Addition of salmeterol to low-dose fluticasone versus higher-dose fluticasone: An analysis of asthma exacerbations

Matz, Jonathan; Emmett, Amanda; Rickard, Kathleen; Kalberg, Chris

doi:10.1067/mai.2001.114709

Cited by 115 publications

(71 citation statements)

References 16 publications

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“…The first, already discussed, is the reduction of exacerbations -and therefore presumably in airway inflammation -with the addition of a LABA to an ICS. However, one analysis of nearly a thousand subjects who received either fluticasone proprionate (FP) 88 mcg plus salmeterol 42 mcg, or FP 220 mcg twice daily, found that there were not only fewer exacerbations with the combination (8.8 percent vs. 13.8 percent) but also that the response to prednisone treatment of the exacerbation was about two days sooner with the combination therapy [25]. Another study suggesting some synergy between LABAs and ICSs is a meta-analysis that compared four studies in which the same doses of salmeterol and of fluticasone were administered either in separate or the same canisters [26].…”

Section: O P Y R Ig H T G E N E R a L P R A C T Ic E A Ir W A Y S Gmentioning

confidence: 99%

Long-Acting Beta-Agonists in Adult Asthma: Evidence that these Drugs are Safe

Nelson

2006

Primary Care Respiratory Journal

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Section: O P Y R Ig H T G E N E R a L P R A C T Ic E A Ir W A Y S Gmentioning

confidence: 99%

Long-Acting Beta-Agonists in Adult Asthma: Evidence that these Drugs are Safe

Nelson

2006

Primary Care Respiratory Journal

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“…For example, in comparison to no treatment, 100 mg budesonide twice daily resulted in a 60% reduced risk of having a severe exacerbation in the OPTIMA (Oxis and Pulmicort Turbuhaler in the Management of Asthma) trial [38]. The addition of a long-acting b 2 -agonist (LABA) to ICS further reduces the frequency [39], severity and duration [40] of exacerbations. Studies such as these were not designed to identify the cause of the exacerbation; however, as viruses are thought to cause o50% of all exacerbations, it is reasonable to assume that some reduction in the incidence of virus-induced exacerbations would occur.…”

Section: Can Current Therapeutic Regimens Prevent Virus-induced Exacementioning

confidence: 99%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

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“…Furthermore, the addition of a LABA to a low dose of an inhaled GC is more efficacious than increasing the dose of a GC. The improved disease control by combination therapy with GCs and LABAs includes a significant decrease in the frequency of exacerbations [2,3,4,5]. Since asthma exacerbations are usually associated with increased airway inflammation, the question has arisen whether LABAs complement the anti-inflammatory effects of GCs, resulting in an enhanced anti-inflammatory efficacy of combination therapy compared to GCs alone.…”

Section: Introductionmentioning

confidence: 99%

“…There is broad clinical agreement that the treatment of asthma with a combination of inhaled glucocorticosteroids (GCs), such as budesonide (BUD) or fluticasone propionate, and long-acting β 2 -agonists (LABAs), such as formoterol (FORM) or salmeterol, improves disease control compared to inhaled GCs alone [1,2,3,4,5]. Furthermore, the addition of a LABA to a low dose of an inhaled GC is more efficacious than increasing the dose of a GC.…”

Section: Introductionmentioning

confidence: 99%

Cooperative Inhibitory Effects of Budesonide and Formoterol on Eosinophil Superoxide Production Stimulated by Bronchial Epithelial Cell Conditioned Medium

Persdotter

Lindahl²,

Malm-Erjefält³

et al. 2007

Int Arch Allergy Immunol

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Background: Improved asthma control by combinations of inhaled glucocorticosteroids (GCs) and long-acting β₂-agonists (LABAs) includes a reduced frequency and severity of exacerbations. In view of the association of exacerbations with increased airway inflammation, the question has arisen as to whether LABAs are able to complement the known anti-inflammatory activity of GCs. To address this, we studied the effects of a LABA, formoterol (FORM), and a GC, budesonide (BUD), alone and in combination, on bronchial epithelial cell-mediated eosinophil superoxide production in vitro.Methods: We employed 2 experimental approaches. First, superoxide production by human eosinophils incubated with conditioned medium (CM) from human bronchial epithelial cells cultured for 24 h with vehicle, BUD, FORM or BUD + FORM was measured (Epi/Eos assay). Second, eosinophils were stimulated with vehicle-CM to which the drugs were added (Eos assay). Superoxide production was determined as the superoxide dismutase-inhibitable reduction of ferricytochrome C. Results: CM increased eosinophil superoxide generation (p < 0.01) and epithelial-derived granulocyte macrophage colony-stimulating factor was the mediator responsible. In both assays, FORM dose-dependently inhibited eosinophil superoxide similarly and in the same concentration range as BUD. The BUD + FORM combination was more effective than BUD alone, and it completely inhibited CM-induced superoxide production in the Epi/Eos assay, suggesting complementary effects of both drugs on bronchial epithelial cells and eosinophils. Conclusions: The cooperative, inhibitory effects of BUD and FORM on eosinophils and bronchial epithelial cells, in terms of their effects on eosinophil superoxide production, may represent a possible mechanism for the enhanced anti-inflammatory efficacy of BUD and FORM combination therapy of asthma.

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Addition of salmeterol to low-dose fluticasone versus higher-dose fluticasone: An analysis of asthma exacerbations

Cited by 115 publications

References 16 publications

Long-Acting Beta-Agonists in Adult Asthma: Evidence that these Drugs are Safe

Long-Acting Beta-Agonists in Adult Asthma: Evidence that these Drugs are Safe

Viral infections and asthma: an inflammatory interface?

Cooperative Inhibitory Effects of Budesonide and Formoterol on Eosinophil Superoxide Production Stimulated by Bronchial Epithelial Cell Conditioned Medium

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