scholarly journals Plasma urate, lung function and chronic obstructive pulmonary disease: a Mendelian randomisation study in 114 979 individuals from the general population

Thorax ◽  
2017 ◽  
Vol 73 (8) ◽  
pp. 748-757 ◽  
Author(s):  
Camilla J Kobylecki ◽  
Signe Vedel-Krogh ◽  
Shoaib Afzal ◽  
Sune F Nielsen ◽  
Børge G Nordestgaard
Keyword(s):  
Lung Function ◽  
General Population ◽  
Respiratory Symptoms ◽  
High Plasma ◽  
Mendelian Randomisation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Plasma Urate ◽  
Genetically Determined

BackgroundUrate is a strong antioxidant in plasma and may protect against lung function impairment. We tested the hypothesis that high plasma urate is causally associated with better lung function and low risk of respiratory symptoms and COPD.MethodsWe measured lung function and plasma urate in 114 979 individuals from the Copenhagen City Heart Study and the Copenhagen General Population Study and genotyped for SLC2A9 rs7442295 and ABCG2 rs2231142 variants, previously associated with high plasma urate, in 110 152 individuals.ResultsIn the two studies combined, multivariable-adjusted 100 µmol/L higher plasma urate was associated with −1.54% (95% CI −1.67 to −1.40) lower FEV1 % predicted and −1.57% (95% CI −1.69 to −1.44) lower FVC % predicted observationally; the corresponding estimates for genetically determined 100 µmol/L higher plasma urate were −0.46% (95% CI −1.17 to 0.25) and −0.40% (95% CI −1.03 to 0.23). High plasma urate was also associated with higher risk of respiratory symptoms; however, genetically determined high plasma urate was not associated with respiratory symptoms. Finally, we identified 14 151 individuals with COPD and found ORs of 1.08 (95% CI 1.06 to 1.11) for COPD observationally and 1.01 (95% CI 0.88 to 1.15) genetically per 100 µmol/L higher plasma urate.ConclusionHigh plasma urate was associated with worse lung function and higher risk of respiratory symptoms and COPD in observational analyses; however, genetically high plasma urate was not associated with any of these outcomes. Thus, our data do not support a direct causal relationship.

scholarly journals Association of bone mineral density with lung function in a Chinese general population: the Xinxiang rural cohort study

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiang Zeng ◽  
Dongling Liu ◽  
Xiangmei Zhao ◽  
Ling Chao ◽  
Yuchun Li ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Lung Function ◽  
General Population ◽  
Bone Mineral ◽  
Chronic Obstructive ◽  
Reference Area ◽  
Mineral Density ◽  
Obstructive Pulmonary Disease ◽  
Lower Lung ◽  
The Relationship

Abstract Background Bone mineral density (BMD) has been positively associated with lung function in patients diagnosed with respiratory diseases such as chronic obstructive pulmonary disease (COPD) and cystic fibrosis. However, the relationship between BMD and lung function is inconsistent in the general population. Methods To investigate the association between BMD and lung function in a Chinese general population, a total of 1024 adults aged 40–70 years old from Qiliying (an industrial polluted exposure area) and Langgongmiao (the reference area with non-industrial pollution) were recruited and underwent BMD and spirometry tests. Results Both BMD and lung function levels were lower in the exposed area compared to the reference area. In addition, BMD and lung function levels were also lower in females compared to males. Both Spearman and partial correlation analyses showed that BMD was positively correlated with FVC and FEV1. After adjusting linear regression analyses for potential confounding factors, every 0.1 g/cm2 drop in BMD was associated with 53.0 mL decrease in FVC and 33.5 mL decrease in FEV1. Conclusions A reduction of BMD is associated with lower lung function in a general population from China.

Childhood maltreatment and lung function: Findings from the general population

2020 ◽  
pp. 2002882
Author(s):  
Carsten Spitzer ◽  
Ralf Ewert ◽  
Henry Völzke ◽  
Stefan Frenzel ◽  
Stephan B. Felix ◽  
...  
Keyword(s):  
Lung Function ◽  
General Population ◽  
Childhood Maltreatment ◽  
Signs And Symptoms ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Childhood Trauma Questionnaire ◽  
Obstructive Pulmonary Disease ◽  
Physical Neglect ◽  
Medical Histories

ObjectiveCumulative evidence indicates that childhood maltreatment (CM) is linked to self-reported asthma and chronic obstructive pulmonary disease. However, the relation between CM 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 also 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 CM. 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 CM. Although participants with CM had numerically lower values for FEV1, FVC and PEF than those without, these differences were non-significant when accounting for relevant covariates like 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 CM was related to spirometrically determined parameters of lung function.ConclusionsOur findings call into question the association of CM with obstructive lung diseases as indicated by prior research relying on self-reported diagnoses. We consider several explanations for these discrepancies.

Smoking, Systemic Inflammation, and Airflow Limitation: A Mendelian Randomization Analysis of 98 085 Individuals From the General Population

2018 ◽  
Vol 21 (8) ◽  
pp. 1036-1044 ◽  
Author(s):  
Yunus Çolak ◽  
Shoaib Afzal ◽  
Peter Lange ◽  
Børge G Nordestgaard
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
General Population ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Tobacco Consumption ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Former Smokers

Abstract Introduction Smoking is associated with systemic and local inflammation in the lungs. Furthermore, in chronic obstructive pulmonary disease, which is often caused by smoking, there is often systemic inflammation that is linked to lung function impairment. However, the causal pathways linking smoking, systemic inflammation, and airflow limitation are still unknown. We tested whether higher tobacco consumption is associated with higher systemic inflammation, observationally and genetically and whether genetically higher systemic inflammation is associated with airflow limitation. Methods We included 98 085 individuals aged 20–100 years from the Copenhagen General Population Study; 36589 were former smokers and 16172 were current smokers. CHRNA3 rs1051730 genotype was used as a proxy for higher tobacco consumption and the IL6R rs2228145 genotype was used for higher systemic inflammation. Airflow limitation was defined as forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) <70%. Results Difference in plasma level of C-reactive protein was 4.8% (95% CI = 4.4% to 5.2%) per 10 pack-year increase and 1.6% (95% CI = 0.4% to 2.8%) per T allele. Corresponding differences were 1.2% (95% CI = 1.1% to 1.3%) and 0.5% (95% CI = 0.3% to 0.8%) for fibrinogen, 1.2% (95% CI = 1.2% to 1.3%) and 0.7% (95% CI = 0.5% to 1.0%) for α1-antitrypsin, 2.0% (95% CI = 1.8% to 2.1%) and 0.7% (95% CI = 0.4% to 1.1%) for leukocytes, 1.9% (95% CI = 1.8% to 2.1%) and 0.8% (95% CI = 0.4% to 1.2%) for neutrophils, and 0.8% (95% CI = 0.7% to 1.0%) and 0.4% (95% CI = 0.1% to 0.7%) for thrombocytes. The differences in these levels were lower for former smokers compared with current smokers. The IL6R rs2228145 genotype was associated with higher plasma acute-phase reactants but not with airflow limitation. Compared with the C/C genotype, the odds ratio for airflow limitation was 0.95 (95% CI = 0.89 to 1.02) for A/C genotype and 0.94 (95% CI = 0.87 to 1.01) for A/A genotype. Conclusions Higher tobacco consumption is associated with higher systemic inflammation both genetically and observationally, whereas systemic inflammation was not associated with airflow limitation genetically. Implications The association between higher tobacco consumption and higher systemic inflammation may be causal, and the association is stronger among current smokers compared to former smokers, indicating that smoking cessation may reduce the effects of smoking on systemic inflammation. Systemic inflammation does not seem to be a causal driver in development of airflow limitation. These findings can help to understand the pathogenic effects of smoking and the interplay between smoking, systemic inflammation, and airflow limitation and hence development and progression of chronic obstructive pulmonary disease.

scholarly journals ABO blood type analysis in patients with chronic obstructive pulmonary disease

Genetika ◽  
2021 ◽  
Vol 53 (2) ◽  
pp. 457-471
Author(s):  
Blazenka Petricevic ◽  
Dragica Pesut
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
General Population ◽  
Pulmonary Disease ◽  
Tobacco Smoking ◽  
Blood Type ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Blood Types ◽  
Abo Blood Type

Tobacco smoking is major risk factor for development of chronic obstructive pulmonary disease (COPD), which appears in 15-20% of smokers. Apart from smoking, exposure to polluted air and various noxae, and several genetic factors influence its development as well. The ABO blood type distribution varies among populations in the world, but also within subpopulations. A large number of studies have shown a correlation between blood types and the pathology of various diseases. These markers, used in population genetic research, have mainly shown deviations in the representation of blood groups in different diseases, compared to the general population. The aim of this study was to determine the ABO blood types distribution in patients with COPD compared to the general population, and their possible association with COPD stage, patients? nutritional status and lung function impairment. This observational, prospective study included 150 patients (68.7% men and 31.3% women), average age 64.80 ? 8.38 years, diagnosed with COPD. Data were collected at the Clinical Center of Montenegro in Podgorica and at the Special Hospital for Lung Diseases Brezovik in Niksic. Determination of blood types of the ABO system and Rh factors for all subjects was performed at the Blood Transfusion Center in Podgorica. Apart from patients? tobacco smoking status (duration of smoking and the number of cigarettes smoked per day expressed in pack/years for current smokers and former smokers), we also analyzed their exposure to various other noxae, their body mass index, and lung function in correlation to ABO blood type and Rh factor, and performed statistical analysis. We found a significant difference in the distribution of ABO blood types in patients with COPD compared to the general population. The highest frequency of blood type A was found in patients with COPD. We also found the lowest average values of spirometry parameters in that group, which represented majority of those patients with respiratory insufficiency having the most severe stage of the disease. Combined blood types A, B and were significantly more common in patients with COPD in comparison to blood type O, which is the least represented (23.3%). The least obstructive disturbance of pulmonary ventilation was found in the patients with B type. Respiratory insufficiency showed differences in gender representation, found in 40.4% of women, and in 25.2% of men with terminal phase of COPD. The prevalence of AB, higher than expected, decreases with the severity of the disease.

scholarly journals Lung function trajectory and biomarkers in the Tasmanian longitudinal health study

2021 ◽  
pp. 00020-2021
Author(s):  
Dinh S. Bui ◽  
Alvar Agusti ◽  
Haydn Walters ◽  
Caroline Lodge ◽  
Jennifer L. Perret ◽  
...  
Keyword(s):  
Lung Function ◽  
Inflammatory Marker ◽  
Health Study ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Inflammatory Protein ◽  
Increased Risk ◽  
Unit Increase ◽  
Circulating Levels

Background and objectiveDifferent lung function trajectories through life can lead to chronic obstructive pulmonary disease (COPD) in adulthood. This study investigates if circulating levels of biomarkers can differentiate those with accelerated (AD) from normal decline (ND) trajectories.MethodsThe Tasmanian Longitudinal Health Study (TAHS) is a general population study that measured spirometry and followed up participants from ages 7 to 53 years. Based on their FEV1 trajectories from age 7 to 53 years, this analysis included those with COPD at age 53 years (60 with AD and 94 with ND) and controls (C, n=720) defined as never smokers with an average FEV1 trajectory. Circulating levels of selected biomarkers determined at 53 and 45 years of age were compared between trajectories.ResultsResults showed that CC16 levels (an anti-inflammatory protein) were lower and CRP (a pro-inflammatory marker) higher in the AD than in the ND trajectory. Higher CC16 levels were associated with a decreased risk of belonging to the AD trajectory (OR=0.79 [0.63–0.98] per unit increase) relative to ND trajectory. Higher CRP levels were associated with an increased risk of belonging to the AD trajectory (OR=1.07 [1.00, 1.13] per unit increase). Levels of CC16 (AUC=0.69 [95%CI: 0.56–0.81], p=0.002), CRP (AUC=0.63 [0.53–0.72], p=0.01) and the combination of both (AUC=0.72 [0.60–0.83], p<0.001) were able to discriminate between the AD and ND trajectories. Other quantified biomarkers (IL4, IL5, IL6, IL10 and TNFα) were not significantly different between AD, ND and C.ConclusionsCirculating levels of CRP and CC16 measured in late adulthood identify different lung function trajectories (AD versus ND) leading to COPD at age 53 years.

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