Meghan E McGarry1, Elizabeth Castellanos2, Neeta Thakur3, Sam S Oh4, Celeste Eng3, Adam Davis5, Kelley Meade5, Michael A LeNoir6, Pedro C Avila7, Harold J Farber8, Denise Serebrisky9, Emerita Brigino-Buenaventura10, William Rodriguez-Cintron11, Rajesh Kumar12, Kirsten Bibbins-Domingo13, Shannon M Thyne14, Saunak Sen15, Jose R Rodriguez-Santana16, Luisa N Borrell17, Esteban G Burchard4. 1. Department of Pediatrics, University of California, San Francisco, CA. Electronic address: DrMeghanMcGarry@gmail.com. 2. Department of Bioengineering and Therapeutic Sciences, University of California, San Francisco, CA. 3. Department of Medicine, University of California, San Francisco, CA. 4. Department of Bioengineering and Therapeutic Sciences, University of California, San Francisco, CA; Department of Medicine, University of California, San Francisco, CA. 5. Children's Hospital and Research Center Oakland, Oakland, CA. 6. Bay Area Pediatrics, Oakland, CA. 7. Department of Allergy-Immunology, Northwestern University, Chicago, IL. 8. Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine and Texas Children's Hospital, Houston, TX. 9. Pediatric Pulmonary Division, Jacobi Medical Center, Bronx, NY. 10. Department of Allergy and Immunology, Kaiser Permanente-Vallejo Medical Center, Vallejo, CA. 11. Veterans Caribbean Health Care System, San Juan, Puerto Rico. 12. Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, IL. 13. San Francisco General Hospital, San Francisco, CA. 14. Department of Pediatrics, University of California, San Francisco, CA. 15. Department of Bioengineering and Therapeutic Sciences, University of California, San Francisco, CA; Department of Epidemiology and Biostatistics, University of California, San Francisco, CA. 16. Centro de Neumología Pediátrica, San Juan, Puerto Rico. 17. Department of Health Sciences, Lehman College, City University of New York, Bronx, NY.
Abstract
BACKGROUND: Obesity is associated with poor asthma control, increased asthma morbidity, and decreased response to inhaled corticosteroids. We hypothesized that obesity would be associated with decreased bronchodilator responsiveness in children and adolescents with asthma. In addition, we hypothesized that subjects who were obese and unresponsive to bronchodilator would have worse asthma control and would require more asthma controller medications. METHODS: In the Study of African Americans, Asthma, Genes, and Environments (SAGE II) and the Genes-environments and Admixture in Latino Americans (GALA II) study, two identical, parallel, case-control studies of asthma, we examined the association between obesity and bronchodilator response in 2,963 black and Latino subjects enrolled from 2008 to 2013 using multivariable logistic regression. Using bronchodilator responsiveness, we compared asthma symptoms, controller medication usage, and asthma exacerbations between nonobese (< 95th% BMI) and obese (≥ 95th% BMI) subjects. RESULTS: The odds of being bronchodilator unresponsive were 24% (OR, 1.24; 95% CI, 1.03-1.49) higher among obese children and adolescents compared with their not obese counterparts after adjustment for age, race/ethnicity, sex, recruitment site, baseline lung function (FEV1/FVC), and controller medication. Bronchodilator-unresponsive obese subjects were more likely to report wheezing (OR, 1.38; 95% CI, 1.13-1.70), being awakened at night (OR, 1.34; 95% CI, 1.09-1.65), using leukotriene receptor inhibitors (OR, 1.33; 95% CI, 1.05-1.70), and using inhaled corticosteroid with long-acting β2-agonist (OR, 1.37; 95% CI, 1.05-1.78) than were their nonobese counterpart. These associations were not seen in the bronchodilator-responsive group. CONCLUSIONS: Obesity is associated with bronchodilator unresponsiveness among black and Latino children and adolescents with asthma. The findings on obesity and bronchodilator unresponsiveness represent a unique opportunity to identify factors affecting asthma control in blacks and Latinos.
BACKGROUND:Obesity is associated with poor asthma control, increased asthma morbidity, and decreased response to inhaled corticosteroids. We hypothesized that obesity would be associated with decreased bronchodilator responsiveness in children and adolescents with asthma. In addition, we hypothesized that subjects who were obese and unresponsive to bronchodilator would have worse asthma control and would require more asthma controller medications. METHODS: In the Study of African Americans, Asthma, Genes, and Environments (SAGE II) and the Genes-environments and Admixture in Latino Americans (GALA II) study, two identical, parallel, case-control studies of asthma, we examined the association between obesity and bronchodilator response in 2,963 black and Latino subjects enrolled from 2008 to 2013 using multivariable logistic regression. Using bronchodilator responsiveness, we compared asthma symptoms, controller medication usage, and asthma exacerbations between nonobese (< 95th% BMI) and obese (≥ 95th% BMI) subjects. RESULTS: The odds of being bronchodilator unresponsive were 24% (OR, 1.24; 95% CI, 1.03-1.49) higher among obesechildren and adolescents compared with their not obese counterparts after adjustment for age, race/ethnicity, sex, recruitment site, baseline lung function (FEV1/FVC), and controller medication. Bronchodilator-unresponsive obese subjects were more likely to report wheezing (OR, 1.38; 95% CI, 1.13-1.70), being awakened at night (OR, 1.34; 95% CI, 1.09-1.65), using leukotriene receptor inhibitors (OR, 1.33; 95% CI, 1.05-1.70), and using inhaled corticosteroid with long-acting β2-agonist (OR, 1.37; 95% CI, 1.05-1.78) than were their nonobese counterpart. These associations were not seen in the bronchodilator-responsive group. CONCLUSIONS:Obesity is associated with bronchodilator unresponsiveness among black and Latino children and adolescents with asthma. The findings on obesity and bronchodilator unresponsiveness represent a unique opportunity to identify factors affecting asthma control in blacks and Latinos.
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