Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary

Respiratory Research Group, Manchester Academic Sciences Health Centre, Manchester, United Kingdom.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 08/2012; 187(4). DOI: 10.1164/rccm.201204-0596PP
Source: PubMed


Chronic obstructive pulmonary disease (COPD) is a global health problem and since 2001 the Global Initiative for Chronic Obstructive Lung Disease (GOLD) has published its strategy document for the diagnosis and management of COPD. This executive summary presents the main contents of the second 5-year revision of the GOLD document that has implemented some of the vast knowledge about COPD accumulated over the last years. Today, GOLD recommends that spirometry is required for the clinical diagnosis of COPD in order to avoid misdiagnosis and to ensure proper evaluation of severity of airflow limitation. The document highlights that the assessment of the COPD patient should always include assessment of 1) symptoms, 2) severity of airflow limitation, 3) history of exacerbations, and 4) comorbidities. The first three points can be used to evaluate level of symptoms and risk of future exacerbations and this is done in a way that split COPD patients into 4 categories - A, B, C and D. Non-pharmacologic and pharmacologic management of COPD match this assessment in an evidence-based attempt to relieve symptoms and reduce risk of exacerbations. Identification and treatment of comorbidities must have high priority and a separate chapter in the document addresses management of comorbidities as well as COPD in the presence of comorbidities. The revised document also contains a new chapter on exacerbations of COPD. The GOLD initiative will continue to bring COPD to the attention of all relevant shareholders and will hopefully inspire future national and local guidelines on the management of COPD.

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Available from: Robert Rodríguez-Roisin, Oct 29, 2015
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    • "The study was conducted in patients with mild to very severe COPD admitted to CIRO, a centre of expertise for chronic organ failure (Horn, the Netherlands) for a comprehensive PR programme [9] in the period between January 2009 and December 2012. The diagnosis of COPD was based on the definition provided by the Global initiative for chronic Obstructive Lung Disease (GOLD) [10]. Part of the patients was included in previous studies concerning coping styles [8] [11]. "

    Full-text · Dataset · Dec 2015
    • "subjects with moderate-to-severe airflow obstruction (defined as Global Initiative for Obstructive Lung Disease (GOLD) severity classes 2 or higher) typically reflects lung hyperinflation, whereas reduced TLC CT can also reflect restriction in individuals with interstitial lung disease, chest wall abnormalities, or neuromuscular weakness. Lung hyperinflation , that is, increased lung gas volume at the end of tidal expiration beyond normal range, is a major comorbidity in COPD [Gibson, 1996; Vestbo et al., 2013], but details of underlying biological mechanisms remain poorly defined [O'Donnell, 2008]. With the availability of efficient algorithms to call structural variations (including deletions and amplifications of chromosomal segments) from raw intensity-level data generated by genome-wide marker panels used for genome-wide association studies (GWAS), useful information about DNA copy number variants (CNVs) can still be extracted from the log R ratios (LRRs) and B allele frequencies (BAFs) generated using this array even when these arrays are not specifically designed for CNV studies. "
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a progressive disease with both environmental and genetic risk factors. Genome-wide association studies (GWAS) have identified multiple genomic regions influencing risk of COPD. To thoroughly investigate the genetic etiology of COPD, however, it is also important to explore the role of copy number variants (CNVs) because the presence of structural variants can alter gene expression and can be causal for some diseases. Here, we investigated effects of polymorphic CNVs on quantitative measures of pulmonary function and chest computed tomography (CT) phenotypes among subjects enrolled in COPDGene, a multisite study. COPDGene subjects consist of roughly one-third African American (AA) and two-thirds non-Hispanic white adult smokers (with or without COPD). We estimated CNVs using PennCNV on 9,076 COPDGene subjects using Illumina's Omni-Express genome-wide marker array. We tested for association between polymorphic CNV components (defined as disjoint intervals of copy number regions) for several quantitative phenotypes associated with COPD within each racial group. Among the AAs, we identified a polymorphic CNV on chromosome 5q35.2 located between two genes (FAM153B and SIMK1, but also harboring several pseudo-genes) giving genome-wide significance in tests of association with total lung capacity (TLCCT ) as measured by chest CT scans. This is the first study of genome-wide association tests of polymorphic CNVs and TLCCT . Although the ARIC cohort did not have the phenotype of TLCCT , we found similar counts of CNV deletions and amplifications among AA and European subjects in this second cohort.
    No preview · Article · Dec 2015 · Genetic Epidemiology
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    • "Previous studies have demonstrated that chronic inflammation and varying degrees of emphysematous alveolar destruction are the key pathological features of the disease (Stockley et al., 2009). Some studies have revealed that an imbalance of endogenous proteinases and antiproteinases, inflammatory cells, proinflammatory mediators, and oxidative stress were responsible for the pathogenesis of COPD (Vestbo et al., 2013). Genetic factors and environmental exposures like tobacco smoke are also involved in the pathogenesis of COPD (Restrepo, 2015). "
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    ABSTRACT: Introduction: Previous studies have shown that glutathione S-transferase P1 (GSTP1) was associated with chronic obstructive pulmonary disease (COPD). However, the association between GSTP1 Ile (105) Val gene polymorphism and COPD remains controversial. To drive a more precise estimation, we performed a meta-analysis based on published case-control studies. Methods: An electronic search of PubMed, EMBASE, Cochrane library, Web of Science and China Knowledge Resource Integrated (CNKI) Database for papers on GSTP1 Ile (105) Val gene polymorphism and COPD risk was performed. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association in the homozygote model, heterozygote model, dominant model, recessive model and an additive mode. Statistical heterogeneity, test of publication bias and sensitivity analysis was performed. The software STATA (Version 13.0) was used data analysis. Results: Overall, seventeen studies with 1892 cases and 2012 controls were included in this meta-analysis. The GSTP1 Ile (105) Val polymorphism showed pooled odds ratios for the homozygote comparison (OR = 1.501, 95%CI [0.862, 2.614]), heterozygote comparison (OR = 0.924, 95%CI [0.733, 1.165]), dominant model (OR = 1.003, 95%CI [0.756, 1.331]), recessive model (OR = 1.510, 95%CI [0.934, 2.439]), and an additive model (OR = 1.072, 95%CI [0.822, 1.398]). Conclusions: In conclusion, the current meta-analysis, based on the most updated information, showed no significant association between GSTP1 Ile (105) Val gene polymorphism and COPD risk in any genetic models. The results of subgroup analysis also showed no significant association between GSTP1 Ile (105) Val gene polymorphism and COPD risk in Asian population and Caucasian population. Further studies involving large populations and careful control with age, sex, ethnicity, and cigarette smoking are greatly needed.
    Full-text · Article · Dec 2015 · Meta Gene
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