Race is associated with differences in airway inflammation in patients with asthma.

Published

Journal Article

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.

Full Text

Cited Authors

  • Nyenhuis, SM; Krishnan, JA; Berry, A; Calhoun, WJ; Chinchilli, VM; Engle, L; Grossman, N; Holguin, F; Israel, E; Kittles, RA; Kraft, M; Lazarus, SC; Lehman, EB; Mauger, DT; Moy, JN; Peters, SP; Phipatanakul, W; Smith, LJ; Sumino, K; Szefler, SJ; Wechsler, ME; Wenzel, S; White, SR; Ackerman, SJ

Published Date

  • July 2017

Published In

Volume / Issue

  • 140 / 1

Start / End Page

  • 257 - 265.e11

PubMed ID

  • 28069248

Pubmed Central ID

  • 28069248

Electronic International Standard Serial Number (EISSN)

  • 1097-6825

International Standard Serial Number (ISSN)

  • 0091-6749

Digital Object Identifier (DOI)

  • 10.1016/j.jaci.2016.10.024

Language

  • eng