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Results for “Chronic Obstructive Pulmonary Disease”

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At least 19 recordsLinked to original sources

PubMed2003

[Clinical aspects of chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease represents a complex syndrome including chronic bronchitis, pulmonary emphysema and chronic asthma, characterised by persistent airway obstruction with different degree of reversibility. Clinical manifestations depend on the relative contribution of these different diseases in the single patient. Relationship between symptoms and severity (as expressed by forced expiratory volume in one second) is weak, and chronic airway obstruction generally precedes symptoms. Cough, sputum, wheezing, and dyspnea are the main symptoms of chronic obstructive pulmonary disease, and they must be carefully inquired and quantified. Symptoms and signs of chronic obstructive pulmonary disease depend on the type of disease (chronic bronchitis or emphysema), and also on the complications and comorbidities. Accurate definition of the heterogeneity of chronic obstructive pulmonary disease can be useful in the prognosis and management of the disease.

Cough↗

PubMed1994

Hypercoagulability state in patients with chronic obstructive pulmonary disease. Chronic Obstructive Bronchitis and Haemostasis Group.

Since there is some clinical evidence that the clinical course of patients with chronic obstructive pulmonary disease (COPD) may be complicated by thrombosis in the pulmonary vessels, we studied whether a hypercoagulability state (HS) does occur in COPD. Plasma levels of prothrombin F1 + 2 fragment, a marker of thrombin generation, D-dimer, a marker of in vivo thrombin and plasmin activation, and fibrinogen were measured in 37 COPD patients and in 30 controls matched for sex and age. COPD patients had significantly higher values of F1 + 2 (p = 0.0001) and fibrinogen (p = 0.0005) than healthy subjects. The difference persisted after excluding smoking patients. F1 + 2 was not correlated with PaO2 (r = 0.02, p > 0.05) and PaCO2 (p = 0.12, p > 0.05). In six patients with stable COPD and F1 + 2 greater than 1.65 nM (mean + 2 SD of controls) subcutaneous calcium-heparin therapy (5000 IU t.i.d. for 15 days) significantly reduced F1 + 2 (p = 0.03) and PaCO2 (p = 0.01). This study shows that COPD patients have an ongoing prothrombotic state which could potentially account for thrombosis occurring in pulmonary vessels. The effect of calcium-heparin treatment on clotting system activation and blood gas may suggest this treatment as potential candidate for prospective study in COPD patients.

Adult↗

PubMed2003

Potential new drugs for therapy of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is a major health problem with cigarette smoking as its major risk factor. Current therapies are directed against the symptoms (e.g., breathlessness and mucus production) or the chronic airway inflammation. However, the excessive annual decline in lung function and the airway inflammation have not yet been shown to be improved by these strategies. New potential drug therapies are directed against specific components of the inflammation. Novel drugs have been developed for treatment of inflammatory diseases including chronic obstructive pulmonary disease in order to antagonise cytokines and chemokines such as TNF-alpha, CXC chemokine ligand 8 (IL-8) or CC chemokine ligand 2 (monocyte chemoattractant protein 1) that orchestrate the inflammatory process. Some of these drugs are shown to be effective in patients with other chronic inflammatory diseases but still have to prove their efficacy in the treatment of chronic obstructive pulmonary disease.

Animals↗

PubMed1999

The role of quinolones in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is a disease state characterized by the presence of airflow obstruction due to chronic bronchitis and/or emphysema. The airflow obstruction is generally progressive. In the past asthma was often confused with chronic obstructive pulmonary disease but as the cellular inflammatory mechanisms are quite different to chronic bronchitis and emphysema it is prudent to separate this condition of airway hyper-responsiveness. Exacerbation of chronic obstructive pulmonary disease is a considerable burden on health service resources in terms of morbidity and mortality. Approximately one half of exacerbations can be attributed to bacterial pathogens, the major pathogens being Haemophilus influenzae, Streptococcus pnemoniae and Moraxella catarrhalis. Resistance to common first-line treatment antibiotics such as the beta-lactams can be variable. Newer fluoroquinolones such as grepafloxacin, levofloxacin, sparfloxacin, clinafloxacin, moxifloxacin, gatifloxacin and gemifloxacin are characterized by improved activity against Gram positive bacteria as well as their Gram negative properties. However, more randomized controlled trials need to be accomplished before the true role of quinolones in exacerbation of chronic obstructive pulmonary disease is clearly ascertained.

Journal Article↗

PubMed2006

[Genetic features during chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease is one of the leading causes of mortality, which is caused by the interaction of genetic susceptibility with environmental factors (especially smoking); however, genetic features of chronic obstructive pulmonary disease still remain unknown. The only proven genetic risk factor is severe deficiency of plasma protease inhibitor, alpha-1 antitrypsin. A large number of candidate genes for chronic obstructive pulmonary disease have already been identified in many experimental and clinical studies; however, polygenic etiology of chronic obstructive pulmonary disease is the main reason for conflicting molecular and genetic findings. This review describes the correlation between single nucleotide polymorphism of alpha-1 antitrypsin, alpha-1 antichymotrypsin, microsomal epoxide hydrolase-1, matrix metalloproteinases-1,-9,-12, glutathione S-transferases, heme oxygenase-1, tumor necrosis factor-alpha, transforming growth factor-beta, interleukins-1,-4,-13, beta2-adrenergic receptor, G-globulin genes and chronic obstructive pulmonary disease. Regions on chromosomes 1, 2, 12, and 17 are indicated as candidate chromosomal regions influencing the decrease in spirometric parameters. Genome-wide scan shows direct evidence for linkage of decreased FEV1/FVC ratio to one or more genes on chromosome 2q influencing the development of airflow obstruction. Genetic markers on chromosome 12p suggest evidence for linkage of FEV1 to this region, and observations on chromosome 1p show the relationship between FVC and genes of this region. All these findings also need to be proven, and linkage analysis among combinations of gene candidates for chronic obstructive pulmonary disease has to be done.

Genetic Linkage↗

PubMed2001

Cytokines in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic obstruction of expiratory flow affecting peripheral airways, associated with chronic bronchitis (mucus hypersecretion with goblet cell and submucosal gland hyperplasia) and emphysema (destruction of airway parenchyma), together with fibrosis and tissue damage, and inflammation of the small airways. Cytokines are extracellular signalling proteins. Increased levels of interleukin (IL)-6, IL-1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-8 have been measured in sputum, with further increases during exacerbations, and the bronchiolar epithelium over-expresses monocyte chemotactic protein (MCP)-1 and IL-8. IL-8 can account for some chemotactic activity of sputum, and sputum IL-8 levels correlate with airway bacterial load and blood myeloperoxidase levels. The expression of chemokines such as regulated on activation, normal T-cell expressed and secreted (RANTES) may underlie the airway eosinophilia observed in some COPD patients. Cytokines may be involved in tissue remodelling. TNF-alpha and IL-1beta stimulate macrophages to produced matrix metalloproteinase-9 (MMP-9), and bronchial epithelial cells to produce extracellular matrix glycoproteins such as tenascin. Increased expression of transforming growth factor-beta (TGFbeta) and of epidermal growth factor (EGF) occurs in the epithelium and submucosal cells of patients with chronic bronchitis. TGFbeta and EGF activate proliferation of fibroblasts, while activation of the EGF receptor leads to mucin gene expression. The cytokine profile seen in chronic obstructive pulmonary disease is different from that observed in asthma. The role of these cytokines needs to be defined and there is a potential for anticytokine therapy in chronic obstructive pulmonary disease.

Cytokines↗

PubMed2026

Integrated salivary proteomic and metabolomic analyses reveal molecular characterization and novel biomarker panels of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a respiratory disorder characterized by chronic inflammation, oxidative stress, and metabolic dysregulation. The lack of convenient and easily-accessible non-invasive diagnostic approaches remains a major clinical challenge. This study applied an integrated saliva-based proteomic and untargeted metabolomic strategy to identify potential biomarkers for COPD classification. Comprehensive multi-omics analyses identified 225 differentially abundant proteins and 60 differentially abundant metabolites between patients with COPD and healthy controls, including 24 biologically relevant endogenous metabolites. Functional enrichment analyses revealed pronounced dysregulation of mitochondrial energy metabolism, redox homeostasis, lipid remodeling, and inflammatory-related pathways in COPD. By integrating salivary proteomic and metabolomic biomarkers, a stepwise feature selection combined with LASSO logistic regression was used to construct diagnostic models, yielding an optimized biomarker panel consisting of 11 proteins and 2 endogenous metabolites. This integrated model achieved excellent diagnostic performance, with an area under the ROC curve of 0.96. Collectively, these findings demonstrate that integrated salivary proteomic and metabolomic profiling provides a robust, non-invasive approach for COPD classification and offers a promising foundation for the development of biosensor-based diagnostic platforms and early disease detection. SIGNIFICANCE: Chronic obstructive pulmonary disease (COPD) remains a major global health burden. Current diagnostic approaches rely largely on spirometry and clinical assessment, which are limited in sensitivity for early-stage disease and unsuitable for large-scale screening. This study employs an integrated saliva-based proteomic and metabolomic strategy to identify non-invasive biomarkers for COPD classification. Our findings reveal coordinated dysregulation of mitochondrial energy metabolism, redox homeostasis, and lipid remodeling in COPD, highlighting the interconnected roles of metabolic reprogramming, oxidative stress, and inflammation in disease pathophysiology. Notably, a robust diagnostic panel comprising 11 proteins and 2 endogenous metabolites was established, achieving excellent classification performance (AUC of 0.96). To our knowledge, the integrated application of salivary proteomics and metabolomics for COPD diagnosis remains largely unexplored, underscoring the significance and translational potential of our findings.

Humans↗

PubMed2006

Lung development and susceptibility to chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease with emphysema has been considered to be an accelerated involutional disease of aging smokers. However, because only a proportion ( approximately 15%) of smokers develop chronic obstructive pulmonary disease with emphysema, clearly genetic susceptibility must play a significant part in determining both the age of onset and the rapidity of decline in lung function. In mice, interference with key genes, either by null mutation, hypomorphism, or gain or loss of function, results in phenotypes comprising either neonatal lethal respiratory distress if the structural effect is severe, or reduced alveolarization and/or early-onset emphysema if the effect is milder. Likewise, null mutants that interfere with matrix assembly and/or integrity, such as elastin, lysyl oxidase, or fibrillin, also result in alveolar dysplasia. Importantly, null mutation of Smad3, which encodes a receptor-activated Smad in the transforming growth factor-beta signaling pathway, results in a more subtle failure to correctly organize the alveolar matrix, which is in turn antecedent to early-onset emphysema mediated by matrix metalloproteinase-9. Furthermore, exposure to side-stream smoke profoundly exacerbates and accelerates alveolar destruction, leading to more severe early-onset emphysema in young Smad3-null mice (unpublished data). Interestingly, polymorphisms in the fibrillin, transforming growth factor-beta type II receptor, and matrix metalloproteinase-9 genes have been described in humans with emphysema. Thus, dysplastic or degraded matrix cannot provide the structural niche for alveolar stem/progenitor cells to assume the correct phenotype and/or repair the alveolar cell lineage niche. The hope is that providing the correct exogenous signals can coax them into doing so.

Age Factors↗

PubMed2003

Systemic inflammation in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is characterised by a chronic inflammation in the pulmonary tissue. The disease is associated with a switch from a self-limiting inflammatory response, mainly initiated by smoke inhalation, to a chronic persistent inflammatory response after prolonged interaction with cigarette smoke. The extent of the inflammatory reaction is correlated with the severity of the disease. Chronic inflammation in the pulmonary tissue is also associated with systemic effects. These effects range from cytokine-induced priming of peripheral leukocytes, to muscle wasting induced by cytokines such as tumour necrosis factor-alpha. Despite a general consensus that chronic inflammation is a characteristic phenomenon of the disease, surprisingly little is known regarding the underlying pathogenetic mechanisms. A clear communication is present between the disease mechanisms in the pulmonary compartment and peripheral tissues, leading to the concept of COPD as a systemic inflammatory disease. This communication can be mediated by: 1) leakage of reactive oxygen species and stress-induced cytokines directly into the peripheral blood, 2) (pre)activation of peripheral blood leukocytes that can result in aberrant homing and activation of inflammatory cells in distant tissues, and 3) the liberation of proinflammatory mediators by leukocytes and/or stromal cells present in the pulmonary tissues during progression of the disease. The current authors hypothesise that the occurrence of a chronic inflammatory response after prolonged interaction of the pulmonary tissue with cigarette smoke causes aberrant homing of leukocytes to the tissue and delayed apoptosis. This leads to the autonomous characteristic of the inflammatory response in patients with chronic obstructive pulmonary disease.

Humans↗

PubMed2003

[Exacerbations of chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease is characterised by a progressive decline in lung function, reduced exercise performance, and worsening of health status. Exacerbations are important clinical events in chronic obstructive pulmonary disease and are defined as sudden worsening of respiratory symptoms and function requiring medical intervention. The most common causes of chronic obstructive pulmonary disease exacerbations are bacterial or viral infections, but comorbidity may be important. A major issue is the decision regarding home management or hospital management of exacerbations. Because of exacerbations, a frequent assessment of severity of chronic obstructive pulmonary disease is required for targeting pharmacological therapy.

Humans↗

PubMed2003

Systemic effects of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is characterised by an inappropriate/excessive inflammatory response of the lungs to respiratory pollutants, mainly tobacco smoking. Recently, besides the typical pulmonary pathology of COPD (i.e. chronic bronchitis and emphysema), several effects occurring outside the lungs have been described, the so-called systemic effects of COPD. These effects are clinically relevant because they modify and can help in the classification and management of the disease. The present review discusses the following systemic effects of chronic obstructive pulmonary disease: 1) systemic inflammation; 2) nutritional abnormalities and weight loss; 3) skeletal muscle dysfunction; and 4) other potential systemic effects. For each of these, the potential mechanisms and clinical implications are discussed and areas requiring further research are highlighted.

Bone Diseases↗

PubMed2006

Corticosteroid therapy and chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is characterized in part by a chronic inflammatory state in the airways (largely from chronic noxious stimuli such as tobacco smoke), punctuated with acute inflammatory exacerbations, which are often infectious. Although pathologically and biochemically different from the inflammation of asthma, the chronic inflammation of chronic obstructive pulmonary disease, especially in subgroups with asthma-like features and especially during exacerbations, might be expected to respond to corticosteroid therapy, as does asthma. Complications from long-term corticosteroid use are important, but they appear less when the corticosteroid is given via the inhaled route. Clinical evidence is particularly strong supporting the use of inhaled corticosteroids to prevent exacerbations and oral corticosteroids to reduce the duration and impact of exacerbations.

Adrenal Cortex Hormones↗

PubMed2006

Pathology of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is one of the leading causes of death and morbidity worldwide. Despite intensive investigation, its pathology and pathophysiology are not well understood. The hallmarks of the disease are irreversible airflow limitation and chronic inflammation. Small airway obstruction due to progressive inflammation and fibrosis, and the loss of elastic recoil mediated by elastolysis and apoptosis equally contribute to pathologic changes. However, it is debated to what extent the obstruction of large airways leads to altered lung function. Three morphologic entities are described in the literature under one disease; chronic bronchitis, obstructive bronchiolitis and emphysema may appear in the same patient at the same time. The authors review pathologic changes observed in chronic obstructive pulmonary disease, including acute exacerbations and secondary pulmonary hypertension as severe but common complications of the disease. Furthermore, we detail recent scientific evidences for major cellular and molecular inflammatory pathway activation. These mechanisms result in accelerated apoptosis, remodeling and increased proinflammatory cytokine release. Targeting intracellular pathological changes may lead to the discovery of a new generation of drugs that could reduce chronic obstruction before airway irreversibility is established.

Humans↗

PubMed2003

An outreach programme for patients with an exacerbation of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is a common clinical condition characterised by airflow obstruction. The clinical course of the disease is characterised by intermittent exacerbations. In Ireland exacerbations of chronic obstructive pulmonary disease are a common cause of admission to acute medical hospitals. The Beaumont Hospital COPD Outreach Programme was designed to provide care at home for patients with an exacerbation of COPD that would otherwise require hospitalisation. Patients recruited to the programme were discharged home within 72 hours of admission and reviewed by the Outreach Team over a two week period. In addition to monitoring clinical progress the Team provided education, smoking cessation and medication advice. Analysis of the outcome of the first 100 patients recruited to the study show that one third of patients admitted to Hospital with an exacerbation of COPD are eligible for this programme and the average length of Hospital stay was 2.6 days. During the fourteen day follow up there was one death (non-respiratory) and six patients were re-admitted to hospital. Forty percent of smokers had abstained from smoking at the end of three months. In summary, the COPD Outreach programme is a safe and effective alternative to acute hospital care for selected patients with exacerbations of COPD.

Home Care Services, Hospital-Based↗

PubMed2001

Epidemiology of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a leading cause of world-wide mortality and disability. On average approximately 5-15% of adults in industrialized countries have COPD defined by spirometry. In 1990, COPD was considered to be at the twelfth position world-wide as a cause of combined mortality and disability but is expected to become the fifth cause by the year 2020. COPD has a chronic long-lasting course characterized by irreversible decline of forced expiratory volume in one second (FEV1), increasing presence of dyspnoea and other respiratory symptoms, and progressive deterioration of health status. After diagnosis the 10-yr survival rate is approximately 50% with more than one-third of patients dying due to respiratory insufficiency. Several environmental exposures such as air pollution increase the risk of death in COPD patients. The aetiology of COPD is overwhelmingly dominated by smoking although many other factors could play a role. Particular genetic variants are likely to increase the susceptibility to environmental factors although little is known about which are the relevant genes. There is clear evidence about the role of the alpha-1-antitrypsin but the fraction of COPD attributable to the relevant variants is only 1%. Phenotypic traits that are considered to play a role in the development of COPD include sex, with females being at a higher risk, bronchial responsiveness and atopy. There is strong causal evidence regarding the relationship between smoking and COPD with decline in FEVI levelling off after smoking cessation. Passive smoking has been found to be associated with a small though statistically significant decline in FEV1. Other risk factors that are likely to be relevant in the development of COPD are occupation, low socioeconomic status, diet and possibly some environmental exposures in early life. Although there is accumulating evidence that oxygen therapy, pharmacological treatment and rehabilitation may improve the course of chronic obstructive pulmonary disease, preventing smoking continues to be the most relevant measure, not only to prevent chronic obstructive pulmonary disease, but also to arrest its development.

Adolescent↗

PubMed2005

Effects of inhaled HFA beclomethasone on pulmonary function and symptoms in patients with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is characterized by progressive airflow limitation and pulmonary inflammation. Inhaled corticosteroids (ICS) have been shown to be effective in the reduction of the number of exacerbations and the rate of deterioration in health status in patients with more advanced chronic obstructive pulmonary disease (COPD). Therefore current international guidelines recommend ICS for patients with severe COPD (FEV1 < 50%) with at least one exacerbation within the last year. We determined the short-term effect of the inhaled corticosteroid beclomethasone in HFA 134 formulation (Ventolair) on Health related Quality of Life (HRQOL), pulmonary function and the release of the cytokines Interleukin-10 (IL-10), Granulocyte-Macrophage Colony-stimulating Factor (GM-CSF), Interferon-gamma (IFN-gamma) and Macrophage Inflammatory Protein-1alpha (MIP-1alpha) from peripheral blood monocytes of patients with COPD (n = 11) in a 12 week double blind cross over placebo-controlled study. Baseline lung function and the St. George Respiratory Questionnaire (SGRQ) were performed at the start and the end of each treatment phase. Monocytes were separated from blood at the end of each treatment phase. The treatment with Ventolair) resulted in an increase of PEF from 4.92 to 5.53 l/s and a decrease of RV% TLC (% predicted) values from 144.52 to 131.36. Inhaled HFA beclomethasone did not affect the cytokine release of IL-10, IFN-gamma, GM-CSF and MIP-1alpha. All cytokines were measured using commercially available Enzyme Linked Immun Sorbent Assay (ELISA) kits. The symptom score of the St. George Respiratory Questionnaire significantly decreased from 55.12 to 47.77 units in the active period compared to the placebo period after the treatment with HFA beclomethasone. The present study shows that a short-term treatment with inhaled steroid beclomethasone in fine particle HFA formulation decreases the hyperinflation and improves the PEF and the COPD symptoms.

Administration, Inhalation↗

PubMed2003

Strategies for screening for chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is easily detected in its preclinical phase, using office spirometry. Successful smoking cessation prevents further disease progression in most patients. Spirometry measures the ratio of the forced expiratory volume in the first second to the forced vital capacity (FEV(1)/FVC), which is the most sensitive and specific test for detecting airflow limitation. Primary care practitioners see the majority of adult smokers, but few primary care practitioners currently have spirometers or regularly order spirometry for their smoker patients. Improvements in spirometry software have made it much easier to obtain good quality spirometry test sessions, thereby reducing the misclassification rate. Respiratory therapists and pulmonary function technologists can help primary care practitioners select good office spirometers for identifying chronic obstructive pulmonary disease and teach staff how to use spirometers correctly.

Adult↗

PubMed2002

New therapeutic drugs in the management of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease remains a major health problem for which new and improved treatments are desperately needed. Recent trials strongly suggest that treatments are improving. Longer-acting bronchodilators will be more convenient and may have additional advantages. Combinations of bronchodilators may offer additive effects and, possibly, synergies. Inhaled glucocorticoids, although unable to alter the loss of forced expiratory volume in 1 second when used alone, may reduce exacerbation frequency and health status deterioration and improve mortality. These clinically meaningful goals represent end points not previously targeted in chronic obstructive pulmonary disease drug development. Moreover, inhaled glucocorticoids may offer benefits in combination with long-acting beta-agonists. Finally, new classes of agents such as the phosphodiesterase inhibitors are on the horizon. The prospect for better treatment of chronic obstructive pulmonary disease looks brighter than ever. Caution is required, however. Much of the excitement has been generated by small studies, presented only in abstract form, and as yet unpublished work. Therapeutic recommendations will require publication of appropriately designed and adequately powered clinical trials.

Albuterol↗