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Background: The allocation of donor lungs for transplantation in Germany was changed on 10 December 2011 to a system based on the Lung Allocation Score (LAS). The aim of the present study is to determine whether this change has prolonged the survival of patients on the transplant waiting list and of those who have undergone lung transplantation (LTx)., Methods: We retrospectively compared data from the three-year periods before and after the change to an LAS-based allocation system (2009-2011 vs. 2012-2014)., Results: The number of patients on the active waiting list declined from 606 on 12/31/2011 to 432 on 12/31/2014, a 29% decrease. The number of patients who died while on the waiting list fell from 306 in 2009-2011 to 226 in 2012-2014 (-26%, p = 0.04). Waiting-list mortality declined across all disease groups. Meanwhile, the number of lung transplantation procedures per year increased by 21% over the period of observation, from 865 to 1045. During the period in which the LAS was used, the proportion of transplant recipients with restrictive lung disease (46% vs. 31%; p<0.001) surpassed the proportion of those with a diagnosis of obstructive lung disease (33% vs. 40%; p = 0.003). The percentage of transplantations in patients treated with mechanical ventilation or extracorporeal respiratory support before transplantation rose from 9% to 13%. The one-year survival rate after lung transplantation was 76% in 2009-2011 and 81% in 2012-2014., Conclusion: The introduction of the LAS in Germany was associated with a decrease in the number of patients on the waiting list, and also in the number of deaths among patients on the waiting list. The distribution of primary diagnoses among transplant recipients shifted away from obstructive and toward restrictive lung diseases. In the future, additional parameters of patients on the waiting list should be considered to enable further improvement of the allocation model.

Background: Ever since higher overall mortality rates due to heat stress were reported during the European heat waves of 2003 and 2006, the relation between heat waves and disease-specific events has been an object of scientific study. The effects of heat waves on the morbidity and mortality of persons with chronic lung disease remain unclear., Methods: We conducted a systematic search using PubMed, the Cochrane Library, and Google Advanced Search to identify relevant studies published between 1990 and 2015. The reference lists of the primarily included articles were searched for further pertinent articles. All articles were selected according to the PRISMA guidelines. The heat-wave-related relative excess mortality was descriptively expressed as a mean daily rate ratio ([incidence 1]/[incidence 2]), and the cumulative excess risk (CER) was expressed in percent., Results: 33 studies with evaluable raw data concerning the effect of heat waves on patients with chronic lung disease (chronic obstructive pulmonary disease, bronchial asthma, pulmonary arterial hypertension, and idiopathic pulmonary fibrosis) were analyzed in this review. By deriving statistics from the overall data set, we arrived at the conclusion that future heat waves will-with at least 90% probability-result in a mean daily excess mortality (expressed as a rate ratio) of at least 1.018, and-with 50% probability-in a mean daily excess mortality of at least 1.028. These figures correspond, respectively, to 1.8% and 2.8% rises in the daily risk of death., Conclusion: Heat waves significantly increase morbidity and mortality in patients with chronic lung disease. The argument that the excess mortality during heat waves is compensated for by a decrease in mortality in the subsequent weeks/months (mortality displacement) should not be used as an excuse for delay in implementing adaptive strategies to protect lung patients from this risk to their health.

The 2009 European Guidelines on Pulmonary Hypertension did not cover only pulmonary arterial hypertension (PAH) but also some aspects of pulmonary hypertension (PH) in chronic lung disease. These guidelines point out that the drugs currently used to treat patients with PAH (prostanoids, endothelin receptor antagonists and phosphodiesterase type-5 inhibitors) have not been sufficiently investigated in other forms of PH. Therefore, the use of these drugs in patients with chronic lung disease and PH is not recommended. This recommendation, however, is not always in agreement with medical needs as physicians feel sometimes inclined to also treat other forms of pulmonary hypertension which may affect the quality of life and survival of these patients in a similar manner as in PAH. In June 2010, a consensus conference was held in Cologne, Germany, to discuss open and controversial issues surrounding the practical implementation of the European Guidelines. The conference was sponsored by the German Society of Cardiology, the German Society of Respiratory Medicine and the German Society of Pediatric Cardiology (DGK, DGP and DGPK). To this end, a number of working groups were initiated, one of which was specifically dedicated to the diagnosis and treatment of PH due to chronic lung disease. This manuscript describes in detail the results and recommendations of this working group which were last updated in October 2011., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

In several papers an increased quantity of cell-free plasma DNA as well as the presence of long DNA fragments in cell-free plasma and serum has been described. We isolated cell-free DNA from plasma, serum, and bronchial lavage supernatants from 33 lung cancer patients and 27 patients with a benign lung disease. The DNA was amplified by real-time PCR, and the quantity as well as the DNA integrity was determined. We did not find significant differences between the patient populations. Our results led us to conclude that this method is not useful in a diagnostic setting and is not able to differentiate between lung cancer patients and patients with a benign lung disease.

Aims The risk of mortality from the coronavirus disease that emerged in 2019 (COVID-19) is increased by comorbidity from cardiovascular and pulmonary diseases. Air pollution also causes excess mortality from these conditions. Analysis of the first severe acute respiratory syndrome coronavirus (SARS-CoV-1) outcomes in 2003, and preliminary investigations of those for SARS-CoV-2 since 2019, provide evidence that the incidence and severity are related to ambient air pollution. We estimated the fraction of COVID-19 mortality that is attributable to the long-term exposure to ambient fine particulate air pollution. Methods and results We characterized global exposure to fine particulates based on satellite data, and calculated the anthropogenic fraction with an atmospheric chemistry model. The degree to which air pollution influences COVID-19 mortality was derived from epidemiological data in the USA and China. We estimate that particulate air pollution contributed ∼15% (95% confidence interval 7–33%) to COVID-19 mortality worldwide, 27% (13 – 46%) in East Asia, 19% (8–41%) in Europe, and 17% (6–39%) in North America. Globally, ∼50–60% of the attributable, anthropogenic fraction is related to fossil fuel use, up to 70–80% in Europe, West Asia, and North America. Conclusion Our results suggest that air pollution is an important cofactor increasing the risk of mortality from COVID-19. This provides extra motivation for combining ambitious policies to reduce air pollution with measures to control the transmission of COVID-19. [ABSTRACT FROM AUTHOR]

Summary Background Lung volume reduction of emphysematous lobes results in clinical improvement for patients with severe emphysema. However, some segments within a lobe are often substantially more diseased than others, thereby warranting a more targeted approach of the emphysematous parts of a lobe. We therefore did a study to assess whether or not selective sequential treatment of the more diseased upper lobe segments with bronchoscopic vapour ablation led to clinical improvement. Methods For the multicentre, parallel-group, randomised, controlled, open-label Sequential Staged Treatment of Emphysema with Upper Lobe Predominance (STEP-UP) trial, adult patients aged 45–75 years with severe, upper lobe-predominant emphysema with a forced expiratory volume in 1 s (FEV 1 ) between 20% and 45%, substantial hyperinflation, and post-rehabilitation 6-min walk test (6MWT) greater than 140 m were enrolled from 13 hospital sites in Europe (ten sites) and Australia (three sites). A computer-generated blocked randomisation scheme (block size three per site based on a random table from an independent biostatistician) stratified by site was used to randomly assign enrolled patients 2:1 to segmental vapour ablation (treatment group) or standard medical management (control group). Patients and investigators were not masked to group assignment. The primary efficacy endpoints were statistically significant changes in FEV 1 and St George's Respiratory Questionnaire (SGRQ-C) scores between trial groups at 6 months, analysed by intention to treat. This study is registered with ClinicalTrials.gov , number NCT01719263 . Findings Between June 30, 2013, and Oct 1, 2014, 134 patients were screened and 70 were enrolled and randomly assigned: 46 to the treatment group and 24 to the control group. One patient in the treatment group did not receive treatment because of physician decision post-randomisation; this patient is excluded from all analyses. The mean relative improvement in FEV 1 between the treatment group versus the control group was 14·7% (95% CI 7·8–21·5%; p<0·0001) and in SGRQ-C was −9·7 points (95% CI −15·7 to −3·7; p=0·0021). COPD exacerbation was the most common serious adverse event, occurring in 11 (24%) of 45 patients in the treatment group and one (4%) of 24 in the control group. One exacerbation resulted in a patient death 84 days after treatment; this was judged by the data and safety monitoring board to be possibly related to treatment. No pneumothorax occurred within 30 days of treatment. Interpretation Compared with standard medical management, targeted thermal vapour ablation of more diseased segments and preservation of less diseased segments resulted in clinically meaningful and statistically significant improvements in lung function and quality of life at 6 months, with an acceptable safety profile. Funding Uptake Medical. [ABSTRACT FROM AUTHOR]

Abstract: Background: In patients with chronic obstructive pulmonary disease (COPD) weight loss frequently occurs that may ultimately lead to cachexia as a serious co-morbidity, indicating severely impaired functional capacity, health status and increased mortality. Increased energy expenditure due to mechanic and metabolic inefficiency and systemic inflammation are determinants of a hypermetabolic state that is not balanced by dietary intake. Anorexia may importantly contribute to weight loss in COPD, however, the association between immune and hormonal derangement and altered appetite has not been studied in detail. Aim: The aim of the present study was to investigate whether anorexia in COPD is related to inflammation and hormonal derangement in association to weight loss. Methods: We prospectively enrolled 103 consecutive patients with COPD (age 59.8±1.3 years, 35% female, mean FEV1 38.3±1.7%) in comparison to healthy controls of similar age (n =15). Results: In 34 patients (33%) cachexia was diagnosed (weight loss >7.5%, BMI≤24 kg/m2). Cachectic COPD patients had lower BMI (19.0±0.5 vs 25.6±0.7 kg/m2) and impaired lung function (FEV1 31±2% vs 42±2%, FVC 51±3 vs 59±3%, both p <0.001). Inflammatory immune activation (IL-6 and IL-6/IL-10 ratio) was significantly higher in cachectic COPD patients. Analysis of the extent of anorexia (visual analogue scale) revealed that cachectic COPD patients had significantly decreased subjective desire to eat compared to non-cachectic patients (3.5±0.3 vs 6.3±0.2, p <0.001). Patients with COPD and cachexia showed evidence of acquired GH resistance (decreased IGF-1/GH ratio) and insulin resistance (HOMA). Anorexia showed a direct correlation with the IGF-1/GH ratio (r =0.34, p <0.05) and was further related to BMI and % weight loss (both p <0.001). Conclusion: In COPD anorexia relates to hormonal derangement and inflammatory immune activation. Anorexia contributes to development of cachexia. The concept of appetite stimulating therapy emerges as a novel therapeutic option in cachectic COPD patients. [Copyright &y& Elsevier]

Abstract: Chronic obstructive pulmonary disease (COPD) is a multisystemic inflammatory disease characterized by pulmonary and extrapulmonary symptoms. The impaired lung function has long-term implications on metabolism and homeostasis of many organ systems such as the skeleton, heart, brain and skeletal muscle. The occurrence and prevalence of anemia in COPD has rarely been studied. Anemia is such a common and simple clinical finding that we may underestimate its physiological relevance in COPD. The aim of the study was to retrospectively investigate the prevalence of anemia in a large population of COPD patients and to compare it to patients with chronic heart failure, renal insufficiency, cancer and asthma. A population of 7337 patients that was treated in the University Hospital Charité, Berlin, Germany, from 1996 to 2003 was subsetted according to the ICD-9/10 code of the discharge diagnoses into the above-mentioned diagnoses groups. The overall prevalence of anemia in COPD patients was 23.1%. It was comparable to the prevalence of anemia we found in patients with chronic heart failure (23.3%). Patients with renal insufficiency and cancer presented the highest anemia frequencies. The high prevalence of anemia in hospitalised COPD patients that were treated mostly for exacerbations gives evidence that anemia is also a comorbidity in COPD and may contribute to exercise limitation and dyspnoea. [Copyright &y& Elsevier]