Table 1. Recognised clinical phenotypes of chronic obstructive pulmonary disease, asthma, and bronchiectasis.
| Phenotype | Basic features |
|---|---|
| Chronic obstructive pulmonary disease (COPD) | |
| Bronchitic phenotype | The presence of productive cough (at least 3 months per year in at least
2 consecutive years) |
| Emphysema phenotype | Presence of emphysema confirmed on imaging (including computed
tomography densitometry) |
| Eosinophil COPD | Presence of eosinophilia, normally defined as at least 2% eosinophils in
either blood or sputum |
| Asthma COPD overlap | Persistent airflow limitation with several features usually associated with
asthma and several features usually associated with COPD |
| Overlap COPD and bronchiectasis | Airflow obstruction consistent with COPD alongside irreversibly dilated
airways, mucus gland hyperplasia and impaired mucus clearance associated with bronchiectasis |
| Frequent exacerbation phenotype | Two or more “exacerbation” events per year; an exacerbation is defined
as an acute worsening of respiratory symptoms that result in additional therapy. |
| Asthma | |
| Atopic asthma | Atopic and eosinophilic with increased fractional exhaled nitric oxide
(FeNO) |
| Non-eosinophilic asthma associated with obesity | Decreased lung function associated with obesity |
| Non-eosinophilic asthma (neutrophilic asthma) | Lack of eosinophilic inflammation. No raised sputum eosinophil count or
FeNO. Neutrophilic inflammation common. |
| Aetiology | Examples of causes |
| Bronchiectasis | |
| Post-infectious damage | Tuberculosis, whooping cough, and so on |
| Muco-ciliary clearance defects | Primary ciliary dyskinesia, cystic fibrosis, and Young’s syndrome |
| Immunodeficiency | Primary (for example, hypogammaglobinaemia)
Secondary (for example, malignancy such as leukaemias or immune modulation with drugs, after transplant) |
| Autoimmune conditions | Rheumatoid arteritis, systemic lupus erythematosus, and inflammatory
bowel disease |
| Congenital | Tracheobronchomegaly, cartilage deficiency, and Marfan syndrome |
| Toxic exposures, obstruction or aspiration | Toxic gas (chlorine, ammonia), foreign body, and smoke exhalation |
The first and second sections provide a table of recognised COPD and asthma phenotypes. Though not exhaustive, these represent phenotypes most often discussed in recent publications (for example, 47, 48) and it is also possible for patients to have more than one phenotype; thus, there can be considerable clinical overlap. In the third section, examples of aetiologies that can lead to bronchiectasis have been given. Again, this list is not exhaustive but for all diseases (COPD, asthma and bronchiectasis) is intended to provide an overview of how disparate clinical phenotypes associated with one umbrella term can be.