[Non-invasive ventilation: indication for acute respiratory failure].

Rev Med Suisse. 2012 Dec 12;8(366):2382-7

Authors: Brunner ME, Lyazidi A, Richard JC, Brochard L

Abstract
Mask or Non-invasive ventilation (NIV) is used for critically ill patients with acute respiratory failure (ARF): acute exacerbation of chronic obstructive bronchopulmonary disease and severe cardiogenic pulmonary edema are considered as the best indications for NIV since it improves the outcome of these patients. This technique is also proposed for hypoxemic respiratory failure, with more various results. To be effective here, NIV must be established early enough and should not delay intubation if required. NIV is also proposed after invasive ventilation or in patients in whom endotracheal intubation is not desirable. Its use has increased and its effectiveness seems to have improved, due to a better understanding of the technique but also thanks to technological progress.

PMID: 23346673 [PubMed - in process]

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Authors: Esquinas Rodriguez AM, Kirakli C

PMID: 23357559 [PubMed - as supplied by publisher]

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Clinical phenotypes of chronic obstructive pulmonary disease and asthma: Recent advances.

J Allergy Clin Immunol. 2013 Jan 26;

Authors: Carolan BJ, Sutherland ER

Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are prevalent obstructive lung diseases, both of which are characterized by airflow limitation. Although both represent distinct pathogenic entities, there can be significant clinical and physiologic overlap between the 2 disorders, creating potential management difficulties for clinicians. Although practice guidelines for both conditions outline diagnostic and management strategies, asthma and COPD are highly heterogeneous, and the symptoms of many patients remain poorly controlled despite adherence to current guidelines. Recent advances in phenotyping studies have elucidated heterogeneity in these airway diseases and might represent the best opportunity to enhance diagnosis, predict outcomes, and personalize treatments in patients with asthma and those with COPD. This review will focus on recent advances in describing phenotypic heterogeneity in asthma and COPD, including the evaluation of multiple clinical variables, molecular biomarkers, physiologic and radiologic data, and factors associated with disease progression and frequent exacerbations.

PMID: 23360757 [PubMed - as supplied by publisher]

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Corticosteroid resistance in patients with asthma and chronic obstructive pulmonary disease.

J Allergy Clin Immunol. 2013 Jan 26;

Authors: Barnes PJ

Abstract
Reduced responsiveness to the anti-inflammatory effects of corticosteroids is a major barrier to effective management of asthma in smokers and patients with severe asthma and in the majority of patients with chronic obstructive pulmonary disease (COPD). The molecular mechanisms leading to steroid resistance are now better understood, and this has identified new targets for therapy. In patients with severe asthma, several molecular mechanisms have been identified that might account for reduced steroid responsiveness, including reduced nuclear translocation of glucocorticoid receptor (GR) α after binding corticosteroids. This might be due to modification of the GR by means of phosphorylation as a result of activation of several kinases (p38 mitogen-activated protein kinase α, p38 mitogen-activated protein kinase γ, and c-Jun N-terminal kinase 1), which in turn might be due to reduced activity and expression of phosphatases, such as mitogen-activated protein kinase phosphatase 1 and protein phosphatase A2. Other mechanisms proposed include increased expression of GRβ, which competes with and thus inhibits activated GRα; increased secretion of macrophage migration inhibitory factor; competition with the transcription factor activator protein 1; and reduced expression of histone deacetylase (HDAC) 2. HDAC2 appears to mediate the action of steroids to switch off activated inflammatory genes, but in patients with COPD, patients with severe asthma, and smokers with asthma, HDAC2 activity and expression are reduced by oxidative stress through activation of phosphoinositide 3-kinase δ. Strategies for managing steroid resistance include alternative anti-inflammatory drugs, but a novel approach is to reverse steroid resistance by increasing HDAC2 expression, which can be achieved with theophylline and phosphoinositide 3-kinase δ inhibitors. Long-acting β(2)-agonists can also increase steroid responsiveness by reversing GRα phosphorylation. Identifying the molecular mechanisms of steroid resistance in asthmatic patients and patients with COPD can thus lead to more effective anti-inflammatory treatments.

PMID: 23360759 [PubMed - as supplied by publisher]