Seven-Year Cumulative Incidence of COPD in an Age-Stratified General Population Sample

Lindberg, Anne; Eriksson, Berne; Larsson, Lars‐Gunnar; Rönmark, Eva; Sandström, Thomas; Lundbäck, Bo

doi:10.1378/chest.129.4.879

Cited by 97 publications

(91 citation statements)

References 24 publications

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“…Besides that, CB has other clinical consequences, including accelerated decline in lung function (6,(8)(9)(10), worse healthrelated quality of life (6,7,11), and increased COPD-related or all-cause mortality (11)(12)(13). Additionally, in the patients without COPD at baseline, CB or chronic respiratory symptoms will increase the risk of airflow limitation (13) and the incidence of COPD on follow-up, independently of smoking habit which is the most common risk factor of developing COPD (14,15). Small data are available on relationship between CB and recovery following exacerbation (16,17).…”

Section: Introductionmentioning

confidence: 99%

Chronic bronchitis is associated with severe exacerbation and prolonged recovery period in Chinese patients with COPD: a multicenter cross-sectional study

Liang

Chen

et al. 2017

J. Thorac. Dis.

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Section: Introductionmentioning

confidence: 99%

Chronic bronchitis is associated with severe exacerbation and prolonged recovery period in Chinese patients with COPD: a multicenter cross-sectional study

Liang

Chen

et al. 2017

J. Thorac. Dis.

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“…8 Spirometry-based COPD prevalence estimates differ extensively based upon the criteria used to diagnose COPD. 9,10 Moreover, the validity of spirometry findings and their utility in the management of patients with COPD to date are unclear and questionable. [11][12][13][14][15] Moreover, spirometry cannot be performed on all patients.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic Utility of Biomarkers in COPD

Ambade¹,

Sontakke

Barthwal³

et al. 2015

Respir Care

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BACKGROUND: COPD will become the third leading cause of death by 2020. There are many situations in which spirometry, the primary tool for diagnosis of COPD, cannot be performed, and thus, the staging and status of these patients cannot be determined. To date, there is no known biochemical marker used for diagnosing COPD. This study aimed to explore the utility of biomarkers for diagnosis of COPD. METHODS: This was an observational study composed of 96 stable subjects with COPD and 96 subjects with normal lung function. Each group contained an equal number of smokers and nonsmokers. Serum levels of superoxide dismutase 3, glutathione peroxidase, catalase, ceruloplasmin ferroxidase activity, C-reactive protein, and surfactant protein D (SPD) were estimated. Ferroxidase activity was estimated by a kinetic method, whereas the other analytes were measured by enzyme-linked immunosorbent assay. The cutoff value, sensitivity and specificity at the cutoff value, and area under the curve for each analyte were determined from receiver operating characteristic curve. RESULTS: Significantly decreased superoxide dismutase 3 and increased ferroxidase activity, SPD, glutathione peroxidase, and C-reactive protein levels were found in subjects with COPD. For all subjects and nonsmoking subjects with COPD, the area under the curve was highest for ferroxidase activity, followed by glutathione peroxidase, SPD, and C-reactive protein, with a sensitivity and specificity of > 73%. For smoking subjects with COPD, the area under the curve was highest for SPD, followed by glutathione peroxidase, ferroxidase activity, and C-reactive protein, with a sensitivity and specificity > 67%. Some combinations of markers were found to give either a sensitivity or specificity of > 95%, which can be utilized to rule in and rule out COPD. CONCLUSIONS: Biomarkers can be reliably utilized in the diagnosis of COPD. Of all the markers, SPD appears to be the most promising in smokers, whereas ferroxidase activity shows promise in nonsmokers. To rule out COPD, ferroxidase activity or glutathione peroxidase can be potentially useful, whereas to rule in COPD, ferroxidase activity and glutathione peroxidase appear to be the most promising combination in both nonsmoking and smoking subjects.

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“…This may be due to the increased incidence of cigarette smoking, as this is the most common risk factor for COPD and contributes to ,85% of all cases. Approximately 15% of smokers will develop COPD, whereas the incidence in nonsmokers is 1.6% [3]. In healthy individuals and smokers without lung obstruction, the lower airways are sterile, but in COPD patients there is often colonisation of the lower respiratory tract, with Streptococcus pneumoniae and Haemophilus influenzae being the most common bacterial pathogens [4].…”

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confidence: 99%

Defective macrophage phagocytosis of bacteria in COPD

Taylor¹,

Finney-Hayward²,

Quint³

et al. 2009

Eur Respir J

312

275

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Exacerbations of chronic obstructive pulmonary disease (COPD) are an increasing cause of hospitalisations and are associated with accelerated progression of airflow obstruction. Approximately half of COPD exacerbations are associated with bacteria and many patients have lower airways colonisation. This suggests that bacterial infection in COPD could be due to reduced pathogen removal. This study investigated whether bacterial clearance by macrophages is defective in COPD.Phagocytosis of fluorescently labelled polystyrene beads and Haemophillus influenzae and Streptococcus pneumoniae by alveolar macrophages and monocyte-derived macrophages (MDM) was assessed by fluorimetry and flow cytometry. Receptor expression was measured by flow cytometry.Alveolar macrophages and MDM phagocytosed polystyrene beads similarly. There was no difference in phagocytosis of beads by MDM from COPD patients compared with cells from smokers and nonsmokers. MDM from COPD patients showed reduced phagocytic responses to S. pneumoniae and H. influenzae compared with nonsmokers and smokers. This was not associated with alterations in cell surface receptor expression of toll-like receptor (TLR)2, TLR4, macrophage receptor with collagenous structure, cluster of differentiation (CD)163, CD36 or mannose receptor. Budesonide, formoterol or azithromycin did not suppress phagocytosis suggesting that reduced responses in COPD MDM were not due to medications.COPD macrophage innate responses are suppressed and may lead to bacterial colonisation and increased exacerbation frequency.

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Seven-Year Cumulative Incidence of COPD in an Age-Stratified General Population Sample

Cited by 97 publications

References 24 publications

Chronic bronchitis is associated with severe exacerbation and prolonged recovery period in Chinese patients with COPD: a multicenter cross-sectional study

Chronic bronchitis is associated with severe exacerbation and prolonged recovery period in Chinese patients with COPD: a multicenter cross-sectional study

Diagnostic Utility of Biomarkers in COPD

Defective macrophage phagocytosis of bacteria in COPD

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