In moderate-to-severe asthma patients monitoring exhaled nitric oxide during exacerbation is not a good predictor of spirometric response to oral corticosteroid

Arthur F. Gelb, Roxanna Moridzadeh, Deepak H. Singh, Christine Fraser, Steven George

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Background: The importance of monitoring exhaled nitric oxide (NO) in asthma remains controversial. Objective: To measure exhaled NO, postnebulized albuterol/ipratropium spirometry, and Asthma Control Test (ACT) during asthma exacerbation requiring 8- to 10-day tapering oral corticosteroid in nonsmoking patients with moderate-to-severe asthma on moderate-dose inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid. Methods: After measuring the fraction of exhaled NO (Feno [ppb]) at 50, 100, 150, and 200 mL/s, the total Feno at 50 mL/s (ppb), large central airway NO flux (J′awNO [nL/s]), and peripheral small airway/alveolar NO concentration (CANO [ppb]) were calculated and corrected for NO axial back-diffusion. Outpatient exacerbation required the patient with asthma to be afebrile with normal chest x-ray and white blood cell count. Results: Group 1 included 17 patients (6 men) with asthma, age 52 ± 12 years, studied at baseline, during 18 exacerbations with abnormal Feno at 50 mL/s, J′awNO, and/or CANO, and post 8- to 10-day tapering 40 mg prednisone (recovery). Baseline: IgE, 332 ± 243 Kμ; total blood eosinophils, 304 ± 266 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.5 ± 0.7 L (86% ± 20% predicted); exacerbation: FEV1, 1.7 ± 0.4 L (60% ± 17%) (P <.001); recovery: FEV1, 2.5 ± 0.7 L (85% ± 13%) (P <.001). Group 2 included 11 (7 men) similarly treated patients with asthma, age 49 ± 14 years, studied at baseline, during 15 exacerbations with normal Feno at 50 mL/s, J′awNO, and C ANO. Baseline: IgE, 307 ± 133 Kμ; total blood eosinophils, 296 ± 149 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.7 ± 0.9 L (71% ± 12% predicted); exacerbation: FEV1, 1.7 ± 0.6 L (54% ± 19%) (P <.006); recovery: FEV1, 2.7 ± 0.9 L (70% ± 14%) (P =.002). On comparing group 1 versus group 2, there was no significant difference for baseline IgE, eosinophils, body mass index, and ACT and similar significant (≤.006) decrease from baseline in FEV1 (L) during exacerbation and similar increase (≤.006) at recovery. Conclusions: Increased versus normal exhaled NO during outpatient exacerbation in patients with moderate-to-severe asthma on inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid does not preclude a robust clinical and spirometric response to tapering oral prednisone.

Original languageEnglish (US)
Pages (from-to)1491-1498
Number of pages8
JournalJournal of Allergy and Clinical Immunology
Volume129
Issue number6
DOIs
StatePublished - Jun 1 2012

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Physiologic Monitoring
Adrenal Cortex Hormones
Nitric Oxide
Asthma
Eosinophils
Immunoglobulin E
Body Mass Index
Prednisone
Outpatients
Maintenance
Spirometry
Leukocyte Count
Thorax
X-Rays

Keywords

  • Asthma
  • asthma mechanisms
  • exhaled nitric oxide

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

In moderate-to-severe asthma patients monitoring exhaled nitric oxide during exacerbation is not a good predictor of spirometric response to oral corticosteroid. / Gelb, Arthur F.; Moridzadeh, Roxanna; Singh, Deepak H.; Fraser, Christine; George, Steven.

In: Journal of Allergy and Clinical Immunology, Vol. 129, No. 6, 01.06.2012, p. 1491-1498.

Research output: Contribution to journalArticle

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abstract = "Background: The importance of monitoring exhaled nitric oxide (NO) in asthma remains controversial. Objective: To measure exhaled NO, postnebulized albuterol/ipratropium spirometry, and Asthma Control Test (ACT) during asthma exacerbation requiring 8- to 10-day tapering oral corticosteroid in nonsmoking patients with moderate-to-severe asthma on moderate-dose inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid. Methods: After measuring the fraction of exhaled NO (Feno [ppb]) at 50, 100, 150, and 200 mL/s, the total Feno at 50 mL/s (ppb), large central airway NO flux (J′awNO [nL/s]), and peripheral small airway/alveolar NO concentration (CANO [ppb]) were calculated and corrected for NO axial back-diffusion. Outpatient exacerbation required the patient with asthma to be afebrile with normal chest x-ray and white blood cell count. Results: Group 1 included 17 patients (6 men) with asthma, age 52 ± 12 years, studied at baseline, during 18 exacerbations with abnormal Feno at 50 mL/s, J′awNO, and/or CANO, and post 8- to 10-day tapering 40 mg prednisone (recovery). Baseline: IgE, 332 ± 243 Kμ; total blood eosinophils, 304 ± 266 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.5 ± 0.7 L (86{\%} ± 20{\%} predicted); exacerbation: FEV1, 1.7 ± 0.4 L (60{\%} ± 17{\%}) (P <.001); recovery: FEV1, 2.5 ± 0.7 L (85{\%} ± 13{\%}) (P <.001). Group 2 included 11 (7 men) similarly treated patients with asthma, age 49 ± 14 years, studied at baseline, during 15 exacerbations with normal Feno at 50 mL/s, J′awNO, and C ANO. Baseline: IgE, 307 ± 133 Kμ; total blood eosinophils, 296 ± 149 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.7 ± 0.9 L (71{\%} ± 12{\%} predicted); exacerbation: FEV1, 1.7 ± 0.6 L (54{\%} ± 19{\%}) (P <.006); recovery: FEV1, 2.7 ± 0.9 L (70{\%} ± 14{\%}) (P =.002). On comparing group 1 versus group 2, there was no significant difference for baseline IgE, eosinophils, body mass index, and ACT and similar significant (≤.006) decrease from baseline in FEV1 (L) during exacerbation and similar increase (≤.006) at recovery. Conclusions: Increased versus normal exhaled NO during outpatient exacerbation in patients with moderate-to-severe asthma on inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid does not preclude a robust clinical and spirometric response to tapering oral prednisone.",
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T1 - In moderate-to-severe asthma patients monitoring exhaled nitric oxide during exacerbation is not a good predictor of spirometric response to oral corticosteroid

AU - Gelb, Arthur F.

AU - Moridzadeh, Roxanna

AU - Singh, Deepak H.

AU - Fraser, Christine

AU - George, Steven

PY - 2012/6/1

Y1 - 2012/6/1

N2 - Background: The importance of monitoring exhaled nitric oxide (NO) in asthma remains controversial. Objective: To measure exhaled NO, postnebulized albuterol/ipratropium spirometry, and Asthma Control Test (ACT) during asthma exacerbation requiring 8- to 10-day tapering oral corticosteroid in nonsmoking patients with moderate-to-severe asthma on moderate-dose inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid. Methods: After measuring the fraction of exhaled NO (Feno [ppb]) at 50, 100, 150, and 200 mL/s, the total Feno at 50 mL/s (ppb), large central airway NO flux (J′awNO [nL/s]), and peripheral small airway/alveolar NO concentration (CANO [ppb]) were calculated and corrected for NO axial back-diffusion. Outpatient exacerbation required the patient with asthma to be afebrile with normal chest x-ray and white blood cell count. Results: Group 1 included 17 patients (6 men) with asthma, age 52 ± 12 years, studied at baseline, during 18 exacerbations with abnormal Feno at 50 mL/s, J′awNO, and/or CANO, and post 8- to 10-day tapering 40 mg prednisone (recovery). Baseline: IgE, 332 ± 243 Kμ; total blood eosinophils, 304 ± 266 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.5 ± 0.7 L (86% ± 20% predicted); exacerbation: FEV1, 1.7 ± 0.4 L (60% ± 17%) (P <.001); recovery: FEV1, 2.5 ± 0.7 L (85% ± 13%) (P <.001). Group 2 included 11 (7 men) similarly treated patients with asthma, age 49 ± 14 years, studied at baseline, during 15 exacerbations with normal Feno at 50 mL/s, J′awNO, and C ANO. Baseline: IgE, 307 ± 133 Kμ; total blood eosinophils, 296 ± 149 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.7 ± 0.9 L (71% ± 12% predicted); exacerbation: FEV1, 1.7 ± 0.6 L (54% ± 19%) (P <.006); recovery: FEV1, 2.7 ± 0.9 L (70% ± 14%) (P =.002). On comparing group 1 versus group 2, there was no significant difference for baseline IgE, eosinophils, body mass index, and ACT and similar significant (≤.006) decrease from baseline in FEV1 (L) during exacerbation and similar increase (≤.006) at recovery. Conclusions: Increased versus normal exhaled NO during outpatient exacerbation in patients with moderate-to-severe asthma on inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid does not preclude a robust clinical and spirometric response to tapering oral prednisone.

AB - Background: The importance of monitoring exhaled nitric oxide (NO) in asthma remains controversial. Objective: To measure exhaled NO, postnebulized albuterol/ipratropium spirometry, and Asthma Control Test (ACT) during asthma exacerbation requiring 8- to 10-day tapering oral corticosteroid in nonsmoking patients with moderate-to-severe asthma on moderate-dose inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid. Methods: After measuring the fraction of exhaled NO (Feno [ppb]) at 50, 100, 150, and 200 mL/s, the total Feno at 50 mL/s (ppb), large central airway NO flux (J′awNO [nL/s]), and peripheral small airway/alveolar NO concentration (CANO [ppb]) were calculated and corrected for NO axial back-diffusion. Outpatient exacerbation required the patient with asthma to be afebrile with normal chest x-ray and white blood cell count. Results: Group 1 included 17 patients (6 men) with asthma, age 52 ± 12 years, studied at baseline, during 18 exacerbations with abnormal Feno at 50 mL/s, J′awNO, and/or CANO, and post 8- to 10-day tapering 40 mg prednisone (recovery). Baseline: IgE, 332 ± 243 Kμ; total blood eosinophils, 304 ± 266 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.5 ± 0.7 L (86% ± 20% predicted); exacerbation: FEV1, 1.7 ± 0.4 L (60% ± 17%) (P <.001); recovery: FEV1, 2.5 ± 0.7 L (85% ± 13%) (P <.001). Group 2 included 11 (7 men) similarly treated patients with asthma, age 49 ± 14 years, studied at baseline, during 15 exacerbations with normal Feno at 50 mL/s, J′awNO, and C ANO. Baseline: IgE, 307 ± 133 Kμ; total blood eosinophils, 296 ± 149 cells/μL; body mass index, 28 ± 6; ACT, 16 to 19; and FEV1, 2.7 ± 0.9 L (71% ± 12% predicted); exacerbation: FEV1, 1.7 ± 0.6 L (54% ± 19%) (P <.006); recovery: FEV1, 2.7 ± 0.9 L (70% ± 14%) (P =.002). On comparing group 1 versus group 2, there was no significant difference for baseline IgE, eosinophils, body mass index, and ACT and similar significant (≤.006) decrease from baseline in FEV1 (L) during exacerbation and similar increase (≤.006) at recovery. Conclusions: Increased versus normal exhaled NO during outpatient exacerbation in patients with moderate-to-severe asthma on inhaled corticosteroid and long-acting β2-agonist but not maintenance oral corticosteroid does not preclude a robust clinical and spirometric response to tapering oral prednisone.

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KW - asthma mechanisms

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