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Asthma and COPD
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Balamugesh Thangakunam, Devasahayam J Christopher
The ‘Dutch hypothesis’ suggested that both asthma and COPD have common genetic origins with environmental factors playing a role in pathogenesis and clinical manifestation (Orie et al. 1961). In asthmatics many Single Nucleotide Polymophisms (SNPs) have been described in genes encoding Th2 cytokines like IL-4, IL-13 and their receptors (Barnes 2006). These are not associated with COPD. In COPD SNPs in genes are responsible for encoding various proteases, antiproteases and antioxidants. The classical genetic predisposition for COPD; alpa-1 antitrypsin deficiency is not associated with atopy or asthma. However, although most SNPs are different in asthma and COPD, there are some that are common to both like the polymorphisms in the promoter region of tumor necrosis factor-alpha (Sakao et al. 2001, Gao et al. 2006). Some novel asthma genes, like ADAM33 and DPP 10, have been associated with COPD as well as asthma (Holgate 2010, van Diemen et al. 2005, Arinir et al. 2004).
Viral-Induced Asthma and Chronic Obstructive Pulmonary Disease
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
It is of interest that experimental studies on viral infection-induced development of disease-like lung features, involving innate immune responses, genetic factors, and environmental exposures have implied roles in onset of both asthma and COPD.25–27 Orie and coworkers originally hypothesized a common origin of asthma and COPD several decades ago, the “Dutch hypothesis” (reviewed in Reference 28). This hypothesis is now frequently revisited.
Therapeutic targets for inflammation-mediated airway remodeling in chronic lung disease
Published in Expert Review of Respiratory Medicine, 2018
Although distinct in their etiology, both AA and COPD share components of airway inflammation, structural remodeling and their disease course punctuated by intermittent exacerbations [6]. The presence of overlapping pathophysiologies and causes of exacerbations has led to a reexamination of the whether both diseases share common origins but are expressed differently through individual variation, a concept known as the ‘Dutch’ hypothesis [7]. Approximately, 15–20% of patients with COPD have features of airway reversibility and eosinophilia. Conversely, a subset of asthmatics develop a fixed airway obstruction. These common features have led to the acceptance of the asthma-COPD overlap syndrome as a distinct disease entity [8]. Although COPD intervention has focused on reducing environmental smoke exposure, large-scale prospective observational studies have identified a potential role of early viral encounters in reduced pulmonary capacity later in life [7]. Irrespective of their etiologies, obstructive lung diseases share common triggers, inflammatory responses and some features of remodeling [9], whose mechanism will be examined in this review.
Comparative safety and effectiveness of inhaled bronchodilators and corticosteroids for treating asthma–COPD overlap: a systematic review and meta-analysis
Published in Journal of Asthma, 2021
Joseph Emil Amegadzie, Jessica Gorgui, Lily Acheampong, John-Michael Gamble, Jamie Farrell, Zhiwei Gao
The notion that asthma and COPD share a common etiology has been discussed and debated since 1961 when Orie and Sluiter proposed the “Dutch hypothesis” (1). The controversy continues today as clinicians assess and treat patients with symptoms of both asthma and COPD. This phenotype of obstructive airway diseases is known as asthma–COPD overlap (ACO). ACO was recently described in 2015 by both The Global Initiative for Asthma (GINA) and Global Initiative for Chronic Obstructive Lung Disease (GOLD) as “persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD”. The GINA guideline also reported that ACO includes different clinical phenotypes with several underlying mechanisms (2,3).