was an attenuation of response to both treatments for only PM PEF (p < 0.05). By contrast, subjects with lower degrees of obesity or overweight did not differ from those with normal weight. The total population exacerbation rate was 2-fold greater in obese III subjects (39%) compared with subjects in other BMI categories (16–21%) (p < 0.05). A potential study limitation is the retrospective analysis of existing data.

Discussion:

Response to treatment was attenuated for PM PEF for subjects with BMI ≥40 and was also associated with an increased rate of asthma exacerbations.

Key words::

• African American
• Asthma
• Body mass index
• Fluticasone propionate
• Salmeterol

Transparency

Declaration of funding

Funding for this research was provided by GlaxoSmithKline.

Declaration of financial/other relationships

C.A.C., E.R.S., W.B., and M.C. were involved with concept and design of the study, analysis and interpretation of the data, and critical review of the manuscript. D.A.S. and S.W.Y. were involved with concept and design of the study, analysis and interpretation of the data, and preparation and review of the manuscript. A.H.E. was involved with concept and design of the study, data generation and critical review of the manuscript.

C.A.C. has received financial support from a variety of groups for participation in conferences, consulting, and medical research; industry sponsors with an interest in asthma: AstraZeneca, Dey, Genentech, GSK, Merck, Novartis, Respironics, and Schering-Plough. E.R.S. serves as a consultant or advisor to Dey, GlaxoSmithKline and Schering-Plough and has research grants from Boehringer-Ingelheim, NIH and Novartis. W.B. has received research grants from Boehringer-Ingelheim and GlaxoSmithKline; consulted for AstraZeneca and GlaxoSmithKline; and is on the speakers’ bureaus of AstraZeneca, Boehringer-Ingelheim, GlaxoSmithKline, and Pfizer. M.C. has no conflicts to report. S.W.Y., A.H.E. and D.A.S. are employees of GlaxoSmithKline.

Peer reviewers may receive honoraria from CMRO for review work. Peer Reviewer 1 has disclosed that he/she is the recipient of research/grant funding from GSK and AstraZeneca and is a consultant/advisor to GSK, Sepracor, AstraZeneca and NovoNordisk. Peer Reviewer 2 has disclosed no relevant financial relationships.

Part of this work has been previously presented at the Annual Meeting of the American Academy of Allergy Asthma & Immunology; March 13–17, 2009, Washington, DC, USA