Global Initiative for Chronic Obstructive Lung Disease 2017 Classification and Lung Function Decline in Chronic Obstructive Pulmonary Disease

Tan, Wan C.; Bourbeau, Jean; Aaron, Shawn D.; Zhou, Guohai; Maltais, François; Hernández, Paul; FitzGerald, J. Mark; Marciniuk, Darcy; Walker, Brandie; Sin, Don D.

doi:10.1164/rccm.201706-1154le

Cited by 25 publications

(30 citation statements)

References 8 publications

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“…The largest contribution of COLD/Can-COLD-related publications may be seen to have advanced knowledge and understanding surrounding appropriate diagnostic approaches and disease characterisation with impact on recommendations for health care services and interventions. More specifically, the larger proportion of studies to date have served to appropriately quantify COPD prevalence and disease determinants 3,4 spirometry testing and prediction equations [5][6][7][8][9] , diagnosis performance and early detection [10][11][12][13][14][15] , novel methods of assessing COPD 16,17 , and COPD clinical impact [18][19][20][21][22] . Consequently, we have elected for this manuscript to summarise key learnings from the CanCOLD study that are relevant to the primary care setting.…”

Section: Resultsmentioning

confidence: 99%

The Canadian Cohort Obstructive Lung Disease (CanCOLD): New Insights for Primary Care Application

Bourbeau¹,

Tan²,

Perrault³

et al. 2021

BRN

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The Canadian Cohort Obstructive Lung disease (CanCOLD) study was launched ten years ago, to provide insight on the natural course of chronic obstructive pulmonary disease (COPD). This project, unique on the world scene for its longitudinal evaluation, is based on random sampling of the population as opposed to more traditional cohorts built on convenience samples of clinical patients. This comprehensive review article has elected to extract and collate from the set of Can-COLD substudies those findings and emerging discoveries that can serve to influence clinical practice, in particular, for primary care. We are presenting findings grouped around three aspects: prevalence of COPD, diagnostic performance, and impacts of COPD. Furthermore, the main results of these studies are supplemented by key messages. From CanCOLD publications we have already learned much, with sufficient substantive data to warrant translation into our clinical practice, guidelines and health policies for the benefit of our COPD patients.

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Section: Resultsmentioning

confidence: 99%

The Canadian Cohort Obstructive Lung Disease (CanCOLD): New Insights for Primary Care Application

Bourbeau¹,

Tan²,

Perrault³

et al. 2021

BRN

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“…Lung function parameters including FVC, FEV 1 and FEV 1 /FVC were mainly used in our study. COPD was defined as FEV 1 /FVC < 70%, which was further classified into four stages according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) [ 24 ]: GOLD 1 (mild: FEV 1 /FVC < 70% and FEV 1 ≥ 80% predicted), GOLD 2 (moderate: FEV 1 /FVC < 70% and 50% ≤ FEV 1 < 80% predicted), GOLD 3 (severe: FEV 1 /FVC < 70% and 30% ≤ FEV 1 < 50% predicted) and GOLD 4 (very severe: FEV 1 /FVC < 70% and FEV 1 < 30% predicted).…”

Section: Methodsmentioning

confidence: 99%

Association of lung function with cardiovascular risk: a cohort study

et al. 2018

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BackgroundThe potential effects of pulmonary dysfunction on cardiovascular diseases (CVD) are receiving attention. We aimed to investigate and quantify the cross-sectional and longitudinal associations between lung function and overall cardiovascular risk among Chinese general population.MethodsWe studied 4019 participants from the Wuhan-Zhuhai cohort, with a follow-up of 3 years. A multivariable risk algorithm generated from the Framingham study was used to calculate individuals’ overall cardiovascular risk i.e. 10-Year CVD Risk, which was further classified into 2 categories: low (< 10%) and high (≥10%) CVD risk. General linear model and logistic regression model were separately used to assess the associations of lung function with continuous and dichotomous 10-Year CVD Risk.ResultsCross-sectionally, each 5% decrease in FEV1/FVC was associated with a 0.47% increase in 10-Year CVD Risk (P < 0.001). The adjusted odds ratio (OR) (95% confidence interval [CI]) for the prevalence of high CVD risk (10-Year CVD Risk≥10%) was 1.12 (1.07, 1.17) corresponding to each 5% decrease in FEV1/FVC. The OR (95% CI) for high CVD risk in the lowest group of FEV1/FVC (< 70% i.e. chronic obstructive pulmonary disease [COPD]) was 2.37 (1.43, 3.91) when compared with the highest group. Longitudinally, the adjusted risk ratio (RR) (95% CI) for the incidence of high CVD risk was 1.14 (1.03, 1.25) with each 5% decrease in baseline FEV1/FVC. Compared with the highest group of FEV1/FVC, the RR (95% CI) for high CVD risk in the lowest group (COPD) was 4.06 (1.46, 11.26). Analyses of 10-Year CVD Risk with FVC or FEV1 showed similar trends and significant associations (all P < 0.05).ConclusionReduced lung function was cross-sectionally and longitudinally associated with increased cardiovascular risk in Chinese general population.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0920-y) contains supplementary material, which is available to authorized users.

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“…Environment (especially smoking) and genetics are the two major factors that are responsible for COPD etiology. In Western countries, more than 90% of COPD cases are caused by chronic smoking [2,3]. The immunopathology of COPD is associated with innate and adaptive in ammatory immune responses to chronic smoking [4].…”

Section: Introductionmentioning

confidence: 99%

miRNA-486-5p Promotes COPD Progression by Targeting HAT1 to Regulate the TLR4-Triggered Inflammatory Response of Alveolar Macrophages

Zhang

Kong

et al. 2020

Preprint

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Background: The aim of this study is to investigate the key regulatory miRNA-486-5p and underlying molecular mechanisms in chronic obstructive pulmonary disease (COPD) progression.Methods: Aberrant miRNA expression in smokers compared to non-smokers and COPD compared to normal was analyzed using microarray datasets and reverse-transcriptase quantitative polymerase chain reaction (qPCR). ELISA assay was used to determine the secretion of inflammatory cytokines in cell supernatants. Inflammatory cytokine expression, including HAT1, TLR4, and miR-486-5p, was determined using qPCR or western blotting. Luciferase reporter assays and fluorescence in situ hybridization were used to confirm the target regulation between miR-486-6p and HAT1. Results: Our results showed that miR-486-5p was significantly up-regulated in the COPD and smoker groups compared to the control group based on bioinformatics analysis and qPCR validation of alveolar macrophages and peripheral monocytes. miR-218-5p expression significantly correlated with IL-6, IL-8, TNF-α, and IFN-γ expression. Luciferase reporter assays confirmed that miR-486-5p directly targets HAT1, and cellular localization showed that miR-486-5p and HAT1 were highly expressed in the cytoplasm. miR-486-5p overexpression led to significant TLR4 up-regulation and significant HAT1 down-regulation. Inversely, miR-486-5p inhibition led to significant TLR4 down-regulation and significant HAT1 up-regulation. HAT1 knockdown using siRNA significantly increased TLR4, IL-6, IL-8, TNF-α, and IFN-γ expression. Conclusions: miR-486-5p was differentially expressed in alveolar macrophages of COPD patients. miR-486-5p overexpression might increase the TLR4-triggered inflammatory response in COPD patients by targeting HAT1.

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Global Initiative for Chronic Obstructive Lung Disease 2017 Classification and Lung Function Decline in Chronic Obstructive Pulmonary Disease

Cited by 25 publications

References 8 publications

The Canadian Cohort Obstructive Lung Disease (CanCOLD): New Insights for Primary Care Application

The Canadian Cohort Obstructive Lung Disease (CanCOLD): New Insights for Primary Care Application

Association of lung function with cardiovascular risk: a cohort study

miRNA-486-5p Promotes COPD Progression by Targeting HAT1 to Regulate the TLR4-Triggered Inflammatory Response of Alveolar Macrophages

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