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Alterations of cognitive functions have been described in COPD. Our study aimed to disentangle the relationship between the degree of cognitive function and COPD characteristics including quality of life (QoL).Data from 1969 COPD patients of the COSYCONET cohort (GOLD grades 1–4; 1216 male/ 753 female; mean (SD) age 64.9 ± 8.4 years) were analysed using regression and path analysis. The DemTect screening tool was used to measure cognitive function, and the St. George‘s respiratory questionnaire (SGRQ) to assess disease-specific QoL.DemTect scores were =60 years of age. For statistical reasons, we used the average of both algorithms independent of age in all subsequent analyses. The DemTect scores were associated with oxygen content, 6-min-walking distance (6-MWD), C-reactive protein (CRP), modified Medical Research Council dyspnoea scale (mMRC) and the SGRQ impact score. Conversely, the SGRQ impact score was independently associated with 6-MWD, FVC, mMRC and DemTect. These results were combined into a path analysis model to account for direct and indirect effects. The DemTect score had a small, but independent impact on QoL, irrespective of the inclusion of COPD-specific influencing factors or a diagnosis of cognitive impairment.We conclude that in patients with stable COPD lower oxygen content of blood as a measure of peripheral oxygen supply, lower exercise capacity in terms of 6-MWD, and higher CRP levels were associated with reduced cognitive capacity. Furthermore, a reduction in cognitive capacity was associated with reduced disease-specific quality of life. As a potential clinical implication of this work, we suggest to screen especially patients with low oxygen content and low 6-MWD for cognitive impairment.

ObjectiveCumulative evidence indicates that childhood maltreatment is linked to self-reported asthma and COPD. However, the relationship between childhood maltreatment and objective measures of lung function as determined by spirometry has not yet been assessed.MethodsMedical histories and spirometric lung function were taken in 1386 adults from the general population. Participants completed the Childhood Trauma Questionnaire for the assessment of emotional, physical and sexual abuse as well as emotional and physical neglect.Results25.3% of the participants reported at least one type of childhood maltreatment. Among them, use of medication for obstructive airway diseases as well as typical signs and symptoms of airflow limitation were significantly more frequent than in the group without exposure to childhood maltreatment. Although participants with childhood maltreatment had numerically lower values for forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and peak expiratory flow than those without, these differences were nonsignificant when accounting for relevant covariates such as age, sex, height and smoking. Likewise, there were no differences in the FEV1/FVC ratio nor in the frequency of airflow limitation regardless of its definition. No specific type of childhood maltreatment was related to spirometrically determined parameters of lung function.ConclusionsOur findings call into question the association of childhood maltreatment with obstructive lung diseases as indicated by prior research relying on self-reported diagnoses. We consider several explanations for these discrepancies.

ObjectiveTo verify the previously reported association between long-term use of β2-adrenoreceptor (β2AR) agonist and antagonist with reduced and increased risk of Parkinson disease (PD), respectively.MethodsWe obtained odds ratios (ORs) associating time of β2AR agonist and antagonist use with PD risk in nationwide Danish health registries.ResultsWe included 2,790 patients with PD and 11,160 controls. Long-term β2AR agonist use was associated with reduced PD risk (OR 0.57, 95% confidence interval [CI] 0.40–0.82) in this cohort. Unexpectedly, short-term β2AR agonist use was equally associated (OR 0.64, 95% CI 0.42–0.98). Because β2AR agonists are prescribed mostly for chronic obstructive pulmonary disease (COPD), often caused by long-term nicotine abuse, we analyzed other markers of smoking. Diagnosis of COPD (OR 0.51, 95% CI 0.37–0.69) and use of inhaled corticosteroids (OR 0.78, 95% CI 0.59–1.02) or inhaled anticholinergics (OR 0.41, 95% CI 0.25–0.67) were also inversely associated with PD. Increased PD risk was not found for all β2AR antagonists but only for propranolol and metoprolol. Associations were markedly stronger for short-term than long-term use.ConclusionWe confirmed β2AR agonist use to be associated with reduced PD risk and β2AR antagonist use with increased PD risk. However, our data indicate the association of β2AR agonists to be indirectly mediated by smoking, which is repeatedly associated with reduced risk of PD. The association of β2AR antagonists indicates reverse causation, with PD symptoms triggering their prescription rather than β2AR antagonists causing PD. Thus, current epidemiologic data do not support a causal link between β2AR agonists and antagonists and PD risk.

Even in large-scale genome-wide association studies, only a fraction of the true associations are detected at the genome-wide significance level. When few or no associations reach the significance threshold, one strategy is to follow-up on the most promising candidates, i.e. the single nucleotide polymorphisms with the smallest association-test p-values, by genotyping them in additional studies. In this communication, we propose an overall test for genome-wide association studies that analyzes the SNP’s with the most promising p-values simultaneously and thereby allows an early assessment of whether the follow- up of the selected SNP’s is likely promising. We theoretically derive the properties of the proposed overall test under the null hypothesis and assess its power based on simulation studies. An application to a GWAS for chronic obstructive pulmonary disease suggests that there are true association signals among the top SNPs and that an additional follow-up study is promising.

Background Chronic inflammatory airway disease (CIAD) has emerged as independent risk factor for cardiovascular mortality and ischemic stroke but the impact of co-existing CIAD in patients with ischemic stroke is less clear. Methods We retrospectively analyzed 1013 patients with acute ischemic stroke who were consecutively admitted to the Department of Neurology, Charité - Universitätsmedizin Berlin, Germany within one year. Mean follow-up was 80 months (IQR 32–85 months). Using multivariable regression models we analyzed the impact of CIAD (defined as chronic obstructive pulmonary disease or asthma bronchiale) on stroke severity and outcome. Results Co-existing CIAD was evident in 7.1 % (n = 72) of all patients with acute ischemic stroke. Baseline characteristics of stroke patients with CIAD did not differ significantly from ischemic stroke patients without CIAD. Age (OR 1.17 [95 % CI 1.03-1.37] per decade), atrial fibrillation (OR 3.43 [95 % CI 2.47-4.78]) and coronary artery disease (OR 1.51 [95 % CI 1.07–2.14]) but not a history of CIAD (p = 0.30) were associated with severe stroke (NIHSS≥11) on hospital admission. Age (HR 1.70 [95 % CI 1.53-1.87] per decade), peripheral artery disease (HR 1.91 [95 % CI 1.35-2.7]), stroke severity at hospital admission (NIHSS per point HR 1.08 [95 % CI 1.06-1.10]), and history of CIAD (HR 1.43 [95 % CI 1.02-2.00]) were independently associated with mortality during long-term follow-up. However, CIAD was not significantly associated with short-term mortality after stroke. Conclusion Co-existing CIAD showed no significant association with stroke severity at hospital admission and early mortality after ischemic stroke. CIAD was negatively associated with long-term survival after ischemic stroke.