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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↗
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↗
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 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

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↗
PubMed2003

[Pathophysiology of chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease (COPD) is a disease state characterised by airflow obstruction that is not fully reversible and progressive. Symptoms, as cough, sputum production and dyspnoea, functional impairment and complications of COPD can all be explained on the basis of the underlying lung inflammation and the resulting pathology. The chronic airflow obstruction is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). On one hand, chronic inflammation causes remodelling and narrowing of the small airways. On the other hand, destruction of the lung parenchyma, also by an inflammatory process, leads to the loss of alveolar attachments to the small airways and decreases lung elastic recoil. In turn, these changes reduce the ability of the airways to remain open during expiration.

Airway Obstruction↗
PubMed2003

Therapy of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease is one of the commonest causes of morbidity and mortality in the world, and is increasing in prevalence. Current therapies are not very effective, and no current treatment prevents the relentless progression of airflow limitation that characterizes this disease. Smoking cessation is the only strategy that reduces this decline in lung function, and although bupropion is the most effective aid to quitting, more effective treatments of nicotine addiction are needed. The mainstay of treatment is bronchodilators for symptom relief, and inhaled anticholinergics and beta(2)-agonists are useful by reducing hyperinflation of the lungs. A new once-daily inhaled anticholinergic is the most effective bronchodilator, but long-acting inhaled beta(2)-agonists are also useful. Theophylline is used as an additional bronchodilator in more severe patients, and may have some anti-inflammatory action. In contrast, inhaled corticosteroids are poorly effective and do not reduce disease progression, although recent studies with combination inhalers (corticosteroid + long-acting beta(2)-agonist) have shown better effects. Long-term oxygen therapy is needed by patients with pulmonary hypertension and right heart failure. There is a pressing need to develop new classes of therapy, and several new drugs are current in development, including interleukin-8 antagonists, phosphodiesterase-4 inhibitors, protease inhibitors, and antioxidants.

Acute Disease↗
PubMed2002

The burden of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by chronic airflow limitation that is not fully reversible, with a precise definition varying between different management guidelines. The burden of COPD is considerable from all relevant viewpoints. From the perspective of society, the mortality is already considerable, and it is likely to increase from the sixth to the third most common cause of death worldwide by 2020. From the patient's perspective, COPD is responsible for disability that restricts many everyday activities, such as walking up stairs. The burden of COPD on physicians includes increasing consultations for the condition. From the perspective of healthcare payers, COPD represents an increasing burden, primarily due to the costs incurred when exacerbations require hospital treatment. Despite this considerable burden, there are many signs that the impact of COPD is not recognized. Research on COPD is currently underfunded in relation to the impact of the disease; patients only present late with symptoms; physicians may fail to diagnose the condition and healthcare payers may be failing to support treatment approaches that could reduce the number of costly hospital exacerbations. Reasons for this overall poor recognition of the burden of COPD include lack of recognition of the disease, difficulties in diagnosis, poor knowledge of COPD and nihilistic attitudes towards the condition and its treatment. Awareness of COPD could be improved with education of the public and healthcare professionals. Long-term epidemiological studies showing the impact on morbidity and mortality of different treatment approaches would also influence the setting of priorities by healthcare payers.

Attitude of Health Personnel↗
PubMed2005

Epidemiology and global impact of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease that causes a heavy health and increasing economic burden both in the United States and around the world. Most of the risk factors for COPD are well known and include smoking, occupational exposures, air pollution, airway hyperresponsiveness, asthma, and certain genetic variations, although many questions, such as why a minority of smokers develop significant airway obstruction, remain. Major medical organizations have agreed on a common definition of COPD, although newer measures, such as functional status or exercise capability, have emerged as important in determining the prognosis of COPD patients. In most of the world, COPD prevalence and mortality are still increasing and will likely continue to rise in response to increases in smoking, particularly by women and adolescents. Resources aimed at smoking cessation and prevention, COPD education and early detection, and better treatment will be of the most benefit in our continuing efforts against this important cause of morbidity and mortality.

Bronchitis, Chronic↗
PubMed2003

[Influence of orthopnoea position on spirometric and plethysmographic parameters in patients with chronic obstructive pulmonary disease ].

Chronic obstructive pulmonary disease (COPD) is characterized by the lack or only slight reversibility of obstruction which can be assessed by spirometry after inhalation of short-acting beta 2-mimetic (e.g. Salbutamol). The aim of the study was to determine if subjective decrease in dyspnoea sensation notified by COPD patients in orthopnoea position is reflected in spirometry and plethysmography. The study was carried out in the group of 30 patients with COPD (FEV1 = 30-70% of predicted value) as well as in 30 sex- and age-matched non-smoking healthy subjects. We observed the increase of spirometric parameters (FEV1, FEV1%VC, FEF75, PEF) and the decrease of plethysmographic parameters (RTOT, RV, RV%TLC) after the change from the initial to orthopnoea position (p < 0.001). The obtained results show that orthopnoea position leads to the decline of obstruction degree, pulmonary hyperinflation and the decrease of dyspnoea sensation.

Adrenergic beta-Agonists↗
PubMed2001

New concepts in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a leading cause of death and disability but has only recently been explored from a cellular and molecular perspective. In COPD, chronic inflammation leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterized by increased numbers of alveolar macrophages, neutrophils, and cytotoxic T lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). There is also a high level of oxidative stress, which may amplify this inflammation. There is increased elastolysis and probable involvement of matrix metalloproteinases. The inflammation and proteolysis in COPD is an amplification of the normal inflammatory response to cigarette smoke. Unlike asthma, this inflammation appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.

Disease Progression↗
PubMed2005

Quantitative computed tomography of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is described as airflow limitation that is not fully reversible. Quantitative assessment of structural changes within the lung that are responsible for this airflow limitation has relied on the examination of tissue obtained from surgical or postmortem specimens. However, in the past two decades, researchers have developed novel and robust tools to measure the structure of the lung parenchyma and airway wall by using computed tomographic (CT) scans, which do not require the removal of lung tissue. These techniques are extremely important because they allow longitudinal studies of the pathogenesis of COPD and the assessment of therapeutic interventions. Another application of this approach is that it potentially allows phenotyping of individuals who predominately have emphysema or small-airway disease, which may be important for the evaluation of pathogenesis and prescription of treatment options. This review describes some of these CT techniques for quantitative assessment of lung structure.

Humans↗
PubMed2005

Sleep in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death, affecting 14 million adults in the United States. Symptoms related to sleep disturbances are common in moderate to severe COPD, particularly in elderly patients, in the form of morning tiredness and early awakenings. One major cause of morbidity in this population is abnormalities in gas exchange and resultant hypoxemia. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying nonapneic oxygen desaturation during sleep. They include decreased functional residual capacity, diminished ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanical effectiveness, diminished arousal responses, respiratory muscle fatigue, diminished nonchemical respiratory drive, increased upper airway resistance, and the position of baseline saturation values on the oxyhemoglobin dissociation curve. Smoking cessation, bronchodilation, and pulmonary rehabilitation are cornerstones of treatment of COPD. Improvement in lung mechanics and gas exchange should lead to better sleep quality and health status.

Humans↗
PubMed2005

Oxygen therapy improves renal function in patients with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) may cause edema independently of cardiac function. This study assessed the effects of oxygen therapy in renal hemodynamics and excretion of sodium and water in COPD patients. Twelve COPD patients without cor pulmonale (PaO2 < or = 60 mmHg), aged 66 +/- 9 years, were studied before and after 72 h of O2 therapy. Oxygen increased PaO2 from 56 +/- 4 to 85 +/- 22 mmHg (p < 0.0001), whereas PaCO2 did not change significantly. Oxygen induced significant increments in glomerular filtration rate (90 +/- 21 to 111 +/- 36 mL/min/1.73 m2, p = 0.03), sodium filtered load (10 +/- 3 to 12 +/- 5 mEq/min, p = 0.004), sodium excreted load (79 +/- 67 to 194 +/- 106 mEq/day, p = 0.0006), fractional excretion of sodium (0.51 +/- 0.49 to 1.30 +/- 1.32%, p = 0.015) diuresis (1048 +/- 548 to 1893 +/- 440 mL/day, p = 0.002), osmolar clearance (1.43 +/- 0.7 to 2.08 +/- 0.6 mOsm/min, p = 0.008) and decreased hematocrit (48 +/- 4 to 44 +/- 3%, p = 0.0038). Renal plasma flow and filtration fraction did not change after oxygen. In summary, use of oxygen caused increases of 36% in GFR, 35% in filtered load of sodium, 118% in diuresis, 258% in excreted load of sodium, and 178% in fractional excretion of sodium. These data suggest that oxygen-induced natriuresis and diuresis were likely more dependent of changes in the tubular manipulation of sodium than in glomerular hemodynamics. These changes occurred with a mild increase in PCO2, showing that oxygen therapy caused renal improvement independently of amelioration of hypercapnia.

Aged↗