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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.



Tracking MET de-addiction in lung cancer: A road towards the oncogenic target. Imprimer Envoyer
Mardi, 29 Août 2017 07:18
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Tracking MET de-addiction in lung cancer: A road towards the oncogenic target.

Cancer Treat Rev. 2017 Aug 20;60:1-11

Authors: Pilotto S, Carbognin L, Karachaliou N, Ma PC, Rosell R, Tortora G, Bria E

Abstract
The discovery of druggable oncogenic drivers (i.e. EGFR and ALK), along with the introduction of comprehensive tumor genotyping techniques into the daily clinical practice define non-small-cell lung cancer (NSCLC) asa group of heterogeneous diseases, requiring a context-personalized clinico-therapeutical approach. Among the most investigated biomarkers, the MET proto-oncogene has been extensively demonstrated to play a crucial role throughout the lung oncogenesis, unbalancing the proliferation/apoptosis signaling and influencing the epithelial-mesenchymal transition and the invasive phenotype. Nevertheless, although different mechanisms eliciting the aberrant MET-associated oncogenic stimulus have been detected in lung cancer (such as gene amplification, increased gene copy number, mutations and MET/HGF overexpression), to date no clinically impactful results have been achieved with anti-MET tyrosine kinase inhibitors and monoclonal antibodies in the context of an unselected or MET enriched population. Recently, MET exon 14 splicing abnormalities have been identified asa potential oncogenic target in lung cancer, able to drive the activity of MET inhibitors in molecularly selected patients. In this paper, the major advancement and drawbacks of MET history in lung cancer are reviewed, underlying the renewed scientific euphoria related to the recent identification of MET exon 14 splicing variants asan actionable oncogenic target.

PMID: 28843992 [PubMed - as supplied by publisher]

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Safety and efficacy of pirfenidone in severe Idiopathic Pulmonary Fibrosis a real-world observational study. Imprimer Envoyer
Mardi, 29 Août 2017 07:18
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Safety and efficacy of pirfenidone in severe Idiopathic Pulmonary Fibrosis a real-world observational study.

Pulm Pharmacol Ther. 2017 Aug 23;:

Authors: Tzouvelekis A, Ntolios P, Karampitsakos T, Tzilas V, Anevlavis S, Bouros E, Steiropoulos P, Koulouris N, Stratakos G, Froudarakis M, Bouros D

Abstract
BACKGROUND: Pirfenidone is a novel anti-fibrotic drug that has shown efficacy in five randomized multicenter clinical trials enrolling patients with Idiopathic Pulmonary Fibrosis of mild-to-moderate disease severity. Scarce data supports the use of pirfenidone in IPF patients with more advanced disease.
OBJECTIVE: To investigate the safety and efficacy profile of pirfenidone in IPF patients with severe lung function impairment.
PATIENTS AND METHODS: This was a retrospective study enrolling patients with advanced IPF (FVC%predicted < 50% and/or (DLco%predicted <35%) receiving pirfenidone for at least 6 months.
RESULTS: Between September 2011 and March 2013, we identified 43 patients with severe IPF (baseline meanFVC%predicted±SD: 63.8 ± 20.3, meanDLCO%predicted: 27.3 ± 8.2), of mean age±SD: 66.3 + 9.7, 34 males (81%) that received pirfenidone (2.403 mg/daily) for one year. Pirfenidone treatment was associated with a trend towards decrease in functional decline compared to 6-months before treatment initiation but failed to show any benefit after one year of treatment (ΔFVC: -3.3 ± 4.6 vs 0.49 ± 11.4 and vs. -5.8 ± 11.8, p = 0.06 and p = 0.04, respectively and ΔDLCO: -13.3 ± 15.2 vs. -10.1 ± 16.6 and vs. 28.3 ± 19.2, p = 0.39 and p = 0.002, respectively). Gastrointestinal disorders (34.9%), fatigue (23.2%) and photosensitivity (18.6%) were the most common adverse events. Adverse events led to treatment discontinuation in 9 patients (20.9%) and dose reduction in 14 (32.5%).
CONCLUSION: Pirfenidone appears to be safe when administered in patients with advanced IPF. Pirfenidone efficacy in IPF patients with severe lung function impairment may fade away after 6 months of treatment.

PMID: 28843616 [PubMed - as supplied by publisher]

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A systematic review of diagnostic methods to differentiate acute lung injury/acute respiratory distress syndrome from cardiogenic pulmonary edema. Imprimer Envoyer
Mardi, 29 Août 2017 07:18
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A systematic review of diagnostic methods to differentiate acute lung injury/acute respiratory distress syndrome from cardiogenic pulmonary edema.

Crit Care. 2017 Aug 25;21(1):228

Authors: Komiya K, Akaba T, Kozaki Y, Kadota JI, Rubin BK

Abstract
BACKGROUND: Discriminating acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) from cardiogenic pulmonary edema (CPE) is often challenging. This systematic review examines studies using biomarkers or images to distinguish ALI/ARDS from CPE.
METHODS: Three investigators independently identified studies designed to distinguish ALI/ARDS from CPE in adults. Studies were identified from PubMed, and the Cochrane Central Register of Controlled Trials database until July 3, 2017.
RESULTS: Of 475 titles and abstracts screened, 38 full texts were selected for review, and we finally included 24 studies in this systematic review: 21 prospective observational studies, two retrospective observational studies, and one retrospective combined with prospective study. These studies compared various biomarkers to differentiate subjects with ALI/ARDS and in those with CPE, and 13 calculated the area under the receiver operator characteristic curve (AUC). The most commonly studied biomarker (four studies) was brain natriuretic peptide (BNP) and the discriminatory ability ranged from AUC 0.67-0.87 but the timing of measurement varied. Other potential biomarkers or tools have been reported, but only as single studies.
CONCLUSIONS: There were no identified biomarkers or tools with high-quality evidence for differentiating ALI/ARDS from CPE. Combining clinical criteria with validated biomarkers may improve the predictive accuracy.

PMID: 28841896 [PubMed - in process]

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