Cause Of Chronic Obstructive Pulmonary Disease Research Articles

Rethinking chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a complex polygenic disease characterized by an abnormal inflammatory response to smoke, and results in a progressive and debilitating condition with declining lung function. The reasons why some smokers get COPD are not known. We suggest that corticosteroid resistance, which derives from oxidative stress, might actually be the cause of COPD and represent the starting point of the pathology. The absence of response to corticosteroids would let the disease develop, impairing the organism capacity to suppress any kind of inflammatory process. Corticosteroid resistance may derive from smoke induced oxidative stress and plausibly impairs the organism capacity to suppress inflammation. Many factors may contribute to the development and persistence of corticosteroid resistance: inefficient antioxidant defences, a corticosteroid response less efficient or more sensitive to oxidative conditions, and also any other concomitant factor, environmental, genetic or intercurrent, which would contribute to amplify inflammation and hence oxidative stress. One or more of these factors might represent the variable component of the disease, which gives origin to COPD heterogeneity. This hypotheses may also explain why the disease persists after quitting smoking, as an inflammatory process severe enough to generate a strong oxidative stress may support itself by maintenance of corticosteroid resistance.

An Official American Thoracic Society Public Policy Statement: Novel Risk Factors and the Global Burden of Chronic Obstructive Pulmonary Disease

Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.

Undiagnosed coeliac disease in patients with emphysema: a fortuitous association?

To the Editors: Chronic obstructive pulmonary disease (COPD) is characterised by progressive and poorly reversible airflow obstruction due to small airway disease and emphysema. Cigarette smoking is the major cause of COPD, but the disease also occurs in nonsmokers. In nonsmokers, environmental factors ( e.g. second-hand smoking and inhalation of toxic gas), genetic factors ( e.g. the rare α1-antitrypsin deficiency) and infectious factors ( e.g. HIV infection) have been implicated in the pathogenesis of the disease. We report on two cases of COPD with emphysema in nonsmokers with long-standing undiagnosed coeliac disease. A 71-yr-old female was referred to our hospital (Hopital Cochin, Assistance Publique-Hopitaux de Paris, Paris, France) for dyspnoea and cough, which had evolved over 5 yrs. She had suffered from alternating diarrhoea and constipation for many years, ascribed to functional bowel disease. She had never been exposed to inhaled toxics and had never smoked. Examination revealed a body mass index (BMI) of 18 kg·m−2 and a chest computed tomography (CT) image revealed pulmonary distension and emphysema (fig. 1). Spirometry revealed severe airflow limitation (table 1). Serum α1-antitrypsin was normal. Treatment with long-acting bronchodilators was initiated. After 7 yrs of follow-up, the patient complained of progressive weight loss (BMI 15 kg·m−2 …

Lipopolysaccharide induced connective tissue growth factor gene expression in human bronchial epithelial cells

Connective tissue growth factor (CTGF) is up-regulated in the lungs of patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke and repeated bacterial infections, both of which are rich sources of LPS, are major causes of COPD. The high levels of LPS in lung epithelial lining fluid also suggest that it may have a considerable impact on the airway epithelium, in terms of cytokine and growth factor production. The aim of this study was to clarify the mechanism of LPS-induced CTGF expression in bronchial epithelial cells. The expression and transcriptional regulation of the CTGF gene were assessed using the cultured human bronchial epithelial cell line, BEAS-2B. LPS significantly up-regulated CTGF mRNA expression in a dose-dependent fashion, with 100 microg/mL LPS causing a twofold increase after 2 h. CTGF protein expression was also up-regulated by LPS after 8 h. Transforming growth factor-beta1 mRNA expression was not changed by LPS treatment. A pharmacological inhibitor of nuclear factor (NF)-kappaB, MG132, inhibited LPS-induced CTGF mRNA expression. Furthermore, luciferase assays demonstrated that deletion of base pairs -253 to -53 from the CTGF promoter, where the Smad and proximal NF-kappaB binding sites are located, decreased the induction of CTGF by LPS. After stimulation with LPS, the p65 subunit of NF-kappaB was shown to be bound to the CTGF promoter in vitro and in situ. LPS directly induced CTGF expression in bronchial epithelial cells, independently of transforming growth factor-beta1, suggesting a possible mechanism for airway remodelling in COPD that is induced by smoking and repeated bacterial infections.

Cigarette smoke promotes dendritic cell accumulation in COPD; a Lung Tissue Research Consortium study

BackgroundAbnormal immune responses are believed to be highly relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD). Dendritic cells provide a critical checkpoint for immunity by their capacity to both induce and suppress immunity. Although evident that cigarette smoke, the primary cause of COPD, significantly influences dendritic cell functions, little is known about the roles of dendritic cells in the pathogenesis of COPD.MethodsThe extent of dendritic cell infiltration in COPD tissue specimens was determined using immunohistochemical localization of CD83+ cells (marker of matured myeloid dendritic cells), and CD1a+ cells (Langerhans cells). The extent of tissue infiltration with Langerhans cells was also determined by the relative expression of the CD207 gene in COPD versus control tissues. To determine mechanisms by which dendritic cells accumulate in COPD, complimentary studies were conducted using monocyte-derived human dendritic cells exposed to cigarette smoke extract (CSE), and dendritic cells extracted from mice chronically exposed to cigarette smoke.ResultsIn human COPD lung tissue, we detected a significant increase in the total number of CD83+ cells, and significantly higher amounts of CD207 mRNA when compared with control tissue. Human monocyte-derived dendritic cells exposed to CSE (0.1-2%) exhibited enhanced survival in vitro when compared with control dendritic cells. Murine dendritic cells extracted from mice exposed to cigarette smoke for 4 weeks, also demonstrated enhanced survival compared to dendritic cells extracted from control mice. Acute exposure of human dendritic cells to CSE induced the cellular pro-survival proteins heme-oxygenase-1 (HO-1), and B cell lymphoma leukemia-x(L) (Bcl-xL), predominantly through oxidative stress. Although activated human dendritic cells conditioned with CSE expressed diminished migratory CCR7 expression, their migration towards the CCR7 ligand CCL21 was not impaired.ConclusionsThese data indicate that COPD is associated with increased numbers of cells bearing markers associated with Langerhans cells and mature dendritic cells, and that cigarette smoke promotes survival signals and augments survival of dendritic cells. Although CSE suppressed dendritic cell CCR7 expression, migration towards a CCR7 ligand was not diminished, suggesting that reduced CCR7-dependent migration is unlikely to be an important mechanism for dendritic cell retention in the lungs of smokers with COPD.

Association of MMP-2 polymorphisms with severe and very severe COPD: a case control study of MMPs-1, 9 and 12 in a European population.

BackgroundGenetic factors play a role in chronic obstructive pulmonary disease (COPD) but are poorly understood. A number of candidate genes have been proposed on the basis of the pathogenesis of COPD. These include the matrix metalloproteinase (MMP) genes which play a role in tissue remodelling and fit in with the protease - antiprotease imbalance theory for the cause of COPD. Previous genetic studies of MMPs in COPD have had inadequate coverage of the genes, and have reported conflicting associations of both single nucleotide polymorphisms (SNPs) and SNP haplotypes, plausibly due to under-powered studies.MethodsTo address these issues we genotyped 26 SNPs, providing comprehensive coverage of reported SNP variation, in MMPs- 1, 9 and 12 from 977 COPD patients and 876 non-diseased smokers of European descent and evaluated their association with disease singly and in haplotype combinations. We used logistic regression to adjust for age, gender, centre and smoking history.ResultsHaplotypes of two SNPs in MMP-12 (rs652438 and rs2276109), showed an association with severe/very severe disease, corresponding to GOLD Stages III and IV.ConclusionsThose with the common A-A haplotype for these two SNPs were at greater risk of developing severe/very severe disease (p = 0.0039) while possession of the minor G variants at either SNP locus had a protective effect (adjusted odds ratio of 0.76; 95% CI 0.61 - 0.94). The A-A haplotype was also associated with significantly lower predicted FEV1 (42.62% versus 44.79%; p = 0.0129). This implicates haplotypes of MMP-12 as modifiers of disease severity.

Relationship between Habit of Cigarette Smoking and Airflow Limitation in Healthy Japanese Individuals: The Takahata Study

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation. The prevalence of airflow limitation in Japan is 10.9% (16.4% of males and 5.0% of females). Cigarette smoking is well known as a major cause of COPD. However, few epidemiological studies have evaluated the effects of cigarette smoking on pulmonary function in healthy subjects. Subjects aged 40 years or older (n=2,917), who had participated in a community-based annual health check in Takahata, Japan, from 2004 through 2005, were enrolled in the study. The smoking histories of these subjects were investigated using a self-reported questionnaire. Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV(1)), and forced expiratory flow at 25-75% of FVC (FEF(25-75)) were measured by standard procedures using spirometric machines. There were 554 current smokers (18.6%) and 403 former smokers (13.8%). The prevalence of airflow limitation defined by FEV(1)/FVC <0.7 in this population was 10.6%, and prevalence of airflow limitation defined by 5th percentile lower limit of normal was 6.4%. In smokers, percent predicted values of measured spirometric parameters (%FVC, %FEV(1) and %FEF(25-75)) decreased significantly with age, except for male %FVC. Also, percent predicted values of measured spirometric parameters decreased significantly with increasing pack-years, except for female %FEF(25-75). Cigarette smoking increased the prevalence and severity of airflow limitation. It is concluded that cigarette smoking increases the risk of airflow limitation in a healthy Japanese population.

Primary Prevention of Chronic Obstructive Pulmonary Disease in Primary Care

Chronic obstructive pulmonary disease (COPD) is a prevalent disease, with cigarette smoking being the main risk factor. Prevention is crucial in the fight against COPD. Whereas primary prevention is targeted on whole populations, patient populations are the focus of primary care; therefore, prevention in this setting is mainly aimed at preventing further deterioration of the disease in patients who present with the first signs of disease (secondary prevention). Prevention of COPD in primary care requires detection of COPD at an early stage. An accurate definition of COPD is crucial in this identification process. The benefits of detecting new patients with COPD should be determined before recommending screening and case-finding programs in primary care. No evidence is available that screening by spirometry results in significant health gains. Effective treatment options in patients with mild disease are lacking. Smoking cessation is the cornerstone of COPD prevention. Because cigarette smoking is not only a major cause of COPD but is also a major cause of many other diseases, a decline in tobacco smoking would result in substantial health benefits.

Recent advances in COPD: pathophysiology, respiratory physiology and clinical aspects, including comorbidities

Owing to its major and better recognised burden from both individual and societal perspectives, chronic obstructive pulmonary disease (COPD) is an area of intensive epidemiological, fundamental and clinical research, leading to the publication of more than 10,000 papers each year in the PubMed database. Among these, many report important advances in the understanding of and care for COPD. Epidemiological aspects are the topic of another manuscript in this issue of the European Respiratory Review [1], while the treatment of COPD and its exacerbations will be addressed in other reviews in upcoming issues. Thus, the present paper will focus on more fundamental aspects of pathophysiology, resting and exercise lung mechanics, respiratory muscles and gas exchange, together with more clinical topics, including respiratory symptoms and comorbidities. The purpose of the authors is clearly not to be exhaustive but to focus on points that are likely to have some impact on clinical practice in the relatively short term. Cigarette smoking is the leading cause of COPD in Western countries. Cigarette-associated noxious agents injure the airway epithelium and drive the key processes that lead to specific airway inflammation and structural changes [2]. Once these agents are removed, repair processes should, ideally, bring the airways back to their normal structure and function. In general, an inadequate repair process is thought to play a key role in the development of chronic airflow obstruction in some, but not all, smokers. Indeed, in many subjects most of the inflammatory changes continue despite smoking cessation [3]. This failure of bronchial inflammation to resolve might contribute to systemic changes and ongoing bronchial and lung matrix degradation. In addition to persistent airway inflammation, other major phenomena involved in the disease initiation and progression include increased oxidative stress and protease–antiprotease imbalance. Several studies have established that …

Living with chronic obstructive pulmonary disease: A survey of patients’ knowledge and attitudes

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition and the fourth leading cause of death in Canada. However, little is known about the impact of COPD on the lives and attitudes of individuals living with this condition. The purpose of this study was to determine whether Canadians with COPD are properly educated and supported, and to recommend solutions to any care gaps identified. A total of 389 Canadians were surveyed who were 40 years of age and older, physician diagnosed with COPD, and current or former smokers. The telephone survey contained 68 items and took 35 min to complete. COPD severity was classified according to symptom severity using the Medical Research Council (MRC) score. Respondents tended to overestimate their disease severity and reported substantial symptom burden and psychosocial impact of living with COPD. Most individuals claimed to be well informed about COPD; however, their knowledge was poor in several domains including the causes of COPD, the consequences of inadequate therapy and the management of exacerbations. Family physicians were the main health care providers. A minority of respondents had seen a lung health educator. Only 34% had ever received a written action plan and only 33% had been told how to prevent an exacerbation. The symptom burden and psychosocial impact of living with COPD is substantial. There are significant gaps in patients' knowledge about the management of COPD and little contact with lung health educators. Increased use of COPD-specific, self-management education programs may help rectify these care gaps.

Cigarette smoke decreases MARCO expression in macrophages: Implication in Mycoplasma pneumoniae infection

Bacterial infections including Mycoplasma pneumoniae (Mp) are a major cause of exacerbations in chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is the leading cause of COPD, and affects the function of alveolar macrophages that act as the first line of defense against the invading respiratory pathogens. Macrophages express a transmembrane receptor called macrophage receptor with collagenous structure (MARCO) that is involved in the clearance of microorganisms. Whether CS down-regulates MARCO and eventually decreases the clearance of Mp has not been investigated. We utilized human monocytic cell line (THP-1)-derived macrophages to examine the effects of CS extract (CSE) on MARCO expression and Mp growth. Specifically, macrophages were pre-exposed to CSE for 6 h, and then infected with or without Mp for 2 h. MARCO was examined at both mRNA and protein levels by using real-time PCR and immunofluorescent staining, respectively. Mp in the supernatants was quantified by quantitative culture. In addition, a neutralizing MARCO antibody was added to macrophages to test if blockade of MARCO impaired Mp clearance. We found that CSE significantly decreased MARCO expression in a dose-dependant manner at 6 h post-CSE. Mp levels in CSE-treated cells were higher than those in non-CSE-treated cells, indicating a decreased pathogen clearance. Additionally, neutralizing MARCO in macrophages markedly increased Mp levels. Our results indicate that cigarette smoke exposure down-regulates MARCO expression in macrophages, which may be in part responsible for impaired bacterial (e.g., Mp) clearance.

The effectiveness of smoking cessation groups offered to hospitalised patients with symptoms of exacerbations of chronic obstructive pulmonary disease (COPD)

Chronic obstructive pulmonary disease (COPD) is a major contributor to morbidity and mortality. Smoking is the leading cause of COPD. Results from randomised trials regarding smoking cessation in hospitalised patients with COPD are few. To assess the effect of smoking cessation groups (SCG) in patients with COPD admitted to hospital. Two hundred and twenty-three patients admitted to hospital were assigned to either a control group (n = 102) or an intervention group (n = 121) by matter of vacancy. The smokers in the intervention group were offered participation in an SCG. Smoking status and change in self-reported symptoms were assessed after 1 year. Smoking status was self-reported and verified with carbohemoglobin measurement. Survival and hospital admissions were assessed after 5 years through national registers. Forty-eight patients participated in an SCG. After 1 year, 36 (30%) patients in the intervention group were abstinent compared with 13 (13%) patients in the control group [odds ratio (95% confidence interval): 2.83 (1.40-5.74)]. There was a significant difference between the intervention group and the control group regarding change in self-reported phlegm. There was a non-significant tendency towards better survival in the intervention group (50.4%) compared with the control group (43.1%). After 3 years, the intervention group had a significantly fewer total number of days admitted to hospital and number of days hospitalised with COPD. This study shows that an intervention consisting of offering participation in an SCG to chronic patients makes it possible to obtain higher abstinence rates. Furthermore, this intervention showed impact on phlegm, survival and hospital readmissions.

Prevalence of COPD: First epidemiological study of a large region in Turkey

Background Although chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality and morbidity worldwide, epidemiological data on COPD is very limited. This study was designed to obtain some baseline data on COPD in the Malatya region of Turkey. Methods Sixty clusters from urban and rural regions were randomly selected. Ten and seven consecutive households were included in the study from each urban and rural cluster, respectively. A validated questionnaire on the epidemiology of COPD was completed for each participant over 18 by a pulmonary physician. Each subject underwent standard spirometric measurement and early bronchodilation testing. Results A total of 1160 participants completed the study (93%). Some 6.9% of the participants were found to have COPD (F/M = 1/4). While the prevalence of COPD was 18.1% in current smokers over 40 years of age, the prevalence was 4.5% among younger smokers. Some 25.5% of the women and 57.2% of the men were current smokers. Biomass exposure, as a sole reason for COPD, was significantly common among female patients living in rural areas (54.5%). In the development of COPD, the relative risk ratio of cigarette smoke was found to be 3.4 and 3.3 times higher than biomass exposure and occupational exposure, respectively. Conclusions Smoking rate and COPD prevalence were found to be unexpectedly high in the region, and biomass exposure is still an important cause of COPD, particularly among females living in rural areas. We think that national policies against smoking and biomass exposure should be implemented immediately.

The COPD Italian Lung Information Needs Questionnaire (LINQ): Development, preliminary validation, and findings

Chronic obstructive pulmonary disease (COPD) patients have poor knowledge about the disease. Until now, it has not been possible to check the information needs of these patients. The Lung Information Needs Questionnaire (LINQ), however, could fill this particular need. The aims of this study were to identify patient perceptions about COPD, and what information patients need, and to verify whether the questionnaire is comprehensible. Data demonstrate that LINQ is easily understood: 82% answered all questions with “I have properly understood the question”. LINQ is quick to apply (approx. 6 min to complete). Sixty-seven per cent of patients had incorrect knowledge about their prognosis. Thirty-six per cent did not know when to call an ambulance. Eight per cent of smokers said that no one had ever told them to stop smoking. Compliance with therapy results was not sufficient. Patients had poor knowledge of the causes of COPD, and they knew little about the whys and wherefores of COPD treatment. LINQ represents a valid means of investigating patients afflicted with COPD and managing pathology control by the doctor and by the patient. LINQ represents a fundamental means of investigating otherwise-unknown COPD issues.

Sygnalizacja zależna od histonów w farmakoterapii przewlekłej obturacyjnej choroby płuc

Chronic obstructive pulmonary disease (COPD) is a 4(th) major cause of morbidity and mortality worldwide. Cigarette smoking and oxidative/nitrosative stress leading to chronic inflammation is considered as a major cause of COPD but up to now, details of molecular pathways responsible for development of disease are unknown. Recent reports indicate the role of disruption in histone function in promoting synthesis of inflammatory cytokines through increased gene transcription which underlies disease development. Core histone acetylation/deacetylation regulate their transcription activity and drug induced changes of its intensity may be an interesting field of further research. In this article the opinions about the role of steroids as inhibitors of the inflammatory process as well as resistance to steroids have been presented. Findings from studies which aimed to explore the anti-inflammatory activity of drugs such as theophylline and N-acetylcysteine and their ability to suppress oxidative stress may suggest the usefulness of these drugs in causative treatment of COPD. However, further studies are necessary to confirm these findings.

An exploration of the smoking‐related health beliefs of older people with chronic obstructive pulmonary disease

To explore the smoking-related health beliefs of older people with chronic obstructive pulmonary disease (COPD). Globally, smoking is a major cause of COPD and symptoms present typically mid to later life. Substantial numbers of people with COPD continue to smoke even though smoking cessation is known to slow the rate of disease progression and prevent further deterioration in lung function. There is evidence to suggest that, although older long-term smokers can successfully quit smoking with the help of specialist structured programmes, those with COPD find it more difficult to achieve sustained cessation. An understanding of the health beliefs of people with COPD will assist professionals to provide the most appropriate support with cessation attempts. A secondary analysis of qualitative interview data. Twenty-two current and former smokers with COPD who used the outreach service of an inner city hospital in Scotland were interviewed in their own homes using semi-structured interviews which were transcribed verbatim. The main concepts of the Health Belief Model were used as an analysis framework. Interviews were carried out with 15 women and seven men with a median age of 68 years. Almost 90% lived in areas of the highest socio-economic deprivation according to DEPCAT scores. Almost two-thirds of the individuals in this study continued to smoke even though they largely perceived smoking as a threat to health. Individuals who continued to smoke cited various barriers to quitting smoking and all had, at some time, attempted smoking cessation. Over half were still attempting to quit. Cues to action came from external sources rather than increasing disease severity. Cessation is challenging and knowledge of a person's health beliefs is a prerequisite to supporting behaviour change. Findings emphasize the need for frontline health professionals to reflect on their current practice with a view to providing sustained encouragement and support towards smoking cessation and relapse prevention for people with COPD.

Preventing Chronic Obstructive Pulmonary Disease: What Is Known and What Needs to Be Done to Make a Difference to the Patient?

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable systemic disease with symptoms that overlap other respiratory illnesses. An estimated 24 million adults in the United States have COPD, but >50% of them are misdiagnosed or undiagnosed. Spirometry remains the “gold standard” for diagnosing COPD and for monitoring the progression of the disease. Cigarette smoking is the main cause of COPD; therefore, smoking cessation is an integral component of any program to reduce COPD risk and delay or limit the progression of airflow obstruction. Influenza vaccinations will also reduce acute respiratory illness in patients with COPD. With increasing awareness of COPD and earlier diagnosis, implementation of treatment guidelines and smoking-cessation efforts may lead to more effective management of this disease, which is projected to be the third leading cause of death in the United States by 2020.

Aspects on pathophysiological mechanisms in COPD

Chronic obstructive pulmonary disease (COPD) is a condition which is characterized by irreversible airway obstruction due to narrowing of small airways, bronchiolitis, and destruction of the lung parenchyma, emphysema. It is the fourth most common cause of mortality in the world and is expected to be the third most common cause of death by 2020. The main cause of COPD is smoking but other exposures may be of importance. Exposure leads to airway inflammation in which a variety of cells are involved. Besides neutrophil granulocytes, macrophages and lymphocytes, airway epithelial cells are also of particular importance in the inflammatory process and in the development of emphysema. Cell trafficking orchestrated by chemokines and other chamoattractants, the proteinase-antiproteinase system, oxidative stress and airway remodelling are central processes associated with the development of COPD. Recently systemic effects of COPD have attracted attention and the importance of systemic inflammation has been recognized. This seems to have direct therapeutic implications as treatment with inhaled glucocorticosteroids has been shown to influence mortality. The increasing body of knowledge regarding the inflammatory mechanism in COPD will most likely have implications for future therapy and new drugs, specifically aimed at interaction with the inflammatory processes, are currently being developed.

Smoking and COPD: what really are the risks?

To the Editors: Chronic obstructive pulmonary disease (COPD) is rapidly becoming a global public health crisis, with around three million people predicted to die from the disease in 2006 1, 2. There is growing awareness of the increasing global burden of COPD not only in terms of mortality, but also its prevalence, morbidity and economic costs 2. In response to these concerns, there has been a renewed research effort to understand the causes of COPD and to develop public health and pharmacological interventions that may reduce the burden. Smoking is recognised as the most important causative factor for COPD, with an individual's susceptibility being a continuous, rather than a categorical characteristic that can interact synergistically with other risk factors. There is now evidence that most smokers develop some respiratory impairment due to COPD 3. One of the most informative recent studies addressing this …

Chronic obstructive pulmonary disease: clinical signs and infections

Chronic obstructive pulmonary disease (COPD) is a pathological condition that involves excessive production of mucus, chronic cough and inflammatory changes leading to airway limitation. The most common cause of COPD is cigarette smoking. COPD can be categorized into either chronic bronchitis or emphysema; both conditions can be differentiated by age and the production of copious, tenacious sputum. Patients with COPD are susceptible to pulmonary infections of bacterial or viral origin. Nurses should be aware of the subtle differences in conditions and the usefulness of antibiotics in the treatment of acute bacterial exacerbations of chronic bronchitis.