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No Significant Detectable Anti-infection Effects of Aspirin and Statins in Chronic Obstructive Pulmonary Disease.

No Significant Detectable Anti-infection Effects of Aspirin and Statins in Chronic Obstructive Pulmonary Disease.

Int J Med Sci. 2015;12(3):280-7

Authors: Yayan J

Abstract
BACKGROUND: Past studies have shown that aspirin and statins decrease the rate and severity of exacerbation, the rate of hospitalization, and mortality in chronic obstructive pulmonary disease (COPD). Although these studies are relatively new, there is evidence that new therapeutic strategies could prevent exacerbation of COPD.
TRIAL DESIGN: This article examines retrospectively the possibility of using aspirin and statins to prevent exacerbation and infection in patients with COPD.
METHODS: All patients with COPD were identified from hospital charts in the Department of Internal Medicine, Saarland University Medical Center, Germany, between 2004 and 2014.
RESULTS: The study examined 514 medical reports and secured a study population of 300 with COPD. The mean age was 69 ± 10 years (206 men, 68.7%, 95% CI, 63.4‒73.9; 94 women, 31.3%, 95% CI, 26.1‒36.6). The study results did not show a causal relationship between aspirin and statins and prevention of exacerbation and infection in patients with COPD.
CONCLUSION: In contrast, in this study, the exacerbation and infection rates increased under medication with aspirin and statins (p = 0.008).

PMID: 25798054 [PubMed - in process]

A SYSTEMATIC REVIEW ON THE EFFICACY AND SAFETY OF A FIXED-DOSE COMBINATION OF UMECLIDINIUM AND VILANTEROL FOR THE TREATMENT OF COPD.

A SYSTEMATIC REVIEW ON THE EFFICACY AND SAFETY OF A FIXED-DOSE COMBINATION OF UMECLIDINIUM AND VILANTEROL FOR THE TREATMENT OF COPD.

Chest. 2015 Mar 12;

Authors: Rodrigo GJ, Neffen H

Abstract
Background: COPD guidelines recommend the combined use of inhaled long-acting beta2-agonists (LABAs) and long-acting muscarinic antagonists (LAMAs) if symptoms are not improved by a single agent. This systematic review tested the hypothesis that the bronchodilator effect of the LABA/LAMA combination, umeclidinium/vilanterol (UMEC/VIL), would translate into better outcomes without incurring increased adverse events (AEs).
Methods: This is a systematic review of randomized, placebo-controlled or cross-over trials (>4 weeks) involving UMEC/VIL compared to its monocomponents, tiotropium or fluticasone/salmeterol. Primary outcomes were trough forced expiratory volume in the first second (FEV1), severe AEs and serious cardiovascular events (SCVEs).
Results: Eleven trials from ten studies (9,609 patients) showed that UMEV/VIL provided superior improvements in lung function compared with UMEC, VIL, tiotropium and FSC (mean trough FEV1 60, 110, 90, and 90 mL respectively, p <0.0001). Also, UMEC/VIL had a greater likelihood of demonstrating a minimal clinical important difference (MCID) in TDI compared with UMEC, and VIL (Number needed to treat for benefit [NNTB] = 14 and 10 respectively). UMEC/VIL therapy significantly reduced the risk of COPD exacerbations compared with UMEC and VIL (NNTB = 42 and 41 respectively). On the contrary, we noted no significant differences with respect to dyspnea, health status, and risk of COPD exacerbation between UMEC/VIL and tiotropium. Regarding safety issues, the incidence of AEs, SAEs, SCVEs and mortality on treatment was similar across treatments suggesting reduced safety concerns with use of UMEC/VIL combination.
Conclusions: Once-daily inhaled UMEC/VIL showed superior efficacy compared with monocomponents, tiotropium and fluticasone/combination in patients with moderate-to-severe COPD.

PMID: 25798635 [PubMed - as supplied by publisher]

Comparison of Clinical Efficacy and Safety between Indacaterol and Tiotropium in COPD: Meta-Analysis of Randomized Controlled Trials.

Comparison of Clinical Efficacy and Safety between Indacaterol and Tiotropium in COPD: Meta-Analysis of Randomized Controlled Trials.

PLoS One. 2015;10(3):e0119948

Authors: Kim JS, Park J, Lim SY, Oh YM, Yoo KH, Park YB, Sheen SS, Kim MJ, Carriere KC, Jung JY, Park HY

Abstract
Two once-daily inhaled bronchodilators, indacaterol and tiotropium, are widely used as first-line therapy in stable COPD patients. This study was performed to compare the clinical efficacy and safety between indacaterol and tiotropium in patients with moderate-to-severe COPD. MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials were searched to identify all published randomized controlled trials (RCTs). The primary outcome was trough forced expiratory volume in 1 second (FEV1) at week 12. Four RCTs were eligible for inclusion (three RCTs with moderate-to-severe COPD patients and one RCT with only severe COPD patients). Trough FEV1 at weeks 12 and 26 were not significantly different between indacaterol and tiotropium by the standardized mean difference with 0.014 (95% CI, -0.036, 0.063, I2= 23.5%) and with 0.037 (95% CI, -0.059 to 0.133, I2= 0%) along with differences in means of 0.003L and 0.014L, respectively. Indacaterol and tiotropium also showed similar St. George`s Respiratory Questionnaire (SGRQ) total scores and percentages of patients with SGRQ improvement (≥ 4 units) at week 26. The incidences of nasopharyngitis, serious cardiovascular events, and serious adverse events were not different between indacaterol and tiotropium, while those of cough (OR = 1.68, P < 0.001, and RR = 1.63) and COPD worsening (OR = 1.18, P = 0.003, and RR = 1.12) were higher for indacaterol than tiotropium. However, when one study with only severe COPD patients was removed from the meta-analysis, the difference in the incidence of COPD worsening between indacaterol and tiotropium became non-significant (OR = 1.13, P = 0.204, and RR = 1.09). The clinical efficacy and serious adverse events between indacaterol and tiotropium were equivocal in patients with moderate-to-severe COPD. Cough is a common complaint associated with indacaterol, and COPD worsening needs to be carefully monitored in severe COPD patients when treated with indacaterol.

PMID: 25799171 [PubMed - as supplied by publisher]

La graisse intramusculaire comme modulateur du risque cardiométabolique chez le BPCO

La perte de masse musculaire périphérique et l’accumulation excessive de graisse sont associés à la mortalité et morbidité cardiovasculaire chez le sujet BPCO. Notre objectif était d’identifier la place de l’infiltration graisseuse musculaire au sein des marqueurs du risque cardiométabolique.

Les paramètres métaboliques et inflammatoires de 78 sujets BPCO (64±9ans) ont été étudiés, ainsi que leur rigidité artérielle et fonction endothéliale, répartis en tertiles d’index de masse corporelle [IMC] : faible [15&lt;IMC≤23], moyen [23&lt;IMC≤28] et haut [28&lt;IMC≤36]kg/m2). À partir de coupes CT à mi-cuisse, étaient déterminé l’infiltration graisseuse musculaire (IGM : volume de graisse intramusculaire/[volume de graisse intramusculaire+volume musculaire]] fondées sur les densités : –190 à –30 ; –30 à +30 and +30 à +70UH pour la graisse, la graisse intramusculaire et le muscle respectivement).

Le tertile le plus élevé des sujets BPCO a montré l’IGM le plus élevé : 52 [43–60] %, pour 47 [38–55] % et 34 [29–38] % des BPCO à IMC moyen et faible respectivement. Un volume musculaire élevé était associé à un NT ProBNP, fibrinogène bas et des thiols plus élevés. Au contraire, le pourcentage de graisse intramusculaire était associé négativement à la capacité anti-oxydante (rapport thiols/protéines : r =–0,50, p =0,009) et à la SaO2 (r =–0,45, p =0,01) dans le groupe avec IMC élevé, mais également avec la fonction endothéliale (r =–0,40, p =0,04) chez les sujets avec IMC bas.

Conclusion L’infiltration de graisse intra-musculaire peut contribuer à une augmentation du risque cardiométabolique non seulement chez le BPCO obèse mais aussi chez le BPCO sans surcharge graisseuse/dénutri.

Les thérapies ciblées dans les cancers bronchiques non à petites cellules en 2014

Depuis quelques années, la perception et la prise en charge du cancer bronchique ont considérablement évolué. L’évolution des techniques de séquençage moléculaire a permis l’identification d’anomalies oncogéniques associées à des profils moléculaires particuliers sensibles à certaines thérapies ciblées. Les mutations du gène de l’EGFR ou du gène de fusion ELM4-ALK sont les plus connues et les seules accessibles à un traitement spécifique de nos jours (ayant une autorisation de mise sur le marché), mais de nombreuses autres cibles ont été identifiées, mettant le concept d’une médecine personnalisée au cœur de la prise en charge du patient atteint d’un cancer bronchique. Le développement de plateformes moléculaires facilite considérablement la détection en routine des mutations EGFR, HER2, KRAS, BRAF, PI3KCA et le réarrangement EML4-ALK.

Nous développerons dans cet article les différents biomarqueurs existants dans le cancer bronchique non à petites cellules (CBNPC), les molécules disponibles ou en cours d’évaluation, ainsi que les principaux axes de recherche clinique dans ce domaine.

For several years, the identification of molecular sequencing alterations has considerably changed the perception and treatment of non-small cell lung cancer (NSCLC). These alterations have been defined as “driver mutations”, such as mutations in EGFR and EML4-ALK fusion gene, and are highly sensitive to specific therapies. Other targets have also been identified recently. Personalized medicine is now a reality for patients with advanced NSCLC on the basis of routine screening for EGFR, HER2, KRAS, BRAF, PI3KCA mutations and EML4-ALK rearrangement.

This article describes identified biomarkers, available targeted therapies, and the main clinical research approaches in NSCLC.

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