Health care education, delivery, and qualityAssociation between IgE levels and asthma severity among African American, Mexican, and Puerto Rican patients with asthma
Section snippets
Study participants
Study participants were from the following ethnic groups: Puerto Rican, Mexican, and African American ethnicity. As part of the GALA study, Mexican subjects with asthma were recruited from the San Francisco Bay Area, California and Mexico City, Mexico, and Puerto Rican subjects with asthma were recruited from New York City and Puerto Rico.25 African Americans with asthma were recruited from the San Francisco–Bay Area as part of SAGE. All subjects with asthma were recruited from community
Subject characteristics
Overall characteristics for the complete GALA and SAGE cohorts are described elsewhere (Naqvi M, et al, unpublished data, 2005).17, 25 In the present analysis, we analyzed a total of 739 patients with asthma (492 with high IgE and 247 with low IgE) who had complete information for IgE, asthma severity, and other variables, including BMI, age, sex, disease onset, and parental histories of asthma and allergies, as described in Methods. No significant differences were noted in drug response,
Discussion
The results of our analysis demonstrate an association between high IgE levels and asthma severity among Mexican, Puerto Rican, and African American patients with asthma. These findings remain significant after accounting for differences in race/ethnicity, age, sex, BMI, and age of asthma onset, and also after stratification of patients with asthma into children and adults. Although asthma has already been shown to be associated with serum IgE levels,1, 2, 3 our results expand on previous
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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.