COPD is a multifaceted disease influenced by both genetic and environmental factors, and its complications (triggered by infections and environmental factors) often require additional treatment, making it a critical health concern.2
There are many endotypes of COPD, which necessitates the classification of patients into distinct subgroups based on biological differences, such as the extent of bacterial colonisation or the presence of eosinophilic inflammation.2
Our current understanding of these COPD subtypes is limited, necessitating further research to enable more precise, individualised treatments rather than a one-size-fits-all approach.2
Why treat COPD?
COPD poses a significant burden on patients and society due to its natural progression, which reduces daily activities, leads to exacerbations, and contributes to work and social isolation, often resulting in psychological conditions like anxiety and depression.3
These factors collectively lower the health-related quality of life and increase mortality compared to the general population. COPD frequently coexists with various comorbidities, some independently arising, and others linked causally or through shared risk factors, such as age, smoking, and systemic inflammation.3
Common comorbidities include bronchiectasis, cardiovascular disease, chronic kidney disease, dyslipidaemia, diabetes, hypertension, lung cancer, mental disorders, osteoporosis, obstructive sleep apnoea, and skeletal muscle dysfunction. Notably, heart failure is a significant predictor of mortality in COPD patients, doubling the risk of death according to some research.3
Subtypes of COPD
The Body mass index-Obstruction-Dyspnoea-Exercise-capacity (BODE) index is a tool often used to identify individuals with COPD who are at increased risk of mortality.4 However, the BODE index does not take into account the underlying pulmonary morphologic abnormalities that are associated with COPD.4
Identifying COPD subtypes that integrate these abnormalities with associated pulmonary dysfunction and risk of mortality could provide insights into potentially modifiable disease pathways and protein biomarkers of disease.4 The most commonly used guidelines for the subclassification of COPD types are the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines.5
According to GOLD, traditional COPD was categorised into spirometric stages 1-4.5 Those lacking airflow obstruction (forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] ≥0.70) and FEV1 ≥80% predicted) were designated as GOLD 0. Those with FEV1/FVC ≥0.70 and FEV1 <80% predicted were labelled as having preserved ratio-impaired spirometry (PRISm).5
How do you know it’s COPD?
The diagnosis of COPD can be challenging, and given its lifelong nature, it is important for clinicians to carefully consider alternative diagnoses. This involves a thorough assessment of the patient’s clinical history, characteristics, exposures, and spirometry results.3 It is important not only to distinguish between obstructive lung diseases (such as asthma, bronchiectasis, and COPD) but also to recognise restrictive lung disease and heart failure, which can sometimes mimic or coexist with COPD.3
Historically, the reversibility of airflow obstruction after bronchodilator administration was used to distinguish between asthma and COPD. However, it is now recognised that significant reversibility (defined as an increase in FEV1 of ≥12% and ≥200 mL from baseline) or an increase in FVC of ≥10% can also occur in COPD, even in the absence of features suggestive of asthma. Furthermore, the degree of reversibility can vary within the same patient over time.3
To definitively exclude asthma and diagnose COPD, a substantial improvement in FEV1 with normalisation of the FEV1/FVC ratio after bronchodilator administration or after four to 12 weeks of inhaled corticosteroid therapy is required. Patients with COPD who develop pneumonia may present with symptoms that are like those of a COPD exacerbation.3 While the treatment of these two conditions is generally similar, the duration of antibiotic therapy for pneumonia may be longer in practice.3
A diagnosis of COPD is possible in any patient who complains of dyspnoea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections and/or a history of exposure to risk factors for the disease but FVC manoeuvre during spirometry showing the presence of a post-bronchodilator FEV1/FVC <0.7 is needed to establish the diagnosis of COPD. The FEV1 also serves to determine the severity of airflow obstruction (GOLD grades 1, 2, 3, and 4, or mild, moderate, severe, and very severe).5
At present, COPD management is primarily focused on alleviating symptoms and minimising the risk of future exacerbations. However, the severity of COPD symptoms, and the possibility of mistaking the condition for any number of other diseases, demands that clinicians actively seek to identify COPD in patients with a history of risk factors and current symptoms.
- Agarwal A, et al. Chronic Obstructive Pulmonary Disease. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559281/
- Vogelmeier CF, et al. Goals of COPD treatment: Focus on symptoms and exacerbations. Respir Med, Volume 166, May 2020, 105938, 2020.
- Sandelowsky H, et al. COPD – do the right thing. BMC Fam Pract, volume 22, Article number: 244, 2021.
- Young KA, et al. Subtypes of COPD Have Unique Distributions and Differential Risk of Mortality. Chronic Obstr Pulm Dis, 6(5): 400–413, 2019.
- Agustí A, et al. Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary. Eur Respir J, Apr 2023, 61 (4).