Why use long acting bronchodilators in chronic obstructive lung diseases? An extensive review on formoterol and salmeterol.

Why use long acting bronchodilators in chronic obstructive lung diseases? An extensive review on formoterol and salmeterol.

Eur J Intern Med. 2015 Jun 3;

Authors: Santus P, Radovanovic D, Paggiaro P, Papi A, Sanduzzi A, Scichilone N, Braido F

Abstract
Long-acting ?2-adrenoceptor agonists, formoterol and salmeterol, represent a milestone in the treatments of chronic obstructive lung diseases. Although no specific indications concerning the choice of one molecule rather than another are provided by asthma and COPD guidelines, they present different pharmacological properties resulting in distinct clinical employment possibilities. In particular, salmeterol has a low intrinsic efficacy working as a partial receptor agonist, while formoterol is a full agonist with high intrinsic efficacy. From a clinical perspective, in the presence of low ?2-adrenoceptors availability, like in inflamed airways, a full agonist can maintain its bronchodilatory and non-smooth muscle activities while a partial agonist may be less effective. Furthermore, formoterol presents a faster onset of action than salmeterol. This phenomenon, combined with the molecule safety profile, leads to a prompt amelioration of the symptoms, and allows using this drug in asthma as an “as needed” treatment in patients already on regular treatment. The fast onset of action and the full agonism of formoterol need to be considered in order to select the best pharmacological treatment of asthma and COPD.

PMID: 26049917 [PubMed – as supplied by publisher]

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Inhaled bronchodilators for acute chest syndrome in people with sickle cell disease.

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Inhaled bronchodilators for acute chest syndrome in people with sickle cell disease.

Cochrane Database Syst Rev. 2014 Aug 2;8:CD003733

Authors: Knight-Madden JM, Hambleton IR

Abstract
BACKGROUND: Bronchodilators are used to treat bronchial hyper-responsiveness in asthma. Bronchial hyper-responsiveness may be a component of acute chest syndrome in people with sickle cell disease. Therefore, bronchodilators may be useful in the treatment of acute chest syndrome.
OBJECTIVES: To assess the benefits and risks associated with the use of bronchodilators in people with acute chest syndrome.
SEARCH METHODS: We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group Trials Register comprising references identified from comprehensive electronic database searches, handsearches of relevant journals and abstract books of conference proceedings. Additional searches were carried out on MEDLINE (1966 to 2002) and Embase (1981 to 2002).Date of the most recent search of the Group’s Haemoglobinopathies Trials Register: 17 March 2014.
SELECTION CRITERIA: Randomised or quasi-randomised controlled trials. Trials using quasi-randomisation methods will be included in future updates of this review if there is sufficient evidence that the treatment and control groups are similar at baseline.
DATA COLLECTION AND ANALYSIS: We found no trials investigating the use of bronchodilators for acute chest syndrome in people with sickle cell disease.
MAIN RESULTS: We found no trials investigating the use of bronchodilators for acute chest syndrome in people with sickle cell disease.
AUTHORS’ CONCLUSIONS: If bronchial hyper-responsiveness is an important component of some episodes of acute chest syndrome in people with sickle cell disease, the use of inhaled bronchodilators may be indicated. There is need for a well-designed, adequately-powered randomised controlled trial to assess the benefits and risks of the addition of inhaled bronchodilators to established therapies for acute chest syndrome in people with sickle cell disease.

PMID: 25086371 [PubMed – as supplied by publisher]

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RGS5 gene and therapeutic response to short acting bronchodilators in paediatric asthma patients.

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RGS5 gene and therapeutic response to short acting bronchodilators in paediatric asthma patients.

Pediatr Pulmonol. 2012 Nov 28;

Authors: Labuda M, Laberge S, Brière J, Bérubé D, Krajinovic M

Abstract
Short-acting ?2-adrenergic receptor agonists are commonly used bronchodilators for symptom relief in asthmatics. Recent evidence demonstrated that prolonged exposure of cultured airway smooth muscle cells to ?2 agonists directly augments procontractile signaling pathways with the change in expression of regulator of G protein signaling 5 (RGS5). The aim of this study was to test whether genetic variants in RGS5 gene affect the response to short acting ?2-agonists. Bronchodilator responsiveness was assessed in 137 asthmatic children by % change in baseline forced expiratory volume in 1?sec (FEV(1) ) after administration of albuterol. The analyses were performed in patients with FEV(1) /FVC ratio below 0.9 (FVC-forced vital capacity, n?=?99). FEV(1) % change adjusted for baseline FEV(1) values was significantly different between genotypes of rs10917696 C/T polymorphism (P?=?0.008). The association remained significant with inclusion of age, sex, atopy, parental smoking, and controller medications into multivariate model (P?=?0.005). We also identified additive effect on the treatment outcome with previously published genetic variant G/A rs1544791 in phosphodiesterase 4 (PDE4D) gene. Carriers of two risk alleles (C and G) had adjusted mean % FEV(1) change value 4.6?±?1.3, while carriers of one and none of the risk alleles had 8.1?±?0.7% and 13.5?±?2.4%, respectively, P?=?0.001. Our work identifies a new genetic variant in RGS5 demonstrating additive effect with PDE4D, both implicated in modulation of asthma treatment. Pediatr Pulmonol. © 2012 Wiley Periodicals, Inc.

PMID: 23193110 [PubMed – as supplied by publisher]

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