Chronic obstructive pulmonary disease (COPD) is characterized by a decline in lung function which is more rapid than that observed with age. In most patients, COPD is due to smoking and non-smoking (pollutants, such as noxious gases and irritants) exposures.
COPD is the fourth leading cause of death and the main cause of morbidity and mortality for chronic disease globally. Due to persistent risk factors, including cigarette smoking and air pollution, and aging of the population, the COPD burden is increasing.
In patients with COPD, pharmacological treatment, which is mostly based on long-acting ?2-adrenoreceptor agonist (LABA) and long-acting muscarinic receptor antagonist (LAMA) bronchodilators and inhaled corticosteroids (ICS) as well as anti-inflammatories, such as phosphodiesterase 4 inhibitor (PDE4 inhibitor), improves clinical and functional outcomes, including symptoms, decline in lung function, frequency of exacerbations, quality of life and exercise tolerance. However, two large prospective randomised clinical trials with ICS/LABA fixed dose combinations (TORCH and SUMMIT) have shown no effect on survival as primary outcome in patients with COPD.
Among new therapeutic options, single inhaler triple therapy for COPD will shortly be available. Two 52-week phase III trials with different triple ICS/LABA/LAMA fixed dose combinations (IMPACT and TRIBUTE) versus dual bronchodilator therapies met the primary outcome represented by the annual rate of COPD exacerbations.
Identifying new, non-invasive, “mechanistic” methods and techniques for COPD assessing and phenotyping, and developing drugs that reduce mortality are priorities in this research area.
COPD is a heterogeneous disease. Clinical phenotypes, including frequent exacerbators or asthma-COPD overlap (ACO), have been identified. Some studies suggest the utility of clinical phenotyping in terms of COPD prognosis or response to pharmacological treatment, but more large prospective studies are required to clarify the implications of this approach for management of patients with COPD.
The importance of COPD phenotyping is also reflected by implementation of more selective strategies in COPD clinical trials as shown by therapies targeting interleukin-5, including mepolizumab and benralizumab, which are in phase III for eosinophilic COPD. In two 52-week phase III trials (METREX and METREO), mepolizumab reduced the annual rate of exacerbations in COPD patients with the eosinophilic phenotype who had a history of moderate or severe exacerbations while taking inhaled glucocorticoid-based triple maintenance therapy.
At present, using the same drug(s) for treating the same phenotype/endotype in different diseases within the same therapeutic area (e.g., mepolizumab and benralizumab in severe asthma and COPD) or even in different therapeutic areas (e.g., an oral selective glucocorticoid receptor modulator in rheumatoid arthritis and respiratory tract disorders) seems to be a feasible strategy in drug development.
Omics technologies provide a powerful tool for exploring the pathophysiology, molecular phenotyping, and identifying new approaches to assessment of respiratory inflammation and drug response in patients with COPD. The latter is currently based on clinical and functional outcomes which are not sufficiently sensitive and do not reflect the mechanisms of action of some classes of drugs for COPD, e.g. anti-inflammatory or anti-oxidant treatment. Omics are potentially useful for identifying biomarkers which, once validated, might improve drug assessment in clinical trials, or identifying new therapeutic targets for development of drugs for COPD.
This Research Topic focuses on current and future trends in assessment, phenotyping and pharmacotherapy of COPD including its co-morbidities. This will also include biomarkers of therapy in assessing the therapeutic efficacy of pharmacotherapy in COPD phenotype/endotype.
The Editors will be willing to consider unsolicited original research or review articles relevant to these topics.
Chronic obstructive pulmonary disease (COPD) is characterized by a decline in lung function which is more rapid than that observed with age. In most patients, COPD is due to smoking and non-smoking (pollutants, such as noxious gases and irritants) exposures.
COPD is the fourth leading cause of death and the main cause of morbidity and mortality for chronic disease globally. Due to persistent risk factors, including cigarette smoking and air pollution, and aging of the population, the COPD burden is increasing.
In patients with COPD, pharmacological treatment, which is mostly based on long-acting ?2-adrenoreceptor agonist (LABA) and long-acting muscarinic receptor antagonist (LAMA) bronchodilators and inhaled corticosteroids (ICS) as well as anti-inflammatories, such as phosphodiesterase 4 inhibitor (PDE4 inhibitor), improves clinical and functional outcomes, including symptoms, decline in lung function, frequency of exacerbations, quality of life and exercise tolerance. However, two large prospective randomised clinical trials with ICS/LABA fixed dose combinations (TORCH and SUMMIT) have shown no effect on survival as primary outcome in patients with COPD.
Among new therapeutic options, single inhaler triple therapy for COPD will shortly be available. Two 52-week phase III trials with different triple ICS/LABA/LAMA fixed dose combinations (IMPACT and TRIBUTE) versus dual bronchodilator therapies met the primary outcome represented by the annual rate of COPD exacerbations.
Identifying new, non-invasive, “mechanistic” methods and techniques for COPD assessing and phenotyping, and developing drugs that reduce mortality are priorities in this research area.
COPD is a heterogeneous disease. Clinical phenotypes, including frequent exacerbators or asthma-COPD overlap (ACO), have been identified. Some studies suggest the utility of clinical phenotyping in terms of COPD prognosis or response to pharmacological treatment, but more large prospective studies are required to clarify the implications of this approach for management of patients with COPD.
The importance of COPD phenotyping is also reflected by implementation of more selective strategies in COPD clinical trials as shown by therapies targeting interleukin-5, including mepolizumab and benralizumab, which are in phase III for eosinophilic COPD. In two 52-week phase III trials (METREX and METREO), mepolizumab reduced the annual rate of exacerbations in COPD patients with the eosinophilic phenotype who had a history of moderate or severe exacerbations while taking inhaled glucocorticoid-based triple maintenance therapy.
At present, using the same drug(s) for treating the same phenotype/endotype in different diseases within the same therapeutic area (e.g., mepolizumab and benralizumab in severe asthma and COPD) or even in different therapeutic areas (e.g., an oral selective glucocorticoid receptor modulator in rheumatoid arthritis and respiratory tract disorders) seems to be a feasible strategy in drug development.
Omics technologies provide a powerful tool for exploring the pathophysiology, molecular phenotyping, and identifying new approaches to assessment of respiratory inflammation and drug response in patients with COPD. The latter is currently based on clinical and functional outcomes which are not sufficiently sensitive and do not reflect the mechanisms of action of some classes of drugs for COPD, e.g. anti-inflammatory or anti-oxidant treatment. Omics are potentially useful for identifying biomarkers which, once validated, might improve drug assessment in clinical trials, or identifying new therapeutic targets for development of drugs for COPD.
This Research Topic focuses on current and future trends in assessment, phenotyping and pharmacotherapy of COPD including its co-morbidities. This will also include biomarkers of therapy in assessing the therapeutic efficacy of pharmacotherapy in COPD phenotype/endotype.
The Editors will be willing to consider unsolicited original research or review articles relevant to these topics.
