Adenosine and related purines have established roles in inflammation, and elevated airway concentrations are predicted in patients with COPD. However, accurate airway surface purine measurements can be confounded by stimulation of purine release during collection of typical respiratory samples.

Airway samples were collected noninvasively as exhaled breath condensate (EBC) from 36 healthy nonsmokers (NS group), 28 healthy smokers (S group), and 89 subjects with COPD (29 with GOLD [Global Initiative for Chronic Obstructive Lung Disease] stage II, 29 with GOLD stage III, and 31 with GOLD stage IV) and analyzed with mass spectrometry for adenosine, adenosine monophosphate (AMP), and phenylalanine, plus urea as a dilution marker. Variable dilution of airway secretions in EBC was controlled using ratios to urea, and airway surface concentrations were calculated using EBC to serum urea-based dilution factors.

EBC adenosine to urea ratios were similar in NS (0.20 ± 0.21) and S (0.22 ± 0.20) groups but elevated in those with COPD (0.32 ± 0.30, P < .01 vs NS). Adenosine to urea ratios were highest in the most severely affected cohort (GOLD IV, 0.35 ± 0.34, P < .01 vs NS) and negatively correlated with FEV₁ (r = –0.27, P < .01). Elevated AMP to urea ratios were also observed in the COPD group (0.58 ± 0.97 COPD, 0.29 ± 0.35 NS, P < .02), but phenylalanine to urea ratios were similar in all groups. Airway surface adenosine concentrations calculated in a subset of subjects were 3.2 ± 2.7 µM in those with COPD (n = 28) relative to 1.7 ± 1.5 µM in the NS group (n = 16, P < .05).

Airway purines are present on airway surfaces at physiologically significant concentrations, are elevated in COPD, and correlate with markers of COPD severity. Purinergic signaling pathways are potential therapeutic targets in COPD, and EBC purines are potential noninvasive biomarkers.

Although high-intensity noninvasive positive pressure ventilation (HI-NPPV) is superior to low-intensity noninvasive positive pressure ventilation (LI-NPPV) in controlling nocturnal hypoventilation in stable hypercapnic patients with COPD, it produces higher amounts of air leakage, which, in turn, could impair sleep quality. Therefore, the present study assessed the difference in sleep quality during HI-NPPV and LI-NPPV.

A randomized, controlled, crossover trial comparing sleep quality during HI-NPPV (mean inspiratory positive airway pressure 29 ± 4 mbar) and LI-NPPV (mean inspiratory positive airway pressure 14 mbar) was performed in 17 stable hypercapnic patients with COPD who were already familiar with HI-NPPV.

Thirteen patients (mean FEV₁ 27% ± 11% predicted) completed the trial; four patients refused to sleep under LI-NPPV. There was no significant difference in sleep quality between the treatment groups (all P > .05), with a mean difference of –3.0% (95% CI, –10.0 to 3.9; P = .36) in the primary outcome, namely non-rapid eye movement sleep stages 3 and 4. However, nocturnal Paco₂ was lower during HI-NPPV compared with LI-NPPV, with a mean difference of –6.4 mm Hg (95% CI, –10.9 to –1.8; P = .01).

In patients with COPD, high inspiratory pressures used with long-term HI-NPPV produce acceptable sleep quality that is no worse than that produced by lower inspiratory pressures, which are more traditionally applied in conjunction with LI-NPPV. In addition, higher pressures are more successful in maintaining sufficient alveolar ventilation compared with low pressures. Thus, HI-NPPV is a very promising new approach, but still requires large, longer-term trials to determine the impact on outcomes such as exacerbation rates and longevity.

German Clinical Trials Register (DRKS); No.: DRKS00000520; URL: www.drks.de

There is considerable evidence that oxidative stress is increased in patients with COPD, although little information is available about its relationship with the structural and functional alterations produced by COPD. In this study, we evaluated the relationship between 8-isoprostane in exhaled breath condensate (EBC) of stable patients with COPD and the main parameters of the disease (such as dyspnea), stages of severity, lung parenchyma densities, lung function impairment, and exercise tolerance in order to identify the predictors of airway oxidative stress.

In a cross-sectional study, we included 76 men with moderate to very severe COPD. 8-Isoprostane levels in EBC were measured by enzyme immunoassay. Regional lung densities were measured by lung densitometry with high-resolution CT scanning. Arterial blood gas levels, lung volumes, and diffusing capacity were determined. Patients performed a 6-min walk test and an incremental exercise test with measurement of breathing pattern and operating lung volumes.

Significant severity-related differences in 8-isoprostane were identified according to the BMI, obstruction, dyspnea, and exercise (BODE) index. 8-Isoprostane levels were related to smoking intensity, lung densities in expiration, static lung volumes, Pao₂, diffusion capacity, distance walked in 6 min, peak oxygen uptake, and anaerobic threshold. Concentration of 8-isoprostane was higher in the 60 patients (79%) who developed dynamic hyperinflation than in the remaining 16 (21%) who did not. In a multivariate linear regression analysis using 8-isoprostane as a dependent variable, end-expiratory lung volume change and Pao₂ were retained in the prediction model (r² = 0.734, P < .001).

In stable patients with COPD, oxygen level and dynamic hyperinflation are related to airway oxidative stress.

The number of oncogeriatric patients with non-small cell lung cancer (NSCLC) is expected to increase in the next decades.

We used the French Society of Thoracic and Cardiovascular Surgery database Epithor that includes information on > 140,000 procedures from 98 institutions. We prospectively collected data from January 2004 to December 2008 on 1,969 patients aged ≥ 70 years with NSCLC stage I or II and matched them with 1,969 control subjects aged < 70 years for sex, American Society of Anesthesia score, performance status, and FEV₁. Surgical treatment and postoperative outcomes were compared between the two age groups.

The absence of radical lymphadenectomy was more frequent in the older patients (14%, n = 269) than in the younger patients (9%, n = 170) (P < .0001). There was no significant difference in type of resection between older and younger patients, respectively (pneumonectomy, 8% [n = 164] vs 11% [n = 216]; lobectomy, 79% [n = 1,559] vs 77% [n = 1,521]; bilobectomy, 4% [n = 88] vs 5% [n = 97]; sublobar resection, 7% [n = 143] vs 6% [n = 118]; P = .08). Differences in number (P = .07) and severity (P = .69) of complications were not significant. Postoperative mortality was higher in elderly patients at every end point (30-day mortality, 3.6% [n = 70] vs 2.2% [n = 43] [P = .01]; 60-day mortality, 4.1% [n = 80] vs 2.4% [n = 47] [P = .003]; 90-day mortality, 4.7% [n = 93] vs 2.5% [n = 50] [P = .0002]).

Elderly patients with NSCLC should not be denied pulmonary resection on the basis of chronologic age alone. Among patients aged ≥ 70 years, 90-day mortality compared acceptably with mortality among younger matched patients. Additionally, the data show that for older patients, a 90-day mortality better represents their real mortality risk than 30- or 60-day figures. Our contemporary, multiinstitutional data importantly reveal that elderly patients, compared with their younger counterparts, do not have increased morbidity, incidence, or severity after pulmonary resection.