Chest
Volume 140, Issue 3, September 2011, Pages 659-666
Journal home page for Chest

Original Research
Asthma
Obesity Is a Determinant of Asthma Control Independent of Inflammation and Lung Mechanics

https://doi.org/10.1378/chest.11-0027Get rights and content

Background

It is unclear why obesity is associated with worse asthma control. We hypothesized that (1) obesity affects asthma control independent of spirometry, airway inflammation, and airway hyperresponsiveness (AHR) and (2) residual symptoms after resolution of inflammation are due to obesity-related changes in lung mechanics.

Methods

Forty-nine subjects with asthma underwent the following tests, before and after 3 months of high-dose inhaled corticosteroid (ICS) treatment: five-item asthma control questionnaire (ACQ-5), spirometry, fraction of exhaled nitric oxide (Feno), methacholine challenge, and the forced oscillation technique, which allows for the calculation of respiratory system resistance (Rrs) and respiratory system reactance (Xrs) as indicators of airway caliber and elastic load, respectively. The effects of treatment were assessed by BMI group (18.5-24.9, 25-29.9, and ≥ 30 kg/m2) using analysis of variance. Multiple regression analyses determined the independent predictors of ACQ-5 results.

Results

At baseline, the independent predictors of ACQ-5 results were FEV1, Feno, and BMI (model r2 = 0.38, P < .001). After treatment, asthma control, spirometry, airway inflammation, and AHR improved similarly across BMI groups. The independent predictors of ACQ-5 results after treatment were Rrs and BMI (model r2 = 0.42, P < .001).

Conclusions

BMI is a determinant of asthma control independent of airway inflammation, lung function, and AHR. After ICS treatment, BMI again predicts ACQ-5 results, but independent of obesity-related changes in lung mechanics.

Section snippets

Subject Characteristics

Adult subjects were recruited from a volunteer's database at The Woolcock Institute of Medical Research by advertising throughout the University of Sydney and by referrals from local respiratory practices. Subjects were eligible if they had a physician diagnosis of asthma and AHR to methacholine, no current smoking (< 10 pack-year smoking history and no smoking within the last 6 months), no chest infections, no antibiotic or oral prednisone use in the previous 4 weeks, and no lung disease other

Before Treatment

Baseline demographics and lung function test results for 49 subjects with asthma are shown in Table 1, according to BMI groups. Subjects were relatively young adults (range 24-51 years). The mean disease duration was 26 years (23-29 years), with no significant difference between BMI groups. There was only one subject who was nonatopic and obese. Subjects who were obese and had asthma tended to be older, had worse FEV1, and had more severe AHR, despite higher use of ICS compared with subjects of

Discussion

The results of this study indicate that obesity is a determinant of asthma control that is independent of airway inflammation, lung function, and AHR. After high-dose inhaled antiinflammatory treatment, obesity and airway caliber remained as independent predictors of asthma control. The effect of obesity on asthma control was similar before and after treatment. However, obesity accounted for the majority of the residual symptoms after treating the steroid-responsive airway abnormalities typical

Acknowledgments

Author contributions: Dr Farah is the guarantor of the manuscript.

Dr Farah: contributed to the study design, data analysis, data interpretation, and writing of the manuscript.

Ms Kermode: contributed to the data collection, data analysis, data interpretation, and writing of the manuscript.

Dr Downie: contributed to the data collection, data analysis, data interpretation, and writing of the manuscript.

Dr Brown: contributed to the data analysis, data interpretation, and writing of the manuscript.

Ms

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    Funding/Support: This study was supported by research grants from the National Health and Medical Research Council of Australia and the Cooperative Research Centre for Asthma and Airways.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).

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