4.7 Article

Obesity's effect on asthma extends to diagnostic criteria

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 141, Issue 3, Pages 1096-1104

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2017.04.047

Keywords

Asthma; obesity; eosinophils; inflammatory markers; fraction of exhaled nitric oxide

Funding

  1. National Heart, Lung, and Blood Institute (NHLBI)/National Institutes of Health (NIH) Asthma Research Network [U10 HL074225, U10 HL074227, U10 HL074231, U10 HL074204, U10 HL074212, U10 HL074073, U10 HL074206, U10 HL074208, U10 HL07421]
  2. NIH training grant [5 T32 AI 007062-36]
  3. NHLBI Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC)

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Background: The use of inflammatory biomarkers to delineate the type of lung inflammation present in asthmatic subjects is increasingly common. However, the effect of obesity on these markers is unknown. Objectives: We aimed to determine the effect of obesity on conventional markers of inflammation in asthmatic subjects. Methods: We performed secondary analysis of data from 652 subjects previously enrolled in 2 Asthma Clinical Research Network trials. We performed linear correlations between biomarkers and logistic regression analysis to determine the predictive value of IgE levels, blood eosinophil counts, and fraction of exhaled nitric oxide values in relationship to sputum eosinophil counts (> 2%), as well as to determine whether cut points existed that would maximize the sensitivity and specificity for predicting sputum eosinophilia in the 3 weight groups. Results: Overall, statistically significant but relatively weak correlations were observed among all 4 markers of inflammation. Within obese subjects, the only significant correlation found was between IgE levels and blood eosinophil counts (r = 0.33, P<.001); furthermore, all other correlations between inflammatory markers were approximately 0, including correlations with sputum eosinophil counts. In addition, the predictive value of each biomarker alone or in combination was poor in obese subjects. In fact, in obese subjects none of the biomarkers of inflammation significantly predicted the presence of high sputum eosinophil counts. Obese asthmatic subjects have lower cut points for IgE levels (268 IU), fraction of exhaled nitric oxide values (14.5 ppb), and blood eosinophil counts (96 cells/mu L) than all other groups. Conclusions: In obese asthmatic subjects conventional biomarkers of inflammation are poorly predictive of eosinophilic airway inflammation. As such, biomarkers currently used to delineate eosinophilic inflammation in asthmatic subjects should be approached with caution in these subjects.

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