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L'essentiel de la littérature réçente en Pneumologie

Dans cette rubrique on vous propose une revue de la littérature à travers une sélection d'abstracts d'articles originaux.
On essaiera de vous tenir informé des dernières nouveautés de recherche en matière de Pneumologie. On ne vous fournit que le résumé de l'article et le lien correspondant, pour accéder à l'article en full text vous devez être inscrits à la revue correspondante.
Cliquez ici pour consulter la liste des revues de Pneumologie disponibles en libre accès.



Inflammatory and Co-Morbid Features of Patients with Severe Asthma and Frequent Exacerbations. Imprimer Envoyer
Jeudi, 25 Août 2016 15:23

RATIONALE: Reducing asthma exacerbation frequency is an important criterion for approval of asthma therapies, but the clinical features of exacerbation prone asthma (EPA) remain incompletely defined.
OBJECTIVE: Describe the clinical, physiological, inflammatory and co-morbidity factors associated with EPA.

METHODS: Baseline data from the NHLBI Severe Asthma Research Program-3 were analyzed. An exacerbation was defined as a burst of systemic corticosteroids lasting ≥3 days. Patients were classified by their number of exacerbations in the past year - none, few (1-2) or exacerbation prone (≥3). Replication of a multivariable model was performed with data from the SARP 1+2 cohort.

MEASUREMENTS AND MAIN RESULTS: Of 709 subjects in the SARP-3 cohort, 294 (41%) had no exacerbations, and 173 (24%) were exacerbation prone in the prior year. Several factors normally associated with severity (asthma duration, age, sex, race, and socioeconomic status) did not associate with exacerbation frequency in SARP-3; bronchodilator responsiveness also discriminated exacerbation proneness from asthma severity. In the SARP-3 multivariable model, blood eosinophils, BMI and bronchodilator responsiveness were positively associated with exacerbation frequency [rate ratios (95%CI); 1.6 (1.2-2.1) for every log unit of eosinophils, 1.3 (1.1-1.4) for every 10 BMI units, and 1.2 (1.1-1.4) for every 10% increase in bronchodilatory responsiveness]. Chronic sinusitis and gastroesophageal reflux were also associated with exacerbation frequency [1.7 (1.4-2.1) and 1.6 (1.3-2.0)], even after adjustment for multiple factors. These effects were replicated in the SARP 1+2 multivariable model.

CONCLUSIONS: EPA may be a distinct susceptibility phenotype with implications for the targeting of exacerbation prevention strategies. Clinical trial registration available at www.clinicaltrials.gov, ID NCT01760915.

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Residual Volume and Total Lung Capacity to Assess Reversibility in Obstructive Lung Disease. Imprimer Envoyer
Jeudi, 25 Août 2016 15:23

BACKGROUND: Reversibility of obstructive lung disease is traditionally defined by changes in FEV1 or FVC in response to bronchodilators. These may not fully reflect changes due to a reduction in hyperinflation or air-trapping, which have important clinical implications. To date, only a handful of studies have examined bronchodilators' effect on lung volumes. The authors sought to better characterize the response of residual volume and total lung capacity to bronchodilators.

METHODS: Responsiveness of residual volume and total lung capacity to bronchodilators was assessed with a retrospective analysis of pulmonary function tests of 965 subjects with obstructive lung disease as defined by the lower limit of normal based on National Health and Nutritional Examination Survey III prediction equations.

RESULTS: A statistically significant number of subjects demonstrated response to bronchodilators in their residual volume independent of response defined by FEV1 or FVC, the American Thoracic Society and European Respiratory Society criteria. Reduced residual volume weakly correlated with response to FEV1 and to FVC. No statistically significant correlation was found between total lung capacity and either FEV1 or FVC.

CONCLUSIONS: A significant number of subjects classified as being nonresponsive based on spirometry have reversible residual volumes. Subjects whose residual volumes improve in response to bronchodilators represent an important subgroup of those with obstructive lung disease. The identification of this subgroup better characterizes the heterogeneity of obstructive lung disease. The clinical importance of these findings is unclear but warrants further study.

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Pulmonary Hypertension in Diffuse Parenchymal Lung Diseases. Imprimer Envoyer
Jeudi, 25 Août 2016 15:23

Pulmonary hypertension (PH) can be triggered by any number of disease processes that result in increased pulmonary vascular resistance. Although historically associated with idiopathic pulmonary arterial hypertension (iPAH), the majority of patients with PH do not have the idiopathic subtype, but rather PH associated with another underlying diagnosis, such as left heart or lung disease. The World Health Organization (WHO) classification of PH helps conceptualize the different categories based on presumed etiology. WHO group 3 is PH associated with lung disease.

This review focuses on PH in diffuse parenchymal lung diseases (DPLD) such as the idiopathic interstitial pneumonias and other more rare forms of DPLD. Although there are clear associations of PH with DPLD, the exact pathophysiologic mechanisms and full clinical significance remain uncertain. Treatment of PH related to DPLD remains investigational, but an area of great interest given the negative prognostic implications and the growing number of available pulmonary vasoactive agents.

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