Chronic Obstructive Pulmonary Disease (COPD) has a specific subtype, known as eosinophilic COPD, defined by the presence of elevated levels of a white blood cell called an eosinophil. These cells contribute to a distinct pattern of airway inflammation. Approximately 25% to 40% of individuals with COPD exhibit this eosinophilic characteristic. Recognizing this subtype is important because the underlying inflammatory process responds differently to certain medications, allowing for a more personalized treatment strategy tailored to the individual’s specific biological profile.
Differentiating Eosinophilic COPD
Eosinophilic COPD is distinguished from other forms of the disease by the specific inflammatory cells driving it. While COPD is traditionally associated with inflammation led by neutrophils, the eosinophilic subtype involves a process more commonly seen in some forms of asthma. In this variant, eosinophils accumulate in the lung tissues, releasing substances that provoke airway inflammation and obstruction. This contrasts with neutrophilic inflammation, which is linked to more severe airway obstruction.
The presence of eosinophilic inflammation is often associated with more frequent symptom flare-ups, known as exacerbations. The inflammation in eosinophilic COPD shares features with asthma, leading to the concept of Asthma-COPD Overlap (ACO). Many individuals with eosinophilic COPD exhibit characteristics of both conditions.
This overlap highlights the heterogeneity of COPD. Patients with ACO may have a history of asthma and allergies, which are less common in purely neutrophilic COPD. The inflammatory pathways in eosinophilic COPD and ACO are linked to what is known as Type 2 inflammation, a pattern of immune response that also drives allergic asthma, which explains why certain treatments that target these specific pathways are more effective in this patient population.
Diagnosis and Identification
The initial diagnosis of COPD is established through a breathing test called spirometry. However, to determine if a patient has the eosinophilic subtype, more specific tests are required. The most common and accessible method is a complete blood count (CBC). This test measures the number of different types of white blood cells, including eosinophils.
A peripheral blood eosinophil count is considered elevated when it is higher than normal levels, which are typically up to 500 cells per microliter (cells/µL). For the purposes of identifying eosinophilic COPD, a count of 300 cells/µL or higher is often used as a threshold to predict a better response to specific treatments and an increased risk of exacerbations.
Another method for identification involves analyzing a sample of sputum, which is mucus coughed up from the lungs. A sputum eosinophil count of 3% or more can also define eosinophilic airway inflammation. While providing a direct measure of airway inflammation, collecting a sputum sample can be more challenging than a blood test. Therefore, the blood eosinophil count remains the most widely used tool in clinical practice to identify patients with this specific COPD phenotype.
Targeted Treatment Approaches
While standard COPD treatments like bronchodilators remain a foundation of care, the identification of eosinophilic COPD allows for more targeted therapeutic strategies. The presence of eosinophilic inflammation indicates that a patient is likely to have a significant response to inhaled corticosteroids (ICS). These medications work to suppress the specific type of inflammation driven by eosinophils, leading to a reduction in exacerbation frequency and improved symptom control. A blood eosinophil count of ≥300 cells/µL is a strong indicator that adding an ICS to a treatment regimen will be beneficial.
For patients who continue to experience frequent exacerbations despite optimal inhaled therapy, including ICS, advanced treatments known as biologics may be considered. These therapies are monoclonal antibodies, which are lab-produced molecules that mimic the immune system’s attack on specific cells. These drugs work by targeting the biological pathways that promote eosinophilic inflammation.
One major class of biologics targets interleukin-5 (IL-5), a signaling molecule for the growth, activation, and survival of eosinophils. Another biologic, dupilumab, targets the receptor for both IL-4 and IL-13, other proteins in the Type 2 inflammatory cascade. These treatments have been shown to significantly reduce exacerbation rates in eligible patients with eosinophilic COPD.
Specific biologics include:
- Mepolizumab and reslizumab, which bind directly to IL-5, preventing it from activating eosinophils.
- Benralizumab, which attaches to the IL-5 receptor on the surface of eosinophils, leading to their depletion.
- Dupilumab, which targets the receptor for both IL-4 and IL-13.
Managing Exacerbations and Prognosis
Patients with eosinophilic COPD often face a higher risk of frequent and severe exacerbations. These flare-ups can lead to a more rapid decline in lung function and an increase in hospital admissions. However, the prognosis for individuals with this subtype can be significantly improved with tailored treatment that directly addresses the underlying eosinophilic inflammation.
The use of targeted therapies, particularly inhaled corticosteroids and biologics, is effective at controlling the disease. These treatments can reduce the frequency and severity of exacerbations. Biologics targeting the IL-5 pathway can lower the annual rate of moderate to severe exacerbations in patients with elevated eosinophil counts.
While this diagnosis once pointed to a more difficult disease course, the outlook has changed with personalized medicine. Interestingly, some studies suggest that during a hospitalization for an exacerbation, patients with high eosinophil counts may have better short-term outcomes, including shorter hospital stays, compared to those with non-eosinophilic flare-ups. With accurate diagnosis and the application of targeted treatments, individuals can achieve better long-term control of their symptoms and a more favorable prognosis.