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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    • "During development of COPD, these normal, physiological, and inflammatory responses of the lungs appear to be amplified, go further out of balance, and consequently result in more permanent chronic inflammation and structural lung damage [3]. Consistent with this, it has been argued that the manifestation of COPD in long-term smokers represents more a quantitative rather than qualitative difference in the underlying biological effects [17]; i.e., at some point the physiological balancing mechanisms are at their limits and permanent structural degradation follows. "
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases. Cigarette smoking is the main risk factor for COPD. In this parallel-group clinical study we investigated to what extent the transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples. We selected 60 age- and gender-matched individuals for each of the four study groups: current asymptomatic smokers, smokers with early stage COPD, former smokers, and never smokers. The cell-free sputum supernatant was analyzed by quantitative proteomics and the cellular mRNA fraction by gene expression profiling. The sputum proteome of current smokers clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins and a prominent xenobiotic/oxidative stress response. The latter response also was observed in the transcriptome, which additionally demonstrated an immune-cell polarization change. The former smoker group showed nearly complete attenuation of these biological effects. Thirteen differentially abundant proteins between the COPD and the asymptomatic smoker group were identified including TIMP1, APOA1, C6orf58, and BPIFB1 (LPLUNC1). In summary, our study demonstrates that sputum profiling can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD. Biological Significance Chronic obstructive pulmonary disease (COPD) is a highly prevalent lung disease. Smoking is the main risk factor and smoking cessation is the most effective known intervention to slow progressive loss of lung function in COPD patients. However, how the transition from a physiological smoke exposure response to early disease is manifested is not fully clear. To date, our study with 240 subjects is the most extensive assessment of how the four states of a chronic-exposure-to-disease model (never, current, and former smokers and subjects with COPD) are reflected in the sputum proteome and transcriptome. Relevant physiological response mechanisms to smoke exposure were identified including the xenobiotic/oxidative stress response, changes in a mucin protein cluster, and a change in immune-cell polarization. Whereas these biological changes appear largely attenuated after long-term smoking cessation, the changes in the sputum proteome appear to be augmented in COPD subjects. This systems-level view of sputum alterations in smokers and COPD subjects provides, and will further facilitate, deeper insights into the chronic-exposure-to-disease transition for COPD, and potentially may serve as a model for other chronic diseases. Copyright © 2015. Published by Elsevier B.V.
    Journal of proteomics 08/2015; 128. DOI:10.1016/j.jprot.2015.08.009 · 3.89 Impact Factor
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    • "As expected, COPD and HF–COPD patients showed evidence of an obstructive ventilatory defect, which, based on both FEV 1 and FEV 1 /FVC, was more severe in COPD patients. Indeed, while the frequency of patients on stage 3 according to the GOLD guidelines [26] "
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    ABSTRACT: Heart failure (HF) and chronic obstructive pulmonary disease (COPD) coexistence increases morbidity and mortality. The intercept of ventilation (V˙Eint) on the V˙E vs. carbon dioxide production (V˙CO2) relationship during exercise has been found to vary in proportion with dead space (VD) in HF. Considering that increased VD is the key pathophysiological abnormality in COPD but a secondary finding in HF we hypothesized that a high V˙Eint would be useful in suggesting COPD as HF co-morbidity. Our aim was to assess whether an elevated V˙Eint suggests the presence of COPD in HF. In a multicenter retrospective study, the V˙E-V˙CO2 relationship was analyzed both as slope and intercept in HF (n=108), HF-COPD (n=106) and COPD (n=95). Patients with pulmonary arterial hypertension (PAH) (n=85) and healthy subjects (HF) (n=56) served as positive and negative controls relative to V˙E-V˙CO2 abnormalities, respectively. Slope and V˙Eint varied in opposite directions in all groups (p<0.05) being V˙E-V˙CO2 slope highest and lowest in PAH and healthy subjects, respectively. No slope differences were observed among HF, HF-COPD and COPD (32±7, 31±7, and 31±6, respectively). V˙Eint was higher in HF-COPD and COPD compared to HF, PAH and controls (4.8±2.4L/min, 5.9±3.0L/min, 3.0±2.6L/min, 2.3±3.3L/min and 3.9±2.5L/min, respectively; p<0.01). A V˙Eint ≥4.07L/min identified patients with high probability of having COPD or HF-COPD (sensitivity of 71.6% and specificity of 72.0%). These data provide novel evidence that a high V˙Eint (≥4.07L/min) should be valued to suggest coexistent COPD in HF patients. Copyright © 2015. Published by Elsevier Ireland Ltd.
    International journal of cardiology 03/2015; 189(1):134-140. DOI:10.1016/j.ijcard.2015.03.422 · 4.04 Impact Factor
    • "Chronic obstructive pulmonary disease (COPD) continues to be a major cause of morbidity and mortality worldwide (Mannino and Buist 2007). It is a syndrome characterized by progressive and irreversible airflow limitation, with clinical symptoms such as chronic and progressive dyspnea, cough, and sputum production (Vestbo et al. 2013). In addition to cigarette smoking, epidemiological evidence has shown that exposure to coal mine dust is a major cause of COPD among coal workers. "
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    ABSTRACT: This case-control study aimed to investigate whether the levels of Hsp70 (HSPA1A) and Hsp27 (HSPB1) in plasma and lymphocytes were associated with the risk of chronic obstructive pulmonary disease (COPD) among coal workers. A total of 76 COPD cases and 48 age-matched healthy controls from a group of coal workers were included. The case group consisted of 35 COPD patients whose condition was complicated with coal workers' pneumoconiosis (CWP) and 41 COPD patients without CWP. Heat shock proteins (Hsps) in plasma and lymphocytes were detected by ELISA and flow cytometry, respectively. Multiple logistic regression models were applied to estimate the association between Hsp levels and COPD risk. Our results showed that plasma Hsp70 and lymphocyte Hsp27 levels were significantly higher and plasma Hsp27 levels were significantly lower in COPD cases than in controls (p < 0.01). No significant differences in lymphocyte Hsp70 levels were found between COPD cases and the matched subjects. Higher plasma Hsp70 levels (odds ratio (OR) = 13.8, 95 % confidence interval (CI) = 5.7-33.5) and lower plasma Hsp27 levels (OR = 4.6, 95 % CI = 2.0-10.5) were significantly associated with an increased risk of COPD after adjusting for confounders. Higher lymphocyte Hsp27 levels were only associated with an increased risk of COPD with CWP (OR = 6.6, 95 % CI = 2.0-22.1) but not with an increased risk of COPD without CWP (OR = 3.0, 95 % CI = 0.9-8.9). Additionally, there were strong joint effects of different Hsps on COPD risk. These results showed that higher levels of plasma Hsp70 and lower levels of plasma Hsp27 might be associated with an increased risk of COPD among coal workers. They may have the potential to serve as monitoring markers for COPD in coal workers.
    Cell Stress and Chaperones 01/2015; 20(3). DOI:10.1007/s12192-015-0572-5 · 3.16 Impact Factor
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