Chronic obstructive pulmonary disease

doi:10.1016/S0140-6736(17)31222-9

The Lancet

Volume 389, Issue 10082, 13–19 May 2017, Pages 1931-1940

https://doi.org/10.1016/S0140-6736(17)31222-9 Get rights and content

Summary

Chronic obstructive pulmonary disease (COPD) kills more than 3 million people worldwide every year. Despite progress in the treatment of symptoms and prevention of acute exacerbations, few advances have been made to ameliorate disease progression or affect mortality. A better understanding of the complex disease mechanisms resulting in COPD is needed. Smoking cessation programmes, increasing physical activity, and early detection and treatment of comorbidities are further key components to reduce the burden of the disease. However, without a global political and economic effort to reduce tobacco use, to regulate environmental exposure, and to find alternatives to the massive use of biomass fuel, COPD will remain a major health-care problem for decades to come.

Introduction

Chronic obstructive pulmonary disease (COPD) is common worldwide and causes a major health-care burden. Although COPD generally manifests at an older age as part of multimorbidity, there is increasing evidence that events early in life contribute to impaired lung function in adults,¹ which suggests that risk factors other than those already known (inhaled particles and gases from cigarette smoking and biomass fuel) are important in the disease's aetiology.

The term COPD might be too general, since the airway abnormalities of chronic bronchitis and the peripheral loss of parenchymal lung texture in emphysema are probably caused by diverse cellular and pathophysiological changes with distinct genetic backgrounds. Advances in lung imaging enable a more detailed view of airway and lung parenchyma abnormalities and novel endoscopic interventions play an increasing role in the management of advanced emphysema. No drug treatment specifically targets emphysema except for the augmentation of α1 antitrypsin in patients with emphysema associated with α1 antitrypsin deficiency.² Although the results of large clinical trials support a shift from anti-inflammatory treatment with inhaled corticosteroids towards dual bronchodilator treatment for airway pathology,³ further prospective studies will help to clarify the role of inhaled corticosteroid treatment in combination with dual bronchodilator therapy in the prevention of exacerbations.⁴ By contrast with asthma, there is little hope that COPD-specific biological therapies can be developed.

Section snippets

Epidemiology and causes

The global prevalence of COPD is difficult to estimate because of the different approaches used to calculate prevalence (eg, spirometry-confirmed airflow limitation or surveys).⁵ The Global Burden of Disease Study 2015 estimated the global prevalence of COPD at about 174 million cases.⁶ In 2010, Adeloye and colleagues⁷ estimated a global prevalence of 384 million cases on the basis of spirometric criteria of fixed airflow limitation applied in several epidemiological cohorts. In Canada, the

Pathophysiology

Clinical treatment guidelines issued by global professional societies tend to oversimplify the definition of COPD, which in fact is a heterogeneous and complex disease.²⁴ Furthermore, most (if not all) knowledge about the pathophysiology of the disease is derived from studies of former or current tobacco smokers. However, COPD caused by biomass fuel exposure, for example, might be substantially different from COPD caused by tobacco smoking in terms of phenotype, comorbidities, and progression

COPD and comorbidities

Patients with COPD are often affected by other diseases, such as cardiovascular disease, osteoporosis, muscle weakness, depression, and lung cancer.50, 51, 52 Smoking is a risk factor for comorbidities; others probably include physical inactivity and yet-to-be-identified inflammatory mechanisms (figure 2).50, 51, 53, 54 Several pulmonary mechanisms of inflammation and oxidative stress that damage DNA and result in an imbalance between tissue repair and cell proliferation seem to promote the

Smoking cessation

Smoking cessation is key to reducing progressive decline in lung function over time, as well as exacerbations and smoking-related comorbidities (lung cancer and cardiovascular disease), which decreases mortality in patients with COPD.15, 69, 70 Reducing indoor air pollution by using a stove instead of cooking on an open fire reduces progressive lung function decline in a manner similar to that of smoking cessation.⁷¹ Patients with COPD who have a high degree of tobacco dependence, and who have

Conclusions and future directions

Globally, COPD will remain a significant public health problem for the foreseeable future. With risk factors largely unchanged, demographic developments in high-income countries and a significant increase in non-communicable diseases in low-income countries will accelerate this health burden. A better genetic molecular and biological understanding of this disease in its distinct endotypes and phenotypes is needed to enable innovative drug development.

Search strategy and selection criteria

We searched Medline and online publications on COPD and tobacco use worldwide (eg, WHO) using the terms COPD, emphysema, tobacco use, epidemiology, cause, emphysema, comorbidities, lung cancer, treatment, pulmonary rehabilitation, physical activity, and exacerbation. We focused on recent publications in English up to 2016 that might be of interest for a general readership.

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