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Clinical Investigations: Miscellaneous |

Racial Differences in T-Lymphocyte Response to Glucocorticoids*

Monica J. Federico, MD; Ronina A. Covar, MD; Eleanor E. Brown, BS; Donald Y. M. Leung, MD; Joseph D. Spahn, MD
Author and Funding Information

*From the Divisions of Pediatric Pulmonary Medicine and Pediatric Allergy & Immunology, National Jewish Medical & Research Center, and Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Ronina A. Covar, MD, National Jewish Medical & Research Center, 1400 Jackson St J316, Denver, CO 80206; e-mail covarr@njc.org



Chest. 2005;127(2):571-578. doi:10.1378/chest.127.2.571
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Background: Asthma morbidity and mortality is increased in blacks.

Objective: The primary objective of this cross-sectional study was to determine if blacks, asthmatic or nonasthmatic, displayed diminished T-lymphocyte response to glucocorticoids in vitro compared to their white counterparts. If differences were noted, this would suggest a racial predisposition to decreased glucocorticoid responsiveness among blacks.

Methods: Asthmatic (n = 395, 27% blacks) and control (n = 202, 52% blacks) subjects recruited from National Jewish Medical and Research Center and from the surrounding community participated in the study. In vitro glucocorticoid responsiveness was determined by assessing the log-transformed concentration of dexamethasone required to suppress phytohemagglutinin-induced T-lymphocyte proliferation by 50% (log10 IC50). Asthma medication history, atopic status, and spirometric lung function measures corrected for race were collected.

Results: Black and white asthmatic subjects had similar FEV1 percentage of predicted values and inhaled and oral glucocorticoid requirements. Black asthmatic subjects displayed significantly diminished glucocorticoid responsiveness compared to white asthmatic subjects, as follows: median (first, third quartile) log10 IC50 values of 1.00 nmol (0.48, 1.83) vs 0.78 nmol (0.29, 1.45) [p = 0.028]. Similar results were found between black and white control subjects, as follows: median, 1.26 nmol (0.70, 2.14) vs 0.95 nmol (0.55, 1.48) [p = 0.01]. Age, race, and basal T-lymphocyte activity were significantly positively correlated to the log10 IC50 values.

Conclusion: Our observation that black asthmatic subjects and non-asthmatic control subjects require greater concentrations of glucocorticoid in vitro to suppress T-lymphocyte activation suggests that blacks have a racial predisposition to diminished glucocorticoid responsiveness, which may contribute to their heightened asthma morbidity.

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