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This study examined the rate of exacerbations among patients with COPD over a period of 3 years. The strongest predictor of an exacerbation in a given year was the presence of an exacerbation in the previous year. The natural history of chronic obstructive pulmonary disease (COPD) is punctuated by exacerbations — acute worsening of symptoms. Exacerbations appear to accelerate the decline in lung function that characterizes COPD, 1 , 2 resulting in reduced physical activity, 3 poorer quality of life, 4 and an increased risk of death, 5 and they are also responsible for a large proportion of the health care costs attributable to this prevalent condition. 6 Consequently, exacerbations are important outcomes in clinical trials, and their prevention is a key component of COPD-management strategies. 7 Despite the importance of exacerbations, we know relatively little about their incidence, their determinants, and their effects . . .

Summary Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow obstruction that is only partly reversible, inflammation in the airways, and systemic effects or comorbities. The main cause is smoking tobacco, but other factors have been identified. Several pathobiological processes interact on a complex background of genetic determinants, lung growth, and environmental stimuli. The disease is further aggravated by exacerbations, particularly in patients with severe disease, up to 78% of which are due to bacterial infections, viral infections, or both. Comorbidities include ischaemic heart disease, diabetes, and lung cancer. Bronchodilators constitute the mainstay of treatment: β2 agonists and long-acting anticholinergic agents are frequently used (the former often with inhaled corticosteroids). Besides improving symptoms, these treatments are also thought to lead to some degree of disease modification. Future research should be directed towards the development of agents that notably affect the course of disease.

More recent studies demonstrate that symptoms are associated with excess exacerbations and radiographic abnormalities (10, 11, 14). [...]features inadequately captured by spirometric airflow limitation are now recognized as independent clinical manifestations of COPD-related disease (15). An 8- to 10-pack-year smoking history has been linked to lung function decline in subjects aged 35 to 53 years (29). [...]contemporary studies confirm that \"chronic bronchitis\" or \"chronic mucus hypersecretion\" predict future COPD incidence (30), especially among younger adults (4). [...]matrix destruction might also cause airway dropout via anoikis, leading to the epithelial apoptosis observed by multiple groups in established disease but unstudied in early COPD. [...]rather than globally suppressing inflammatory cell function, future therapies to arrest early COPD might focus on containing the microbial invasion that drives inflammation.

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity, mortality, and health-care use worldwide. COPD is caused by exposure to inhaled noxious particles, notably tobacco smoke and pollutants. However, the broad range of factors that increase the risk of development and progression of COPD throughout the life course are increasingly being recognised. Innovations in omics and imaging techniques have provided greater insight into disease pathobiology, which might result in advances in COPD prevention, diagnosis, and treatment. Although few novel treatments have been approved for COPD in the past 5 years, advances have been made in targeting existing therapies to specific subpopulations using new biomarker-based strategies. Additionally, COVID-19 has undeniably affected individuals with COPD, who are not only at higher risk for severe disease manifestations than healthy individuals but also negatively affected by interruptions in health-care delivery and social isolation. This Seminar reviews COPD with an emphasis on recent advances in epidemiology, pathophysiology, imaging, diagnosis, and treatment.

A pair of review articles examines our current understanding of the biology, diagnosis, and treatment of chronic obstructive pulmonary disease. This article focuses on the clinical aspects of COPD.

In this trial, long-term supplemental oxygen treatment did not result in longer survival than no use of supplemental oxygen among patients with stable COPD and moderate resting desaturation (Spo2, 89 to 93%) or moderate exercise-induced desaturation. Two trials that were conducted in the 1970s showed that long-term treatment with supplemental oxygen reduced mortality among patients with chronic obstructive pulmonary disease (COPD) and severe resting hypoxemia. 1 , 2 These results led to the recommendation that supplemental oxygen be administered to patients with an oxyhemoglobin saturation, as measured by pulse oximetry (Spo 2 ), of less than 89%. 3 , 4 In the 1990s, two trials evaluated long-term treatment with supplemental oxygen in patients with COPD who had mild-to-moderate daytime hypoxemia; neither trial showed a mortality benefit, but both were underpowered to assess mortality. 5 , 6 The effects of oxygen treatment on . . .

Patients with COPD have increased peripheral airway resistance. In this study, increased peripheral airway resistance was strongly associated with a reduction in the number of terminal bronchioles rather than narrowing of airways. Direct measurement of the distribution of resistance in the lower respiratory tract has established that small airways (i.e., <2 mm in internal diameter) become the major sites of obstruction in patients with chronic obstructive pulmonary disease (COPD). 1 – 3 Resistance to flow through tubes is inversely related to the reduction in the radius raised to the fourth to fifth power. Since loss of half of such airways will only double the total peripheral resistance because of their parallel arrangement, 4 the increase in peripheral airway resistance by a factor of 4 to 40, as has been reported in patients with COPD, 1 is . . .

It had been thought that most people with chronic obstructive pulmonary disease had normal lung function in mid-adult life and then lost it rapidly. In this study, many people with COPD already had low lung function in mid-adult life, before COPD developed. Chronic obstructive pulmonary disease (COPD) is a major cause of illness and death worldwide. 1 Since the research by Fletcher and colleagues in the 1970s, 2 , 3 the prevailing paradigm of COPD pathogenesis has been that, in susceptible persons, exposure to particulate matter — especially tobacco smoke — leads to clinical disease through acceleration of the age-related decline in lung function, as assessed by the forced expiratory volume in 1 second (FEV 1 ). Subsequent population studies supported this paradigm and led to therapeutic trials aimed at reducing the rapid decline in FEV 1 . 4 – 11 Surprisingly, the observed declines in FEV . . .

Chronic obstructive pulmonary disease diagnosis rests on chronic pulmonary symptoms and airflow obstruction. This study showed that people may have chronic COPD symptoms but no airflow obstruction. Such patients have more COPD exacerbations than those without chronic symptoms. Among the criteria that are needed to make a diagnosis of chronic obstructive pulmonary disease (COPD) are deficits in the rate at which one can forcefully exhale. Most experts consider a low ratio (<0.70) of the forced expiratory volume in 1 second (FEV 1 ) to the forced vital capacity (FVC) after bronchodilator use to be a key diagnostic criterion. 1 Once the diagnosis of COPD has been established, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) nomenclature grades severity according to the degree to which the measured FEV 1 is lower than the patient’s predicted value. GOLD stage 1, . . .

Global Strategy for the Diagnosis, Management, and Prevention of COPD 2018 is a consensus report published periodically since 2001 by an international panel of health professionals from respiratory medicine, socioeconomics, public health, and education comprising the Global Initiative for Chronic Obstructive Lung Disease (GOLD). The GOLD documents endeavor to incorporate latest evidence and expert consensus and are intended for use as “strategy documents” for implementation of effective care for chronic obstructive lung disease (COPD) on a global level. The GOLD 2018 report defines COPD as a “common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases,” with the criteria of “persistent respiratory symptoms” being a new and controversial inclusion since 2017. With the availability of newer pharmacotherapy options, treatment recommendations are made on the basis of a review of the latest literature and directed by symptom burden and health care utilization. Apart from the change in definition, a major shift in the recommendations is the exclusion of severity of airflow limitation as one of the major factors in guiding therapy. We review the salient features of the GOLD 2018 document and provide commentary on features that merit further discussion based on our clinical experience and practice as well as literature review current as of February 2018.