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Scholarly Works (2 results)

  • Article
  • Peer Reviewed
ICTS Publications (2011)

To determine the relationship of poor asthma control to bronchodilator response (BDR) phenotypes in children with normal spirometry.

Children with asthma were assessed for clinical indexes of poorly controlled asthma. Pre- and post-bronchodilator spirometry were performed, and the percent BDR was determined. Multivariate logistic regression assessed the relationship of the clinical indices to BDR at ≥ 8%, ≥ 10%, and ≥ 12% BDR thresholds.

There were 510 controller naïve children and 169 on controller medication. In the controller naïve population the mean age (± 1 SD) was 9.5 (3.4); 57.1% were male, 85.7% Hispanic. Demographics were similar in both populations. In the adjusted profile, significant clinical relationships were found particularly to positive BDR phenotypes ≥ 10% and ≥ 12% versus negative responses including younger age, (OR 2.0, 2.5; P < .05), atopy (OR 1.9, 2.6; P < .01), nocturnal symptoms in females (OR 3.4, 3.8; P < .01); β₂ agonist use (OR 1.7, 2.8; P < .01); and exercise limitation (OR 2.2, 2.5; P < .01) only in the controller naïve population.

The BDR phenotype ≥ 10% is significantly related to poor asthma control, providing a potentially useful objective tool in controller naïve children even when the pre-bronchodilator spirometry result is normal.

    Cover page: The relationship of the bronchodilator response phenotype to poor asthma control in children with normal spirometry.
    • Article
    • Peer Reviewed
    UC Irvine Previously Published Works (2010)
    Background: The exhaled nitric oxide (eNO) signal is a marker of inflammation, and can be partitioned into proximal [J'aw(NO) (nl/s), maximum airway flux] and distal contributions [CA(NO)(ppb), distal airway/alveolar NO concentration]. We hypothesized that J'awNO and CANO are selectively elevated in asthmatics, permitting identification of four inflammatory categories with distinct clinical features. Methods: In 200 consecutive children with asthma, and 21 non-asthmatic, non-atopic controls, we measured baseline spirometry, bronchodilator response, asthma control and morbidity, atopic status, use of inhaled corticosteroids, and eNO at multiple flows (50, 100, and 200 ml/s) in a cross-sectional study design. A trumpet-shaped axial diffusion model of NO exchange was used to characterize J'awNO and CANO. Results: J'awNO was not correlated with CANO, and thus asthmatic subjects were grouped into four eNO categories based on upper limit thresholds of non-asthmatics for J'aw(NO) (>= 1.5 nl/s) and CA(NO) (>= 2.3 ppb): Type I (normal J'aw(NO) and CA(NO)), Type II (elevated J'aw(NO) and normal CA(NO)), Type III (elevated J'aw(NO) and CA(NO)) and Type IV (normal J'aw(NO) and elevated CA(NO)). The rate of inhaled corticosteroid use (lowest in Type III) and atopy (highest in Type II) varied significantly amongst the categories influencing J'aw(NO), but was not related to CA(NO), asthma control or morbidity. All categories demonstrated normal to near-normal baseline spirometry; however, only eNO categories with increased CA(NO) (III and IV) had significantly worse asthma control and morbidity when compared to categories I and II. Conclusions: J'aw(NO) and CA(NO) reveal inflammatory categories in children with asthma that have distinct clinical features including sensitivity to inhaled corticosteroids and atopy. Only categories with increase CANO were related to poor asthma control and morbidity independent of baseline spirometry, bronchodilator response, atopic status, or use of inhaled corticosteroids.
      Cover page: Clinical patterns in asthma based on proximal and distal airway nitric oxide categoriesCreative Commons 'BY' version 4.0 license
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