Nicole L Grossman1, Victor E Ortega2, Tonya S King3, Eugene R Bleecker4, Elizabeth A Ampleford5, Leonard B Bacharier6, Michael D Cabana7, Juan C Cardet8, Tara F Carr9, Mario Castro10, Loren C Denlinger11, Joshua L Denson12, Nicolas Fandino13, Anne M Fitzpatrick14, Gregory A Hawkins15, Fernando Holguin16, Jerry A Krishnan17, Stephen C Lazarus18, Sharmilee M Nyenhuis17, Wanda Phipatanakul19, Sima K Ramratnam20, Sally Wenzel21, Stephen P Peters5, Deborah A Meyers4, Michael E Wechsler12, Elliot Israel13. 1. Department of Internal Medicine, Division of Pulmonary and Critical Care, Lahey Hospital and Medical Center, Burlington, Mass. 2. Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC. Electronic address: vortega@wakehealth.edu. 3. Department of Public Health Sciences, Pennsylvania State University School of Medicine, Hershey, Pa. 4. Department of Medicine, Division of Genetics, Genomics, and Precision Medicine, University of Arizona College of Medicine, Tucson, Ariz. 5. Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC. 6. Department of Pediatrics, Division of Allergy, Immunology, and Pulmonary Medicine, Washington University School of Medicine, St Louis, Mo. 7. Department of Pediatrics, University of California San Francisco, San Francisco, Calif. 8. Deparment of Internal Medicine, Divison of Allergy and Immunology, Morsani College of Medicine, University of South Florida, Tampa, Fla. 9. Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, University of Arizona, Tucson, AZ. 10. Department of Internal Medicine, Division of Pulmonary Diseases and Critical Care Medicine, University of Kansas, Kansas City, Kan. 11. Department of Medicine, University of Wisconsin School of Medicine, Madison, Wis. 12. Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, Colo. 13. Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass. 14. Department of Pediatrics, Emory University, Atlanta, Ga. 15. Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC. 16. Department of Medicine, University of Colorado Anschutz Medical Campus, Denver, Colo. 17. Department of Medicine, University of Illinois Hospital & Health Sciences System, Chicago, Ill. 18. Department of Medicine, University of California San Francisco, San Francisco, Calif. 19. Division of Pediatric Allergy and Immunology, Boston Children's Hospital, Harvard Medical School, Boston, Mass. 20. Department of Pediatrics, University of Wisconsin School of Medicine, Madison, Wis. 21. Department of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pa.
Abstract
BACKGROUND: Minority groups of African descent experience disproportionately greater asthma morbidity compared with other racial groups, suggesting that genetic variation from a common ancestry could influence exacerbation risk. OBJECTIVE: We evaluated clinical trial measures in the context of self-reported race and genetic ancestry to identify risk factors for asthma exacerbations. METHODS:One thousand eight hundred forty multiethnic subjects from 12 Asthma Clinical Research Network and AsthmaNet trials were analyzed for incident asthma exacerbations with Poisson regression models that included clinical measures, self-reported race (black, non-Hispanic white, and other), and estimates of global genetic African ancestry in a subgroup (n = 760). RESULTS:Twenty-four percent of 1840 subjects self-identified as black. Black and white subjects had common risk factors for exacerbations, including a history of 2 or more exacerbations in the previous year and FEV1 percent predicted values, whereas chronic sinusitis, allergic rhinitis, and gastroesophageal reflux disease were only associated with increased exacerbation risk in black subjects. In the combined multiethnic cohort, neither race (P = .30) nor percentage of genetic African ancestry as a continuous variable associated with exacerbation risk (adjusted rate ratio [RR], 1.26 [95% CI, 0.94-1.70; P = .13]; RR per 1-SD change [32% ancestry], 0.97 [95% CI, 0.78-1.19; P = .74]). However, in 161 black subjects with genetic data, those with African ancestry greater than the median (≥82%) had a significantly greater risk of exacerbation (RR, 3.06 [95% CI, 1.09-8.6; P = .03]). CONCLUSION:Black subjects have unique risk factors for asthma exacerbations, of which global African genetic ancestry had the strongest effect.
RCT Entities:
BACKGROUND: Minority groups of African descent experience disproportionately greater asthma morbidity compared with other racial groups, suggesting that genetic variation from a common ancestry could influence exacerbation risk. OBJECTIVE: We evaluated clinical trial measures in the context of self-reported race and genetic ancestry to identify risk factors for asthma exacerbations. METHODS: One thousand eight hundred forty multiethnic subjects from 12 Asthma Clinical Research Network and AsthmaNet trials were analyzed for incident asthma exacerbations with Poisson regression models that included clinical measures, self-reported race (black, non-Hispanic white, and other), and estimates of global genetic African ancestry in a subgroup (n = 760). RESULTS: Twenty-four percent of 1840 subjects self-identified as black. Black and white subjects had common risk factors for exacerbations, including a history of 2 or more exacerbations in the previous year and FEV1 percent predicted values, whereas chronic sinusitis, allergic rhinitis, and gastroesophageal reflux disease were only associated with increased exacerbation risk in black subjects. In the combined multiethnic cohort, neither race (P = .30) nor percentage of genetic African ancestry as a continuous variable associated with exacerbation risk (adjusted rate ratio [RR], 1.26 [95% CI, 0.94-1.70; P = .13]; RR per 1-SD change [32% ancestry], 0.97 [95% CI, 0.78-1.19; P = .74]). However, in 161 black subjects with genetic data, those with African ancestry greater than the median (≥82%) had a significantly greater risk of exacerbation (RR, 3.06 [95% CI, 1.09-8.6; P = .03]). CONCLUSION: Black subjects have unique risk factors for asthma exacerbations, of which global African genetic ancestry had the strongest effect.
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