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Exercise testing in chronic lung disease
Published in R. C. Richard Davison, Paul M. Smith, James Hopker, Michael J. Price, Florentina Hettinga, Garry Tew, Lindsay Bottoms, Sport and Exercise Physiology Testing Guidelines: Volume II – Exercise and Clinical Testing, 2022
Oliver J. Price, Karl Sylvester, Joanna Shakespeare, Mark A. Faghy
Lung disease affects one in five people and is a leading cause of morbidity and mortality in the UK (Taskforce for Lung Health, 2018). Broadly, lung diseases can be classified into obstructive (e.g., asthma and chronic obstructive pulmonary disease [COPD]) or restrictive disorders (e.g., interstitial lung disease [ILD]). In reality, however, patients often present with comorbidities such as asthma/COPD overlap syndrome (ACOS) and/or cardiovascular disease. Specifically, obstructive lung disease is typically characterised by a reduction in forced expiratory volume in one second (FEV1) to forced vital capacity (FVC) ratio (FEV1 / FVC) but with normal relaxed vital capacity (VC). In severe obstructive lung diseases, increases in measured residual volume (RV) are evident, as a consequence of early airway closure and gas trapping and an increase in functional residual capacity (FRC) due to dynamic hyperinflation. In contrast, restrictive lung disease is characterised by a reduction in lung volume, either due to a reduction in the ability of the lungs to expand (e.g., ILD) or the inability to generate the force required to allow sufficient lung expansion (e.g., respiratory muscle weakness) (see Maynard et al. [2020], West and Luks [2015] and Association for Respiratory Technology and Physiology [ARTP] [2020a] for a detailed overview of respiratory physiology and lung function assessment).
Pathophysiology of asthma
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
The association of asthma and COPD features in a single patient has been recognized for a long time, but interest about this condition called Asthma–COPD Overlap has increased recently with the reports of an increased morbidity associated with this condition. The 2017 GINA report stresses that: “ACO is not a single disease or phenotype and mentions that ACO is characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. Asthma–COPD overlap is therefore identified in clinical practice by the features that it shares with both asthma and COPD. This is not a definition, but a description for clinical use, as asthma–COPD overlap includes several different clinical phenotypes and there are likely to be several different underlying mechanisms.” The pathophysiology of ACO has not been well studied up to now but recent reports suggest various mechanisms potentially involved [65, 66].
Bronchus-associated lymphoid tissue and immune-mediated respiratory diseases
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Dale T. Umetsu, Bart Lambrecht
Asthma and chronic obstructive pulmonary disease (COPD) are two major chronic inflammatory diseases of the lung. Asthma is a major public health problem, affecting 300 million persons worldwide, and has increased markedly in prevalence in Westernized countries over the past three decades. Asthma is a complex trait caused by multiple environmental factors in combination with more than 100 major and minor susceptibility genes. Asthma is characterized by reversible obstruction of the airways, with symptoms of shortness of breath, coughing, wheezing, and chest tightness, and is a major cause of emergency room visits, hospitalization, and school absences. The estimated health-related annual costs for asthma amount to $80 billion in the United States alone. COPD is also a major public health problem; worldwide it is the fourth leading cause of death (shared with human immunodeficiency virus/acquired immunodeficiency syndrome). Both asthma and COPD are characterized by airway obstruction, which in asthma is variable and reversible, but in COPD is progressive and irreversible, and associated with symptoms of shortness of breath, which is progressive, and sputum overproduction. Both chronic diseases are characterized by acute exacerbations, with a great increase in symptoms and inflammation; these exacerbations are frequently caused by infections or air pollution. In addition, the medications for these two diseases overlap, and patients with long-standing asthma may evolve into a picture that mimics COPD, particularly when there is a history of smoking in asthmatics. Although many differences exist between asthma and COPD, the similarities between asthma and COPD suggest that asthma and COPD may be the ends of a single spectrum of inflammatory lung diseases modulated by environmental and genetic factors (the Dutch hypothesis, more recently called Asthma COPD Overlap Syndrome [ACOS]). An alternative hypothesis (the British hypothesis), suggests that asthma and COPD are fundamentally different diseases, with asthma caused by allergy and COPD by cigarette smoking.
Efficacy and safety of add-on tiotropium in the management of uncontrolled asthma: a patient case series
Published in Journal of Asthma, 2022
Giselle Mosnaim, md, Brian K. Bizik, md, Christy Wilson, pa-c, Gregory Bensch, pa-c
The degree of obstruction is measured by a positive bronchodilator response, which is defined as an increase of ≥12% and ≥200 ml in FEV1 or FVC from baseline (26). Our final case report of a 29-year-old female patient had a post-bronchodilator change in FEV1 of 7% at presentation and indicated a patient subtype with fixed obstructive asthma. Such patients have severe airway obstruction (27), indicated by an FEV1/FVC ratio of <0.7 and no change in postbronchodilator FEV1% (1). These patients may exhibit characteristics of an asthma-COPD overlap. Given the efficacy of tiotropium in COPD, tiotropium could be an effective add-on therapy in this subset of patients (28). It is important to note that tiotropium bromide when administered for the treatment of COPD in 5 µg (2 puffs of 2.5 µg per puff, once daily (6)) differs from the dosage approved for asthma (2.5 µg; 2 puffs of 1.25 µg per puff, once daily (6)). Moreover, tiotropium has not specifically been studied in a randomized controlled trial for patients with asthma and COPD overlap (ACO).
Updated simplified approach of pharmacological treatment of stable COPD: Do common co-morbidities have a role?
Published in Postgraduate Medicine, 2021
Georgios Hillas, Anastasia Papaporfyriou, Katerina Dimakou, Andriana I. Papaioannou
In our previously published simplified therapeutic algorithm, we have proposed to emphasize to the main aspects of COPD and to use long-acting bronchodilators as the cornerstone of COPD treatment. We have recognized that a small percentage of COPD patients would benefit from single long acting bronchodilators, named anticholinergics. However, the grand majority will continue to experience symptoms and/or exacerbations requiring dual bronchodilator treatment. Inhaled corticosteroids (ICS) as an add-on treatment was recommended in the specific groups of patients: a) patients with Asthma COPD overlap, b) patients with blood eosinophils ≥2% and ≥150–200 cells/μL and a history of exacerbations, c) patients with frequent exacerbations (≥2 per year, ≥1 leading to hospital admission) despite treatment with LAMA/LABA, and finally d) symptomatic patients with FEV1 < 50% predicted and ≥1 moderate/severe exacerbation in the previous year.
Prevalence of COPD among workers with work-related asthma
Published in Journal of Asthma, 2020
Katelynn E. Dodd, Jacek M. Mazurek
An estimated 52% (1.1 million) of adults with WRA had a physician diagnosis of COPD, which is higher than that reported by Ojanguren et al. among persons with occupational asthma (28). In their study, the authors found that 13.8% of 304 subjects with occupational asthma had asthma-COPD overlap. However, Ojanguren et al. assessed asthma-COPD overlap only among those who had smoked ≥10 pack-years. Research has shown that nonsmokers can develop COPD and patients with asthma may develop features of COPD (29,30). Accelerated decline in lung function and fixed air-flow obstruction may be a result of recurrent exacerbations characteristic of WRA, and may explain the elevated proportion of COPD found among adults with WRA in this study (17). The pathology of this disease progression is unknown, however (31).