| | Association between IgE levels and asthma severity among African American, Mexican, and Puerto Rican patients with asthmaReceived 27 September 2006; received in revised form 10 February 2007; accepted 19 February 2007. published online 11 May 2007. BackgroundHigh levels of IgE are associated with asthma. Whether higher levels of IgE are associated with more severe asthma is still unclear. ObjectiveTo determine whether IgE is associated with asthma severity among Latino and African American subjects with asthma. MethodsWe assessed lung function and asthma severity among African American, Mexican, and Puerto Rican patients with asthma with high IgE levels (≥100 IU/mL; n = 492) and compared these values to those of patients with asthma with low IgE levels (<100 IU/mL; n = 247). We also examined IgE as a continuous variable among these groups. ResultsPatients with asthma with high IgE had a lower mean FEV1 (87.6 ± 17.1, percent of predicted) than patients with asthma with low IgE (91.5 ± 17.0; P = .031). Regardless of race and ethnicity, baseline FEV1, forced expiratory flow, and FEV1/forced vital capacity were lower among subjects with high IgE than among subjects with low IgE (P = .031, P < .0001, P = .0001, respectively). In addition, 54.7% of patients with asthma with high IgE had been previously hospitalized, compared with 44.1% of patients with asthma with low IgE (odds ratio, 1.33; 95% CI, 1.04-1.71). ConclusionHigher IgE is associated with lower baseline lung function and more severe asthma among these populations. Clinical implicationsAmong patients with asthma from 3 ethnically distinct groups, total IgE levels are inversely correlated with baseline lung function and asthma severity. San Francisco and Oakland, Calif, San Juan, Puerto Rico, Mexico City, Mexico, and Evanston, Ill Abbreviations used: ANCOVA, Analysis of covariance, BMI, Body mass index, ETS, Environmental tobacco smoke, FEF25-75, Forced expiratory flow at 25% to 75% of forced vital capacity, FVC, Forced vital capacity, GALA, Genetics of Asthma in Latino Americans, ICU, Intensive care unit, MFI, Median family income, OR, Odds ratio, SAGE, Study of African Americans, Asthma, Genes and Environments, SES, Socioeconomic status a From the University of California, San Francisco b San Juan Veterans Affairs Medical Center, University of Puerto Rico School of Medicine c Pediatric Pulmonary Program of San Juan d Instituto Nacional de Enfermedades Respiratorias, Mexico City e James A. Watson Wellness Center, Oakland f Children's Hospital and Research Institute, Oakland g Bay Area Pediatrics, Oakland h Northwestern University, Evanston Reprint requests: Esteban Gonz´lez Burchard, MD, MPH, University of California, San Francisco, San Francisco, CA 94143-2911.
Supported by the National Institutes of Health (R01 HL078885, K23 HL04464, HL07185, GM61390, American Lung Association of California, Robert Wood Johnson Amos Medical Faculty Development Award, National Center for Minority Health Disparities Health Disparities Scholar, Extramural Clinical Research Loan Repayment Program for Individuals from Disadvantaged Backgrounds, 2001-2003, to E.G.B.), (HL51823, HL074204, 3M01RR000083-38S30488, HL56443, and HL51831 to the Asthma Clinical Research Network), an American Thoracic Society Breakthrough Opportunities in Lung Disease grant (ATS-05-078) and a Tobacco-Related Disease Research Program New Investigator Award (15KT-0008) to S.C., the American Lung Association of California (Research Training Fellowship to H.-J.T.), San Francisco General Hospital General Clinical Research Center M01RR00083-41, U01-HL 65899, University of California, San Francisco-Children's Hospital of Oakland Pediatric Clinical Research Center (M01 RR01271), Oakland, Calif, Sandler Center for Basic Research in Asthma, and the Sandler Family Supporting Foundation, Ernest S. Bazley Grant to Northwestern University. Disclosure of potential conflict of interest: M. LeNoir has consulting arrangements with GlaxoSmithKline and is on the speakers' bureau for GlaxoSmithKline, Aventis, and Alocon. P. C. Avila has received grant support from Genentech and Novartis. The rest of the authors have declared that they have no conflict of interest. PII: S0091-6749(07)00614-8 doi:10.1016/j.jaci.2007.02.045 © 2007 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. | |
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