Sharmilee M Nyenhuis1, Jerry A Krishnan2, Alalia Berry3, William J Calhoun4, Vernon M Chinchilli5, Linda Engle5, Nicole Grossman6, Fernando Holguin7, Elliot Israel6, Rick A Kittles8, Monica Kraft8, Stephen C Lazarus9, Erik B Lehman5, David T Mauger5, James N Moy10, Stephen P Peters11, Wanda Phipatanakul12, Lewis J Smith13, Kaharu Sumino14, Stanley J Szefler15, Michael E Wechsler16, Sally Wenzel7, Steven R White17, Steven J Ackerman18. 1. Department of Medicine, University of Illinois at Chicago, Chicago, Ill; University of Illinois Hospital & Health Sciences System, Chicago, Ill. Electronic address: snyenhui@uic.edu. 2. Department of Medicine, University of Illinois at Chicago, Chicago, Ill; University of Illinois Hospital & Health Sciences System, Chicago, Ill. 3. Division of Allergy, Pulmonary and Critical Care, Department of Medicine, the University of Wisconsin School of Medicine and Public Health, University of Wisconsin, Madison, Wis. 4. Division of Pulmonary Critical Care & Sleep Medicine, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Tex. 5. Department of Public Health Sciences, Pennsylvania State University, Hershey, Pa. 6. Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Mass. 7. Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pa. 8. University of Arizona College of Medicine, Tucson, Ariz. 9. Division of Pulmonary and Critical Care, Department of Medicine, University of California, San Francisco, Calif. 10. Stroger Hospital of Cook County, Chicago, Ill. 11. Division of Pulmonary, Critical Care, Allergy and Immunologic Diseases, Department of Medicine, Wake Forest School of Medicine, Winston-Salem, NC. 12. Division of Allergy and Immunology, Department of Pediatrics, Boston Children's Hospital, Boston, Mass. 13. Division of Pulmonary and Critical Care, Department of Medicine Northwestern University, Feinberg School of Medicine, Chicago, Ill. 14. Division of Pulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St Louis, Mo. 15. Division of Pulmonary Medicine, Department of Pediatrics, Children's Hospital of Colorado, Aurora, Colo. 16. Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Mass; Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colo. 17. Division of Pulmonary/Critical Care, Department of Medicine, University of Chicago, Chicago, Ill. 18. Department of Medicine, University of Illinois at Chicago, Chicago, Ill.
Abstract
BACKGROUND: African American subjects have a greater burden from asthma compared with white subjects. Whether the pattern of airway inflammation differs between African American and white subjects is unclear. OBJECTIVE: We sought to compare sputum airway inflammatory phenotypes of African American and white subjects treated or not with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively). METHODS: We performed a secondary analysis of self-identified African American and white subjects with asthma enrolled in clinical trials conducted by the National Heart, Lung, and Blood Institute-sponsored Asthma Clinical Research Network and AsthmaNet. Demographics, clinical characteristics, and sputum cytology after sputum induction were examined. We used a sputum eosinophil 2% cut point to define subjects with either an eosinophilic (≥2%) or noneosinophilic (<2%) inflammatory phenotype. RESULTS: Among 1018 participants, African American subjects (n = 264) had a lower FEV1 percent predicted (80% vs 85%, P < .01), greater total IgE levels (197 vs 120 IU/mL, P < .01), and a greater proportion with uncontrolled asthma (43% vs 28%, P < .01) compared with white subjects (n = 754). There were 922 subjects in the ICS+ group (248 African American and 674 white subjects) and 298 subjects in the ICS- group (49 African American and 249 white subjects). Eosinophilic airway inflammation was not significantly different between African American and white subjects in either group (percentage with eosinophilic phenotype: ICS+ group: 19% vs 16%, P = .28; ICS- group: 39% vs 35%, P = .65; respectively). However, when adjusted for confounding factors, African American subjects were more likely to exhibit eosinophilic airway inflammation than white subjects in the ICS+ group (odds ratio, 1.58; 95% CI, 1.01-2.48; P = .046) but not in the ICS- group (P = .984). CONCLUSION: African American subjects exhibit greater eosinophilic airway inflammation, which might explain the greater asthma burden in this population. Published by Elsevier Inc.
BACKGROUND: African American subjects have a greater burden from asthma compared with white subjects. Whether the pattern of airway inflammation differs between African American and white subjects is unclear. OBJECTIVE: We sought to compare sputum airway inflammatory phenotypes of African American and white subjects treated or not with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively). METHODS: We performed a secondary analysis of self-identified African American and white subjects with asthma enrolled in clinical trials conducted by the National Heart, Lung, and Blood Institute-sponsored Asthma Clinical Research Network and AsthmaNet. Demographics, clinical characteristics, and sputum cytology after sputum induction were examined. We used a sputum eosinophil 2% cut point to define subjects with either an eosinophilic (≥2%) or noneosinophilic (<2%) inflammatory phenotype. RESULTS: Among 1018 participants, African American subjects (n = 264) had a lower FEV1 percent predicted (80% vs 85%, P < .01), greater total IgE levels (197 vs 120 IU/mL, P < .01), and a greater proportion with uncontrolled asthma (43% vs 28%, P < .01) compared with white subjects (n = 754). There were 922 subjects in the ICS+ group (248 African American and 674 white subjects) and 298 subjects in the ICS- group (49 African American and 249 white subjects). Eosinophilic airway inflammation was not significantly different between African American and white subjects in either group (percentage with eosinophilic phenotype: ICS+ group: 19% vs 16%, P = .28; ICS- group: 39% vs 35%, P = .65; respectively). However, when adjusted for confounding factors, African American subjects were more likely to exhibit eosinophilic airway inflammation than white subjects in the ICS+ group (odds ratio, 1.58; 95% CI, 1.01-2.48; P = .046) but not in the ICS- group (P = .984). CONCLUSION: African American subjects exhibit greater eosinophilic airway inflammation, which might explain the greater asthma burden in this population. Published by Elsevier Inc.
Entities:
Keywords:
African American; Asthma; airway inflammation; body mass index; clinical trial; corticosteroid; eosinophil; induced sputum; race
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