Related Articles

STOP accelerating lung aging for the treatment of COPD.

Exp Gerontol. 2014 Apr 5;

Authors: Ito K, Mercado N

Abstract
Life expectancy is assumed to rise continuously and consequently global burden of age-associated diseases is expected to increase. All vital organs begin to lose some function during aging with different rates, and the same happens on the lung. Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs, which progresses very slowly and the majority of patients are therefore elderly. COPD is a major and increasing global health problem with enormous amount of expenditure of indirect/direct health care costs, and therefore, there is urgent need to clarify the molecular mechanism of COPD and develop novel treatments. We here hypothesize that environmental gases, such as cigarette smoke and kitchen pollutants, may accelerate the aging of lung or worsen aging-related events in the lung, leading to defective resolution of inflammation, reduced anti-oxidant capacity and defective disposal of abnormal proteins, and this consequently induces progression of COPD. Recent studies identified some anti-aging small molecules (geroprotectors) that may open up new avenues for the treatment of COPD.

PMID: 24709339 [PubMed - as supplied by publisher]

Publication date: April 2014 Source:Respiratory Medicine, Volume 108, Issue 4

Author(s): Sang-Do Lee , Ming-Shyan Huang , Jian Kang , Ching-Hsiung Lin , Myung Jae Park , Yeon-Mok Oh , Namhee Kwon , Paul W. Jones , Dimitar Sajkov

We evaluated the predictive value of the COPD assessment test (CAT™) for exacerbation in the following six months or time to first exacerbation among COPD patients with previous exacerbations. COPD outpatients with a history of exacerbation from 19 hospitals completed the CAT questionnaire and spirometry over six months. Exacerbation events were prospectively collected using a structured questionnaire. The baseline CAT score categorised into four groups (0–9, 10–19, 20–29, and 30–40) showed strong prediction for time to first exacerbation and modest prediction for any exacerbation or moderate-severe exacerbation (AUC 0.83, 0.64, and 0.63 respectively). In multivariate analyses, the categorised CAT score independently predicted all three outcomes (p = 0.001 or p < 0.001). Compared with the lowest CAT score category, the higher categories were associated with significantly shorter time to first exacerbation and higher exacerbation risks. The corresponding adjusted median time was >24, 14, 9, and 5 weeks and the adjusted RR was 1.00, 1.30, 1.37, and 1.50 in the category of 0–9, 10–19, 20–29, and 30–40 respectively. Exacerbation history (≥2 vs. 1 event in the past year) was related to time to first exacerbation (adjusted HR 1.35; p = 0.023) and any exacerbation during the study period (adjusted RR 1.15; p = 0.016). The results of this study support the use of the CAT as a simple tool to assist in the identification of patients at increased risk of exacerbations. This could facilitate timely and cost-effective implementation of preventive interventions, and improve health resource allocation. Trial registration Clinicaltrials.gov: NCT01254032.

Publication date: April 2014 Source:Respiratory Medicine, Volume 108, Issue 4

Author(s): Kai-Michael Beeh , Stephanie Korn , Jutta Beier , Dalal Jadayel , Michelle Henley , Peter D'Andrea , Donald Banerji

Introduction QVA149 is a novel, inhaled, once-daily dual bronchodilator containing a fixed-dose combination of the long-acting β2-agonist indacaterol and the long-acting muscarinic antagonist glycopyrronium (NVA237), for the treatment of chronic obstructive pulmonary disease (COPD). This study evaluated the effects of QVA149 on exercise tolerance, hyperinflation, lung function and lung volumes versus placebo and tiotropium. Methods Patients with moderate-to-severe COPD were randomized to QVA149 110/50 μg, placebo or tiotropium 18 μg once daily in a blinded, 3-period crossover study for 3 weeks. The primary endpoint was exercise endurance time at Day 21 for QVA149 versus placebo. Results Eighty-five patients were randomized; 86% completed the study. QVA149 significantly improved exercise endurance time at Day 21 compared with placebo (least squares mean treatment difference 60 s [p = 0.006]). No significant improvements in exercise endurance time at Day 21 between QVA149 and tiotropium were found. Dynamic inspiratory capacity (IC) at exercise isotime, trough forced expiratory volume in 1 s, residual volume and functional residual capacity showed significant improvements with QVA149 from Day 1 of treatment that were maintained throughout the study. The safety profiles were similar across groups. Conclusions In patients with moderate-to-severe COPD, once-daily QVA149 significantly improved exercise endurance time compared with placebo which was associated with sustained reductions of lung hyperinflation as indicated by significant improvement in IC at rest and during exercise. Trial registration: ClinicalTrials.gov NCT01294787. Take home message: Dual bronchodilation with QVA149 decreases lung hyperinflation and improves exercise tolerance and lung function in patients with moderate-to-severe COPD.

Publication date: April 2014 Source:Respiratory Medicine, Volume 108, Issue 4

Author(s): M. Molimard , L. Mala , I. Bourdeix , V. Le Gros

Introduction Severe persistent asthma represents a major and costly public health issue. There is evidence that long-term treatment with omalizumab might have disease-modifying activity but data on the consequences of discontinuing treatment after a positive response are limited. The purpose of this study was to investigate—in real-life prescribing conditions—what happens when omalizumab is discontinued in patients with severe, persistent allergic asthma who have responded well to omalizumab treatment. Methods An observational, descriptive, cross-sectional, retrospective study to establish the time to loss of asthma control after the discontinuation of courses of omalizumab treatment of varying duration. Results 24 lung specialists reviewed data from 61 responder patients who had discontinued omalizumab after a mean duration of 22.7 ± 13.1 [range: 2.5; 59.5] months of treatment. Loss of asthma control was documented in 34 patients (55.7%) with a median interval between discontinuation and loss of control of 13.0 months (mean 20.4 ± 2.6 [95% CI: 8.3–28.1]). No correlation was detected between time to loss of control and duration of treatment, although control tended to be sustained for longer in patients whose response had been classified as “excellent” as opposed to “good” (median: 17.0 vs. 12.8 months; NS). Discussion The discontinuation of omalizumab was not associated with any rebound effect or exacerbation of the disease, and control was sustained throughout the follow-up period of at least 6 months in nearly half of all patients, including all of those who had been treated for 3.5 years or more. After the reintroduction of omalizumab, 4 out of 20 patients did not respond again.