scholarly journals Cessation of long-acting β2-agonist in children with persistent asthma on inhaled corticosteroids

2016 ◽  
Vol 48 (2) ◽  
pp. 558-560 ◽  
Author(s):  
Francine M. Ducharme ◽  
Roxanne Gagnon ◽  
Brigitte Bénard ◽  
Sze Man Tse ◽  
Robert Thivierge
Keyword(s):  
Inhaled Corticosteroids ◽  
Persistent Asthma ◽  
Long Acting ◽  
Β2 Agonist

Wirksamkeit und Sicherheit von Dupilumab bei ganzjähriger allergischer Rhinitis und gleichzeitigem Asthma

2019 ◽  
Vol 7 (1) ◽  
pp. 27-28
Author(s):  
Susanne Lau
Keyword(s):  
Allergic Rhinitis ◽  
Inhaled Corticosteroids ◽  
Persistent Asthma ◽  
High Dose ◽  
Specific Response ◽  
Pivotal Phase ◽  
Runny Nose ◽  
Asthma Patients ◽  
Long Acting ◽  
Snot 22

Background: Dupilumab, an anti-IL-4 receptor a mAb, inhibits IL-4/IL-13 signaling, key drivers of type 2/TH2 immune diseases (eg, atopic/allergic disease). In a pivotal, phase 2b study (NCT01854047), dupilumab reduced severe exacerbations, improved lung function and quality of life, and was generally well tolerated in patients with uncontrolled persistent asthma despite using medium-to-high-dose inhaled corticosteroids plus long-acting b2-agonists. Objective: To examine dupilumabʼs effect on the 22-item Sino-Nasal Outcome Test (SNOT-22) total score and its allergic rhinitis (AR)-associated items in asthma patients with comorbid perennial allergic rhinitis (PAR). Methods: A post hoc analysis reporting data from the phase 2b study for the 200 and 300 mg every 2 week (q2w) doses under investigation in phase 3 (NCT02414854) was carried out. PAR was defined at study entry as a specific response to typical perennial antigens (IgE >0.35 Ku/L). Results: Overall, 241 (61%) patients had PAR. In asthma patients with PAR, dupilumab 300 mg q2w versus placebo significantly improved SNOT-22 total score (least squares mean difference, 25.98; 95% CI, 210.45 to 21.51; P 5.009) and all 4 AR-associated symptoms evaluated (nasal blockage, 20.60; 95% CI, 20.96 to 20.25; runny nose, 20.67; 95% CI, 21.04 to 20.31; sneezing, 20.55; 95% CI, 20.89 to 20.21; postnasal discharge, 20.49; 95% CI, 20.83 to 20.16; all P < .01). Dupilumab 200 mg q2w demonstrated numerical, but not statistically significant, decreases in SNOT-22 total score (21.82; 95% CI, 26.46 to 2.83; P 5 .443 vs placebo) and in each ARassociated symptom. In patients without PAR, no differences were observed for these measures versus placebo. Conclusions: Dupilumab 300 mg q2w significantly improved AR-associated nasal symptoms in patients with uncontrolled persistent asthma and comorbid PAR.

scholarly journals Association of Inhaled Corticosteroids and Long-Acting Muscarinic Antagonists With Asthma Control in Patients With Uncontrolled, Persistent Asthma

JAMA ◽  
2018 ◽  
Vol 319 (14) ◽  
pp. 1473 ◽  
Author(s):  
Diana M. Sobieraj ◽  
William L. Baker ◽  
Elaine Nguyen ◽  
Erin R. Weeda ◽  
Craig I. Coleman ◽  
...  
Keyword(s):  
Asthma Control ◽  
Inhaled Corticosteroids ◽  
Persistent Asthma ◽  
Muscarinic Antagonists ◽  
Long Acting

scholarly journals Rapid nongenomic actions of inhaled corticosteroids on long-acting β2-agonist transport in the airway

2011 ◽  
Vol 24 (6) ◽  
pp. 654-659 ◽  
Author(s):  
Gabor Horvath ◽  
Eliana S. Mendes ◽  
Nathalie Schmid ◽  
Andreas Schmid ◽  
Gregory E. Conner ◽  
...  
Keyword(s):  
Inhaled Corticosteroids ◽  
Long Acting ◽  
Β2 Agonist

β 2-Adrenoceptor polymorphism and bronchoprotective sensitivity with regular short- and long-acting β2-agonist therapy

1999 ◽  
Vol 96 (3) ◽  
pp. 253-259 ◽  
Author(s):  
B. J. LIPWORTH ◽  
I. P. HALL ◽  
I. AZIZ ◽  
K. S. TAN ◽  
A. WHEATLEY
Keyword(s):  
Inhaled Corticosteroids ◽  
Forced Expiratory Volume ◽  
Double Blind ◽  
Geometric Means ◽  
Once Daily ◽  
Regular Treatment ◽  
Parallel Group ◽  
Long Acting ◽  
To Receive ◽  
Β2 Agonist

The aim of the present study was to investigate bronchoprotective sensitivity in patients receiving regular treatment with short- and long-acting β2-agonists and to evaluate any possible association with genetic polymorphism. Thirty-eight patients with stable mild to moderate asthma and receiving inhaled corticosteroids were randomized in a parallel group, double-blind, double-dummy fashion to receive 2 weeks of treatment with either formoterol (12μg once daily, 6μg twice daily or 24μg twice daily) or terbutaline (500μg four times daily). Bronchoprotection against methacholine challenge (as a provocative dose to produce a 20% fall in forced expiratory volume in 1.0 ;s: PD20) was measured at baseline (unprotected) after an initial 1 week run-in without β2-agonist, and at 1 ;h after the first and last doses of each treatment. The PD20 values were log-transformed and calculated as change from baseline. Percentage desensitization of log PD20 for first- versus last-dose bronchoprotection was calculated and analysed according to effects of treatment and β2-adrenoceptor polymorphism at codon 16 or 27. The mean degree of desensitization for bronchoprotection was comparable with all four treatments and there were no significant differences in absolute PD20 values after 2 weeks of chronic dosing. The PD20 values were (as μg of methacholine, geometric means±S.E.M.): formoterol, 12μg once daily, 99±42μg; formoterol, 6μg twice daily, 107±44μg; formoterol, 24μg twice daily, 108±45μg; terbutaline, 500μg four times daily, 88±37μg. All patients receiving formoterol, 24μg twice daily, exhibited a loss of protection greater than 30% which was unrelated to polymorphism at codon 16 or 27. For codon 16, the use of lower doses of formoterol (12μg once daily or 6μg twice daily) showed wider variability in the propensity for protection loss in patients who were heterozygous, in contrast to a more uniform protection loss seen with homozygous glycine patients. The amount of protection loss was not significantly related to polymorphism at codon 16 or 27, expressed as values (mean±S.E.M.) for percentage desensitization according to each genotype (pooled treatments): Gly-16, 66±11%; Het-16, 53±8%; Arg-16, 69±18%; Glu-27, 68±12%; Het-27, 58±8%; Gln-27, 52±12%. The results of this preliminary study showed that bronchoprotective desensitization occurred readily in response to short- or long-acting β2-agonist exposure irrespective of β2-adrenoceptor polymorphism at codon 16 or 27. Further studies with larger patient numbers are required to further evaluate the effects of polymorphisms with lower doses of regular formoterol.

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