Chronic Obstructive Pulmonary Disease

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Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease

How common is chronic obstructive pulmonary disease? COPD is common and important. It is estimated that about three million people in the UK have COPD. However, in many of these people, the condition has not been formally diagnosed (normally these would be mild cases). This is because in the early stages, many people put up with a cough or mild breathlessness without seeing their doctor. They may only see see their doctor when symptoms get worse.

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Sirtuins and Chronic Obstructive Pulmonary Disease

Sirtuins and Chronic Obstructive Pulmonary Disease

C. Carollo * , C. Urso, R. Lo Presti, G. Caimi Biomedical Department of Internal and Specialistic Medicine, University of Palermo, Palermo, Italy Abstract Chronic obstructive pulmonary disease (COPD) is one of the world leading causes of death. It has been recently related to aging and inflammation, as well as sirtuins are actually recognized to be involved in both these pheno- mena. Sirtuins are a family of highly conserved protein deacetylases and they influence the factors that worsen physiological aging such as glucose meta- bolism, DNA stability and cancer, neurodegenerative processes, etc. Among the seven sirtuins, SIRT1 and SIRT6 have been deeply investigated in COPD.
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Autoantibodies in Chronic Obstructive Pulmonary Disease

Autoantibodies in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death world- wide, is characterized by irreversible airflow limitation based on obstructive bronchiolitis, emphysema, and chronic pulmonary inflammation. Inhaled toxic gases and particles, e.g., cigarette smoke, are major etiologic factors for COPD, while the pathogenesis of the dis- ease is only partially understood. Over the past decade, an increasing body of evidence has been accumulated for a link between COPD and autoimmunity. Studies with clinical samples have demonstrated that autoantibodies are present in sera of COPD patients and some of these antibodies correlate with specific disease phenotypes. Furthermore, evidence from animal models of COPD has shown that autoimmunity against pulmonary antigens occur during disease development and is capable of mediating COPD-like symptoms. The idea that autoimmunity could contribute to the development of COPD provides a new angle to understand the pathogenesis of the disease. In this review article, we provide an advanced overview in this field and critically discuss the role of autoantibodies in the pathogenesis of COPD.
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Models of chronic obstructive pulmonary disease

Models of chronic obstructive pulmonary disease

Chronic obstructive pulmonary diseaseCOPDasthmaanimalmiceratguinea pigtobacco smokenitrogen dioxidesulfur dioxide Abstract Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations.
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Exacerbation Of Chronic Obstructive Pulmonary Disease

Exacerbation Of Chronic Obstructive Pulmonary Disease

250 Med J Malaysia Vol 64 No 3 September 2009 SUMMARY Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in COPD patients and place a large burden on healthcare resources. COPD patients with frequent exacerbations have accelerated decline in lung function, poorer health status and are at higher risk of mortality. The mainstay of treatment includes increasing short acting bronchodilator therapy and systemic glucocorticosteroids with or without antibiotics. Non invasive ventilation is indicated in those with respiratory failure with acidosis or hypercapnia. Preventive strategies to reduce exacerbations include smoking cessation, immunisation against influenza and S. pneumonia, chronic maintenance inhaled pharmacotherapy, pulmonary rehabilitation and self management education.
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Microbiome in chronic obstructive pulmonary disease

Microbiome in chronic obstructive pulmonary disease

Correspondence to: Eduard Monsó. Respiratory Diseases Department, Parc Taulí University Hospital, Parc Tauli 1, 08208 Sabadell, Barcelona, Spain. Email: emonso@tauli.cat or eduardmonsomolas@gmail.com. Abstract: The introduction of culture-independent techniques for the microbiological analysis of respiratory samples has confirmed that the respiratory system hosts a large number of microorganisms, which include a wide range of bacteria. The regular exposure to tobacco smoke changes the microbiome in healthy smokers, first in the oropharynx, increasing the presence of a restricted number of genera which attain high relative abundance, a pattern that may be considered as dysbiosis. In chronic obstructive pulmonary disease (COPD), microbiome analyses of sputum samples have demonstrated an important decline in bacterial diversity, with a change to a restricted flora with an overrepresentation of the Proteobacteria phylum, which include most of the bacteria commonly considered as potentially pathogenic microorganisms, paralleled by a decline in the relative abundance of microorganisms part of the Firmicutes phylum. In exacerbations, specific bacteria overrepresented in microbiome analyses and potentially causal of the acute episode may not be recovered by sputum culture, while colonizing microorganisms grow easily, in spite that their relative abundance have not changed from previous stability. This situation has been described in patients showing chronic colonization by Pseudomonas aeruginosa, who suffer from exacerbations that in most cases are due to other PPMs, in spite of the persistence of positive cultures for the colonizing Pseudomonas strains.
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The genetics of chronic obstructive pulmonary disease

The genetics of chronic obstructive pulmonary disease

Abstract Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease caused by the interaction of genetic susceptibility and environmental influences. There is increasing evidence that genes link to disease pathogenesis and heterogeneity by causing variation in protease anti-protease systems, defence against oxidative stress and inflammation. The main methods of genomic research for complex disease traits are described, together with the genes implicated in COPD thus far, their roles in disease causation and the future for this area of investigation.
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Pathogenesis of chronic obstructive pulmonary disease

Pathogenesis of chronic obstructive pulmonary disease

3 Richard L. Roudebush Veteran Affairs Medical Center, Indiana University, Indianapolis, Indiana. The current epidemic of chronic obstructive pulmonary disease (COPD) has produced a worldwide health care burden, approaching that imposed by transmittable infectious diseases. COPD is a multidimensional disease, with varied intermediate and clinical phenotypes. This Review discusses the pathogenesis of COPD, with particular focus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by exposure to ciga- rette smoke, pollutants, and infectious agents), progression, and consolidation. Tissue damage entails complex interactions among oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death. Lung damage by cigarette smoke ultimately leads to self-propagating processes, resulting in macromo- lecular and structural alterations — features similar to those seen in aging.
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An update on chronic obstructive pulmonary disease

An update on chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. It is a chronic condition which affects the respiratory system and worsens over time. Cigarette smoking and advancing age are the two major risks associated with this disease. It is concerning that the global incidence of this chronic illness is on the rise. Current projections indicate that it will become the third leading cause of death by the year 2020. Inflammatory changes underlie the pathophysiology of COPD. Irreversible damage and progressive narrowing of the air passages follow. COPD is characterised by the progressive loss of lung function. In addition, the Global Initiative for Chronic Obstructive Lung Disease released the latest update on its global strategy for the diagnosis, management, and prevention of COPD in 2015. This article provides an overview of the causative risk factors, underlying disease process, pathophysiological changes, and the classification and management of COPD, including the latest perspectives on this highly prevalent condition.
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An update on chronic obstructive pulmonary disease

An update on chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. It is a chronic condition which affects the respiratory system and worsens over time. Cigarette smoking and advancing age are the two major risks associated with this disease. It is concerning that the global incidence of this chronic illness is on the rise. Current projections indicate that it will become the third leading cause of death by the year 2020. Inflammatory changes underlie the pathophysiology of COPD. Irreversible damage and progressive narrowing of the air passages follow. COPD is characterised by the progressive loss of lung function. In addition, the Global Initiative for Chronic Obstructive Lung Disease released the latest update on its global strategy for the diagnosis, management, and prevention of COPD in 2015. This article provides an overview of the causative risk factors, underlying disease process, pathophysiological changes, and the classification and management of COPD, including the latest perspectives on this highly prevalent condition.
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Phenotypes in chronic obstructive pulmonary disease

Phenotypes in chronic obstructive pulmonary disease

m ots - clés : Broncho-Pneumopathie Chronique Obstructive - Phénotype - Bronchite chronique - Emphysème P henotyPes in chRonic obstRuctive PulmonaRy disease s ummaRy : Chronic Obstructive Pulmonary Disease (COPD) is a multi-dimensional disorder with multiple phenotypes. The GOLD guidelines, used for the diagnosis, staging and treat- ment of COPD, do not fully reflect the heterogeneous nature of the disease. Historically, the two most recognized clinical phenotypes of COPD are emphysema and chronic bronchitis. Most COPD patients encountered in practice actually share both of these features. Genetic background, clinical presenta- tion, variation in the response to treatment and propensity to exacerbations may also identify other phenotypes. Recently, using a mathematical approach, such as cluster analysis, which is based on pre-selected parameters, other interesting phenotypes were identified. A precise definition of COPD phe- notypes should lead to a more targeted therapeutic approach based on these phenotypes. The purpose of this article is to point out that COPD is a heterogeneous disease and to sum- marize the current data available about the phenotypes of this disease.
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Angiogenesis in Chronic Obstructive Pulmonary Disease

Angiogenesis in Chronic Obstructive Pulmonary Disease

Beyond the widely recognized role in cancer, angiogenesis is important in other lung disorders that have a lung vascular disease component, such as pulmonary hypertension, chronic obstructive pulmonary disease (COPD) and tuberculosis. In fact, the lung is characterized by double vascularization: the bronchial vasculature, deriving from thoracic aorta (intercostal and mammarian arteries), has a trophic role, while pulmonary system is part of air/blood barrier that plays respiratory function of the lung. 12 The burden of vasculogenesis and angiogenesis in pneumology can be better understood if one considers that in humans the volume of the lungs increases by more than 20 times during the first 2 years of life. A number of studies in animal models showed that the inhibition of angiogenesis in embryonic lung displays a variety of vascular defects including a significant reduction in formation of air space and capillaries, resulting in distended and under-developed alveoli. 13, 14
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A Review on Chronic Obstructive Pulmonary Disease

A Review on Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a disorder that causes a huge degree of human suffering. Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded). Emphysema, on the other hand, is defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Airflow limitation in emphysema is due to loss of elastic recoil and decrease in airway tethering, whereas chronic bronchitis leads to narrowing of airway caliber and increase in airway resistance. Although some patients predominantly display signs of one or the other, most fall somewhere in the middle of the spectrum.The past definitions of COPD have been pessimistic at best, suggesting that the disease process is irreversible with little therapy to offer. More recently, however, a more optimistic definition has become widely accepted. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines define COPD as a disease state characterized by airflow limitation that is not fully reversible, is usually progressive, and is associated with an abnormal inflammatory response of the lungs to inhaled noxious particles or gases. This definition shifts the paradigm of the disease, suggesting that it is both treatable and preventable.
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Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD)

go away. What is COPD? COPD stands for “Chronic Obstructive Pulmonary Disease” COPD is a term used to refer to these chronic respiratory diseases including 1) chronic bronchitis and 2) emphysema. Most people with COPD have a mix of both emphysema and bronchitis. COPD is not contagious.

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Consequences of chronic kidney disease in chronic obstructive pulmonary disease

Consequences of chronic kidney disease in chronic obstructive pulmonary disease

Additional file Additional file 1: Table S1. Laboratory values. (DOCX 18 kb) Abbreviations 6MWT: Six-minute walk test; BMI: Body mass index; CAD: Coronary artery disease; CAT: COPD assessment test; CKD: Chronic kidney disease; CKD- EPI: Chronic kidney disease epidemiology collaboration; COPD: Chronic obstructive pulmonary disease; CRP: C-reactive protein; CVI: Cardiovascular index; DM: Diabetes mellitus; EC: Exercise capacity; eGFR: Estimated glomerular filtration rate; EQ-5D: EuroQol- 5 dimension; FEV 1 : Forced expiratory volume in 1 s; FS: Functional status; HbA1c: Glycosylated haemoglobin; HDL: High density lipoprotein; ITGV: Intrathoracic gas volume;
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Summary Guide. Living Well. Living Well. Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Disease

Summary Guide. Living Well. Living Well. Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Disease

Introduction Chronic obstructive pulmonary disease (COPD) – a chronic, respiratory disease – is a leading cause of disability and death in Canada. Unfortunately, it is also increasing in prevalence. COPD is not a hopeless diagnosis. Use this patient information booklet to learn about COPD, medications and your action plan in treating and managing your disease.

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Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease

Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease

[Indian J Chest Dis Allied Sci 2018;60:233-237] Key words: COPD, Severity, Exacerbations, Inflammatory markers. Introduction Chronic obstructive pulmonary disease (COPD) is a common disease of the respiratory system and has extremely high morbidity and mortality rates. At present, COPD is the fourth highest cause of death worldwide and is expected to become the third leading cause of mortality by the year 2020. 1 Exacerbations of respiratory symptoms in COPD are of major importance because of their profound adverse effects, like accelerated deterioration of lung function, poor quality of life, and increased mortality. 2 Forced expiratory volume in one second (FEV 1 ) is used as a global marker of pathophysiological changes and severity of COPD. However, FEV 1 often fails to reflect the severity of dyspnoea, functional impairment, prognosis, and systemic manifestations of patients with COPD. 3 Hence, there is a constant search for the factors that can predict the exacerbation risk better. One such marker is acute-phase proteins, which has been implicated in both stable and COPD
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Metabolic syndrome in chronic obstructive pulmonary disease

Metabolic syndrome in chronic obstructive pulmonary disease

Study methods Both cases and controls were interviewed to obtain relevant data. Based on inclusion and exclusion criteria, about 51 cases of chronic obstructive pulmonary disease patients were compared with an equal number of healthy controls. Global initiative for chronic obstructive pulmonary disease (GOLD) guidelines were used for diagnosing COPD and Metabolic Syndrome diagnosed based on Modified NCEP: ATP III criteria. 5,10

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Epidemiology of Comorbidities in Chronic Obstructive Pulmonary Disease

Epidemiology of Comorbidities in Chronic Obstructive Pulmonary Disease

13. COPD, comorbidities and frailty INTRODUCTION With the aging of our population and the reduction in early deaths from acute illnesses and infections, more people are living longer but frequently suffer from chronic illnesses such as Chronic Obstructive Pulmonary Disease (COPD). COPD is characterized by various systemic manifestations in addition to the progressive chronic airflow limitation. 24 The most prevalent known comorbidities are cardiovascular disease, metabolic syndrome, osteoporosis, depression, and lung cancer. 24 Other systemic manifestations of COPD include skeletal muscle wasting, cachexia and normocytic anemia. 373, 407 These comorbid conditions have a clear impact on the clinical presentation and prognosis of patients with COPD and the identification and treatment of comorbid diseases are key elements in COPD management. 1 In contrast to organ-specific diagnoses and treatment, frailty points more to a holistic viewpoint of the elder patient and their predicament. 37 The definition of frailty describes a biological syndrome in which a progressive, cumulative decline in the reserve capacity of multiple physiological systems elicits an abnormal vulnerability to common stressors. 38 Frailty is a distinct syndrome associated with functional decline, loss of independence, and mortality, and is characterized by the disability to compensate function loss. 38 Frailty is defined as meeting 3 or more of five established criteria for frailty, evaluating nutritional status, physical activity, mobility, strength and energy. 38 Individuals with one or two criteria are defined as intermediate frail or pre-frail and have been found to be at increased risk of becoming frail. 38 Previously, we have demonstrated that frailty is common in the general elderly population. 408 Moreover, we demonstrated that frail elderly subjects had more falls and hospitalizations and an increased risk of mortality independent of age, sex and comorbidity. 408 Distinction of frail elderly people from those who are not frail is essential in an aging population to better outweigh benefits and risks of invasive procedures or potentially harmful medication in vulnerable elderly. 37
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Ambulatory Oxygen in Chronic Obstructive Pulmonary Disease

Ambulatory Oxygen in Chronic Obstructive Pulmonary Disease

Received September 8, 2011; revised October 2, 2011; accepted October 20, 2011 Abstract Ambulatory oxygen has been shown to improve pulmonary hemodynamics and reduce dynamic hyperinfla- tion in patients with Chronic Obstructive Pulmonary Disease. Therefore, it is hypothesized to be of benefit in patients with either exertional desaturation or dyspnoea. There is evidence of short-term improvements in exercise distance, exercise time, breathlessness, oxygen saturation and minute ventilation. However, longer term studies only identified improvements in oxygenation and minute ventilation. The benefits were even more limited in patients with no resting hypoxemia. The role in improving exercise training in pulmonary rehabilitation by increasing exercise time and reducing dyspnoea was marginal and no improvements were detected in walking distance or quality of life. Practical considerations make compliance with ambulatory oxygen therapy a major issue with the weight of oxygen and social unacceptability the most often quoted problems. The evidence for any benefit of ambulatory oxygen is therefore limited despite the theoretical benefits.
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