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Chronic Respiratory Disease: History
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Please note this is an old version of this entry, which may differ significantly from the current revision.
Subjects: Respiratory System
Contributor: Yong Qin Lee

Chronic respiratory diseases are major contributors to the global burden of disease. Chronic respiratory diseases are pathologies of the airways and respiratory tract, for example, asthma, chronic obstructive pulmonary disease (COPD), and bronchiectasis.

  • treatable trait
  • chronic respiratory disease
  • asthma
  • COPD
  • bronchiectasis
  • individualised therapy

1. Introduction

While these approaches are largely effective in chronic-disease control, it is recognised that patients with heterogenous diseases consisting of multiple phenotypes, like asthma, do not respond equally to the same type of treatment and have differing risks of exacerbation and prognosis [1]. Hence, a relatively recent treatment strategy proposed to tackle these limitations is a “treatable traits” approach.
The “treatable traits” approach involves treating specific traits possessed by patients, defined by specific trait markers, which are subsequently targeted by specific therapies. This differs from the current broad, stepwise treatment of the disease entity, such as the Global Initiative for Asthma guidelines, which has been shown to be limited in its ability to predict exacerbations when used by itself [1]. Multidimensional assessment incorporating treatable traits has the potential to improve care and provide more individualised therapy, allowing management principles to be tailored to each patient’s characteristics or traits [2].

2. Treatable Traits in Chronic Respiratory Disease

2.1. Physiological Traits

For physiological treatable traits (Table 1), these were studied mostly in the setting of asthma, COPD, and bronchiectasis. These studies described traits including airflow limitation, hypoxemia/hypercapnia, lung hyperinflation, and ciliary dysfunction.
Table 1. Overview of physiological treatable traits.
Condition Treatable Trait Trait-Identification Marker Average Prevalence Treatment Description and Benefits Prognostic Implications Author (Year)
Asthma Airway limitation Post-bronchodilator FEV1/FVC < 0.7
FEV1 < 80% predicted		 52.5% (45.5–54.5%) LAMA: ↑ Lung function, exacerbations
Bronchial Thermoplasty: ↑ control, ↑ QoL, ↓ exacerbations
SABA
Short-acting anticholinergics: ↓ risk of admission
Magnesium: ↓ odds of admission		 Patients with poor PEFR response to salbutamol:
↑ airway obstruction, symptom duration and healthcare utilisation
↑ exacerbation risk		 Hiles (2020) [3]
Cazzola (2020) [4]
Connolly (2018) [5]
Simpson (2018) [6]
Papaioannou (2018) [7]
Hinks (2020) [8]
Martin (2020) [1]
McDonald (2019) [9]
Asthma Hypoxemia/hypercapnia SpO2 < 90% at rest or during 6 min walk test 10.9% Investigation and implementation of domiciliary oxygen therapy and nasal CPAP - Hiles (2020) [3]
Asthma Lung hyperinflation >10% reduction in in inspiratory capacity - Systemic Corticosteroids: ↓ of dynamic hyperinflation Dynamic hyperinflation ↑ in placebo group Meer (2019) [10]
Bronchiectasis Airway limitation Low nasal NO, electron microscopic abnormalities, abnormal ciliary beating pattern - Inhaled saline, airway clearance, ongoing trial of ENaC inhibition - Shteinberg (2020) [11]
Bronchiectasis Ciliary dysfunction Elevated sweat chloride,
characteristic electrophysiological
abnormalities, CFTR mutations on
two alleles		 - CFTR modulators - Shteinberg (2020) [11]
Chronic airway disease Airway limitation FEV1/FVC < 0.7 and
FEV1 < 80% predicted		 - LAMA
LABA-ICS: Significant functional and symptomatic improvement,
Pulmonary rehabilitation		 - Llano (2020) [12]
COPD Airway limitation Post-bronchodilator FER < 70% and FEV1 < 80% predicted 88.9% LAMA, LABA-ICS, Pulmonary rehabilitation - Hiles (2020) [3]
Llano (2020) [12]
COPD Hypoxemia/hypercapnia PO2/PCO2 38.9% Oxygen, NIV Marker of poor prognosis Llano (2020) [12]
Gonçalves (2018) [13]
Hiles (2020) [3]
COPD Lung hyperinflation RV > 175% predicted or RV/TLC ≥ 0.58 - Endobronchial valves, coils: ↑ in lung function, ↓ dyspnoea, ↑ QoL, ↑ exercise tolerance, ↓ residual volume
lung volume reduction surgery
Bronchoscopic thermal vapour ablation: ↑ lung function and QoL in upper lobe prominent emphysema		 - Dijk (2020) [14]
Abbreviations: BMI, body mass index; CFTR, cystic fibrosis transmembrane conductance regulator; CPAP, continuous positive airway pressure; COPD, chronic obstructive pulmonary disease; EnaC, epithelial sodium channel; FER, forced expiratory ratio; FEV1, forced expiratory volume in the first second; FVC, forced vital capacity; ICS, inhaled corticosteroids; LABA, long-acting beta 2-agonists; LAMA, long-acting muscarinic antagonists; NIV, non-invasive ventilation; NO, nitric oxide; PCO2, partial pressure of carbon dioxide; PEFR, peak expiratory flow rate; QoL, quality of life; PO2, partial pressure of oxygen; RV, residual volume; SABA, short-acting beta-agonists; SpO2, peripheral capillary oxygen saturation; TLC, total lung capacity; ↑, increased/improved; ↓, decreased/reduced.
The most prominent physiological trait is airflow limitation, being the most common trait in asthma and COPD. The average prevalence was 52.5% in asthma [5][3][6], with the prevalence varying from 45.5–54.5% between studies [5][3][6]. As defined by a post-bronchodilator forced expiratory volume in the first second < 80% predicted, the prevalence in COPD was the highest, at 88.9% [3]. Airflow limitation has prognostic implications on asthma, leading to worsened severity of symptoms and increased exacerbations and healthcare utilisation [1]. Treatment of airflow limitation in asthma with long-acting muscarinic antagonists (LAMA) and bronchial thermoplasty have been shown to decrease exacerbations, improve lung function, and improve disease control [4][8][7], while short-acting anticholinergics and magnesium were found to decrease hospital admissions [1]. Similar treatments with LAMA, long-acting beta-agonists (LABA), inhaled corticosteroids (ICS), and pulmonary rehabilitation have been proposed to treat airflow limitation in COPD [3][12]. Airflow limitation was also described in bronchiectasis, with inhaled saline and airway clearance being the suggested treatment and with an ongoing trial on epithelial sodium channel inhibition [11].
Lung hyperinflation was also a trait targeted in the management of COPD patients, with endobronchial valves and bronchoscopic thermal vapour ablation showing improved lung function and quality of life [14]. 

2.2. Biochemical Traits

Type-2 inflammation is widely documented as a treatable trait in chronic airway diseases like asthma and COPD (Table 2), with a prevalence of 42.0% in asthma patients [6]. Type-2 inflammation is characterised by T2-high expression, such as IL-13 induced genes or high eosinophil count. Chung et al. [15] reported that asthma patients with type-2 inflammation were predisposed to corticosteroid insensitivity and may be dependent on oral corticosteroids in severe cases. Treatment options include bronchodilators containing inhaled corticosteroids (ICS), which have been shown to be effective for asthma. ICS-LABA and ICS-LABA-LAMA combinations have similarly been effective for patients with COPD [12]. Anti-T2 biologics have also been shown to significantly reduce the risk of severe asthma exacerbation and improve lung function and quality of life of patients [15].
Table 2. Overview of biochemical treatable traits.
Condition Treatable Trait Trait-Identification Marker Prevalence (Range) Treatment Description Prognostic Implications Author (Year)
Asthma Eosinophilia Blood/Sputum Eosinophilia 54.3% (51.4–56.4%) Corticosteroids: ↑ FEV1
Omalizumab: Significant ↓ in exacerbations and ↑ in CARAT and AQLQ. FEV1 ↑, RV ↓, mean BE ↓
Mepolizumab/Anti IL-5
Anti IL4/IL -13: High FeNO responds to anti-IL4/IL13 therapies		 Associated with severe asthma, frequent exacerbations, ↓ lung function at baseline Chung (2019) [15]
Connolly (2018) [5]
Dean (2017) [16]
Feng (2019) [17]
Santos (2018) [18]
Pavord (2020) [19]
Llano (2019) [20]
Papaioannou (2018) [7]
Hiles (2020) [3]
Hinks (2020) [8]
Asthma FeNO FeNO levels - FeNO-guided ICS treatment: Improved symptoms, ↑ asthma control, ↓ exacerbations, ↑ QoL   Dean (2017) [16]
Honkoop (2019) [21]
Kuo (2019) [22]
Asthma Neutrophil elastase/inflammation; CXCR2R2 Sputum neutrophilis ≥ 61% 36.5% (27.3–40%) Macrolides: ↓ exacerbation. May result in antibiotic resistance
Smoking cessation: ↓ of neutrophilic inflammation, lung-function improvement in asthmatics		 ↑ exacerbation risk Connolly (2018) [5]
Dean (2017) [16]
Simpson (2018) [6]
Papaioannou (2018) [7]
Hiles (2020) [3]
Hinks (2020) [8]
McDonald (2019) [9]
Asthma Paucigranulocytic phenotype Neutrophil levels <61% and eosinophil levels <2% - Macrolides, bronchodilators, bronchial thermoplasty ↑ risk of moderate-severe acute exacerbations, ↑ all-cause mortality. Higher airflow limitation and dyspnoea present in these patients. Papaioannou (2018) [7]
Asthma Proteins (periostin, galectin-3) Sputum galectin-3 - Anti-IgE therapy (omalizumab) - Dean (2017) [16]
Asthma Type 2 inflammation T2-high expression 42.0% Salbutamol: Improved bronchodilator response
Anti-T2 biologics: Major ↓ in severe exacerbations, small improvement in FEV1, improvement in asthma QoL scores		 Corticosteroid insensitivity and oral corticosteroid dependence in severe patients Chung (2019) [15]
Simpson (2018) [6]
Bronchiectasis Eosinophilia IL-5, IL-13 and Gro-α in sputum - ICS, Bronchodilators, macrolides: Treatment showed little difference in clinical parameters between groups - Shteinburg (2020) [11]
Shoemark (2019) [23]
Bronchiectasis Neutrophil elastase/inflammation; CXCR2R2 Sputum neutrophils - Neutrophil elastase inhibitor: Significant ↑ in FEV1 and QoL.
CXCR2 antagonist: ↓ sputum neutrophils, no difference in exacerbations. Macrolides
Corticosteroids		 ↑ frequency of exacerbations and more rapid decline in FEV1 in some patients.
Disease severity worse with ↑ BSI score, sputum volume, and ↓ predicted FEV1%		 Chalmers (2018) [24]
Shoemark (2019) [23]
Chronic airway disease FeNO Exhaled CO - Primary prevention ↑ acute exacerbations + major public health problem. McDonald (2019) [25]
Chronic airway disease T2-low inflammation Eosinophil <100 - Azithromycin, roflumilast, LABA-LAMA - Llano (2020) [12]
Chronic airway disease Type 2 inflammation Sputum/blood eosinophilia - ICS-LABA, ICS-LABA-LAMA, biologics - Llano (2020) [12]
McDonald (2019) [25]
COPD Eosinophilia Sputum/blood eosinophilia 60.1% (22.2–60.1%) Corticosteroids: Beneficial during exacerbations for patients with eosinophilia
Anti-IL5		 ↑ number of moderate exacerbations, risk of future exacerbations. Exacerbations characterised by enhanced airway eosinophilic inflammation; generally milder, with ↓ mortality and ↓ hospital stay. Garudadri (2018) [26]
Gonçalves (2018) [13]
Soriano (2018) [27]
Müllerová (2018) [28]
Müllerová (2018) [29]
Hiles (2020) [3]
Mathioudakis (2020) [30]
Matsunaga (2020) [31]
Matthes (2018) [32]
COPD Neutrophil elastase/inflammation; CXCR2R2 Sputum neutrophils > 61% 44.4% Macrolides - Hiles (2020) [3]
COPD Proteins (periostin, galectin-3) Specific marker - Specific therapy - Llano (2020) [12]
COPD T2-low inflammation Eosinophil < 100 - Azithromycin, Roflumilast, LABA-LAMA - Llano (2020) [12]
COPD Type 2 Inflammation Eosinophil > 300/>100 if on OCS - ICS-LABA, ICS-LABA-LAMA, Biologics - Llano (2020) [12]
COPD Vitamin D Serum 25-hydroxycholecalciferol levels - Vitamin D supplementation: ↓ risk of respiratory tract infection. VDD was associated with ↓ FEV1 at baseline and faster decline in FEV1 Llano (2020) [12]
Rhinitis/rhinosinusitis Airway/nasal inflammation Nasal cytology; nasal polyps biopsy - Corticosteroids, biologicals - Heffler (2019) [33]
United Airways Dz Eosinophilia Blood/sputum eosinophilia, blood periostin, high FeNO, absent specific IgE, non- reactive skin prick tests - Corticosteroids, anti-IL-5, IL-4, IL-13, anti-TSLP, CRTh2 antagonist - Yii (2018) [34]
United Airways Dz Environmental exposure Total IgE, skin prick tests Peak flow monitoring Specific bronchoprovocation challenge - Exposure avoidance, respiratory protection devices, anti-IgE - Yii (2018) [34]
United airways Dz Neutrophil elastase/inflammation; CXCR2R2 IL-8, sputum neutrophilia - Smoking cessation, macrolides - Yii (2018) [34]
Abbreviations: AQLQ, Asthma Quality of Life Questionnaire; BE, base excess; BSI, bronchiectasis severity index; CARAT, Control of Allergic Rhinitis and Asthma Test; CO, carbon monoxide; CRTh2, prostaglandin D2 receptor 2; FeNO, fractional exhaled nitric oxide; FEV1, forced expiratory volume in the first second; FVC, forced vital capacity; ICS, inhaled corticosteroids; LABA, long-acting beta 2-agonists; LAMA, long-acting muscarinic antagonists; OCS, oral corticosteroids; QoL, quality of life; ↑, increase/improved; ↓, decreased/reduced.
Specifically, eosinophilia is one of the most prominent biochemical traits studied, with its prevalence ranging from 51.4% to 56.4% in asthma and 22.2% to 60.1% in COPD [3][32][28]. Eosinophil levels can be measured using blood or sputum eosinophils, and high eosinophil levels are associated with increased risk of exacerbations in both asthma and COPD. In particular for asthma, Feng et al. [17] showed that patients with exacerbation-prone asthma had increased blood eosinophil and reduced lung function at baseline. Treatment for asthma and COPD patients with eosinophilia involves corticosteroid usage, which has been shown to be beneficial in acute exacerbations and to improve FEV1 of patients. Among patients with eosinophilia, monoclonal antibodies, such as anti-IL5, have also been reported to reduce exacerbations in COPD [32]. Specifically for asthma, omalizumab has been shown to significantly reduce both eosinophilia and exacerbations, with improved lung function and quality of life [18].
Neutrophil-related inflammation was also prominent in patients with asthma, bronchiectasis, and COPD, and it is identified by high sputum neutrophil counts [3]. It was associated with increased exacerbation risk for each of the above conditions [9], and high sputum neutrophil counts predicted more rapid decline in FEV1 in patients with bronchiectasis. Macrolides were shown to reduce exacerbations in asthma and COPD, while smoking cessation was additionally recommended for asthma patients. Neutrophil elastase inhibitors were also shown to improve lung function and quality of life for patients with bronchiectasis [24].
As for environmental exposure in united airway diseases identified by immunoglobulin E (IgE) levels and skin-prick tests, proposed treatment options included exposure avoidance, respiratory protection devices, and anti-IgE therapy [34]. However, data on the prevalence of these traits were lacking, and studies evaluating the clinical benefits of the proposed treatment strategies were not available either.

2.3. Psychosocial Traits

Two main psychosocial traits identified were treatment adherence/technique and smoking history (Table 3). Education and medication reconciliation are the main treatment options, targeting inhaler technique, self-management action plans, and minimising the number of inhaler devices [3].
Table 3. Overview of psychosocial treatable traits.
Condition Treatable Trait Trait-Identification Marker Prevalence (Range) Treatment Description Prognostic Implications Author (Year)
Asthma Adherence and technique Adherence check
Adherence rating scales		 44.0% (26.9–61.8%) Self-management education and WAP
Treatment changed when possible to minimise devices
Inhaler technique skills
Self-management education with adherence-aiding strategies		 Inhaler-device polypharmacy is one of the best predictors of exacerbation risk
↑ exacerbation risk		 Connolly (2018) [5]
Simpson (2018) [6]
Hiles (2020) [3]
McDonald (2019) [9]
Asthma Smoking/ex-smoker Medical history of smoking or exhaled CO ≥ 10 ppm 14.3% (13.9–14.5%) Counseling and NRT or varenicline, bupropion - Connolly (2018) [5]
Simpson (2018) [6]
Hiles (2020) [3]
Milne (2020) [35]
Chronic airway disease Adherence and technique Adherence check
Adherence rating scales		 - Understanding reason
for non-adherence,
directing education
of adherence-aiding
strategies accordingly: Good adherence associated with ↓ severe exacerbations of asthma and COPD		 Suboptimal inhaler technique and inhaler device polypharmacy associated with ↑ healthcare
utilisation		 Llano (2020) [12]
McDonald (2019) [25]
Chronic airway disease Smoking/ex-smoker Medical history of smoking or exhaled CO ≥ 10 ppm - Counseling and NRT or varenicline, bupropion: Cessation ↓ lung function decline and future risk of exacerbations Smoking is a risk factor for exacerbation Llano (2020) [12]
McDonald (2019) [25]
Chronic Airway Disease Social issues Interview - Activate support services Poor family and social support and deprived socioeconomic status associated with ↑ symptom deterioration and exacerbation McDonald (2019) [25]
COPD Adherence and technique Does not possess a WAP or does not use WAP during exacerbations
Test of adherence to inhalers		 55.6% Self-management education and WAP
Treatment changed when possible to minimise devices
Inhaler technique skills
Self-management education with adherence-aiding strategies		 - Hiles (2020) [3]
Llano (2020) [12]
COPD Smoking/ex-smoker Medical history of smoking or exhaled CO ≥ 10 ppm 19.4% Counseling and NRT or varenicline, bupropion - Hiles (2020) [3]
Llano (2020) [12]
Abbreviations: CO, carbon monoxide; COPD, chronic obstructive pulmonary disease; NRT, nicotine replacement therapy; WAP, written action plan; ↑, increased/improved; ↓, decreased/reduced.
Smoking was prevalent among patients with chronic respiratory diseases, with a mean prevalence of 14.3% in asthma and 19.4% in COPD [3]. Smoking status was usually assessed through interview or the use of exhaled carbon monoxide and was shown to be a significant risk factor for exacerbation in chronic airway diseases [25]. Smoking cessation was shown to reduce lung-function decline and risk of recurrent exacerbations, highlighting the importance of opportunistic implementation of smoking cessation strategies during acute exacerbations [25]. Management options include counselling with pharmacologic adjuncts, such as nicotine replacement therapy, varenicline, and bupropion [3][25][12].
Low socioeconomic status and poor family support in chronic airway disease were also associated with increased symptomatic deterioration and exacerbations, with social support services proposed as a possible treatment option [25].

2.4. Microbiological Traits

Microbiological treatable traits were mostly found in asthma, bronchiectasis, COPD, and united (combined upper and lower) airway diseases. The most prevalent trait was chronic respiratory infection in both asthma and COPD, with an average prevalence of 45.0% and a prevalence range of 34.8–47.3% among the studies on asthma [3][36][6]. Various treatment options, such as antibiotics, mucolytics, roflumilast, education, and inhaled interferon-β treatment, were suggested [1][5][3]. However, evidence was lacking regarding their efficacy. In patients with COPD, chronic respiratory infection was present in 55.6% of the patients [3], with prognostic implications on their quality of life and dyspnoea severity [31]. Macrolides have been shown to decrease hospital admissions resulting from exacerbations, but their usage must be balanced against the risk of colonisation with macrolide-resistant organisms [31].
Another prominent microbiological trait is microbial colonisation, present in an average of 18.9% of asthmatics, with a range varying from 12.7 to 55.6% [5][3]. Microbial colonisation was present in an average of 44.8% of COPD patients, with prevalence ranging from 38.9 to 45% [3][30]. This is a separate trait from infection, as colonisation refers to the presence of organisms, while infection refers to the presence of signs and symptoms due to these organisms. Microbial colonisation nonetheless had prognostic significance, demonstrated particularly in COPD patients, with implications on quality of life and increment in dyspnoea [30]. Treatment options for this trait in patients with asthma include education and antibiotic-based written action plans (e.g., using macrolides) [3][8]. However, information regarding treatment options for this trait was inadequate in COPD. Interestingly, patients with microbial colonisation had lower mortality for exacerbations associated with viral infections compared to bacterial infections, though the clinical significance of this is uncertain [30].

2.5. Comorbidity Traits

Impaired physical function is a comorbidity seen in almost all chronic respiratory conditions, with a prevalence of 36.1% in COPD and 10.9% in asthma [3]. Impaired physical function can present in different forms, such as low appendicular skeletal muscle mass, limitations in mobility, and low muscle strength and has been shown to be an independent predictor of hospital admission and mortality in COPD. Patients with lower 6 min walking distance were also reported to have higher readmission risk [25]. Various management measures targeted at physical function can be implemented. For instance, Hiles et al. [3] recommended a high-protein diet, strength training, and regular pulmonary rehabilitation for patients with low appendicular skeletal muscle mass.
Another prevalent comorbidity trait is the presence of psychiatric conditions, particularly depression and anxiety in asthma and COPD. Treatments included counselling, cognitive behavioural therapy, and paroxetine [3][31].
Nutrition (underweight) is another common comorbidity, with a prevalence of 52.8% in COPD [3] and 38.1% in asthma, with a range of 35.1–58.2% [3]. These traits had similar prognostic implications, with decreased quality of life, increased severity of symptoms, and increased exacerbations [31][9][7][37]. Treatments to normalise body mass index, such as supplementation and weight loss, have also been shown to decrease asthma severity [7]. However, treatment benefits for COPD were not described in the literature.
Some of the other comorbidity traits with high prevalence include systemic inflammation, which was present in 56.4% of asthmatics and 63.9% of COPD patients, and sleep disorders, with a prevalence of 60.0% and 30.6% in patients with asthma and COPD, respectively [3]. For the mitigation of systemic inflammation, McDonald et al. showed that statin therapy improved C-reactive protein levels in COPD patients [2]. Separately, positive airway pressure has been shown to reduce overall mortality and exacerbation risk in COPD patients with sleep disorders, though its efficacy may be limited by patient adherence [31].

This entry is adapted from the peer-reviewed paper 10.3390/cells10113263

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