ED: COPD significantly impacts quality of life. Optimising pharmacological treatment can be tricky.
COPD is a functional abnormality with a number of pathologies.
Chronic obstructive pulmonary disease (COPD) is defined as a reduction in the FEV1 to <80% of the predicted value and a reduction of the FEV1/FVC ratio to <0.7 (assuming correctly done spirometry) that is not reversible. An FEV1/FVC ratio greater than 0.7 does not exclude airflow limitation (mixed restrictive/obstructive pattern of lung function requiring full lung function testing). Considerable degrees of emphysema can exist in the presence of a normal FEV1 in some smokers. Emphysema should be diagnosed by measurement of gas transfer and CT chest.
COPD – how did I get here?
The FEV1 measured in adult life is the result of cumulative lifetime events – fetal development, perinatal exposures, early childhood insults and adult exposures. For example, the deficit in lung function associated with asthma, combined with the accelerated rate of lung function decline due to smoking, result in lower levels of lung function in later adult life than either alone (Figure 1). Stopping smoking stops the rapid decline in FEV1, within a month.
Personalised treatment applies – go for ‘GOLD’!
Pharmacological therapy in airway diseases, especially ‘COPD’ currently presents a bewildering array of options. Large-scale trials of combined therapies demonstrate modest improvements in FEV1 and quality of life and reduced exacerbation rates. Subsequently it has been recognised that inhaled corticosteroids (ICS) use in COPD is associated with an increased risk of pneumonia and not all patients obtain benefit. COPD patients with “asthma-like” features (e.g. allergy, reversibility/variability of lung function, past history of asthma and sputum eosinophilia) appear to do best with ICS.
Therefore, it would seem beneficial to use ICS in patients with COPD who have “asthma-like” features and/or sputum eosinophilia, and to use only bronchodilators in the rest since they may be at increased of pneumonia. But how to assess sputum eosinophilia and what bronchodilators to use?
Both exhaled nitric oxide and blood eosinophil levels are good predictors of sputum eosinophils. Blood eosinophil levels have been shown to relate well to sputum eosinophils and a value >300 cells/µl (0.3 cells x 109/litre) identifies a group of patients with COPD more likely to benefit from ICS.
Combinations of long-acting beta-agonists (LABAs) and long-acting anti-muscarinic antagonists (LAMAs) achieves greater (modest) FEV1 improvements and quality of life outcomes than either alone. In patients with moderate fixed reductions in FEV1 it is recommended to use both, in combination. Agent choice also depends on patient convenience, ease of use and side effects which are few and usually mild. There is no evidence of superiority of the different LAMAs and LABAs when used at recommended doses. The evidence-based GOLD guidelines (2017) are recommended.
Take Home Points
- COPD is an acronym, not a disease, which describes a functional abnormality.
- Defined by correct spirometry, COPD may result from a number of pathologies.
- Reversible and irreversible airflow obstruction may co-exist.
- Cumulative life-course host factors and exposures can cause COPD.
- COPD – bronchodilators for most, inhaled corticosteroids for some – go for ‘GOLD’.
References available on request.
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Author competing interests: nil relevant disclosures.
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