When doctors talk about chronic obstructive pulmonary disease, they often write it as Chronic Obstructive Pulmonary Disorder (COPD) is a progressive lung disease characterized by airflow limitation that is not fully reversible. COPD and asthma often get mentioned together because they share symptoms-shortness of breath, cough, wheeze-yet the reasons they overlap are far from simple. This article unpacks how the two conditions intersect, why the overlap matters for treatment, and what patients can do to keep their lungs working as best as possible.
COPD develops slowly, usually over decades, as the lungs endure repeated insults-most commonly cigarette smoke. The disease creates permanent changes in the airway walls and destroys the tiny air sacs (alveoli). This leads to chronic bronchitis (excess mucus) and emphysema (loss of elastic recoil). The hallmark is a reduced forced expiratory volume in one second (FEV1) that does not fully recover after a bronchodilator test.
Asthma is a chronic inflammatory disorder of the airways that causes reversible airflow obstruction and hyper‑responsiveness. Triggers range from allergens (pollen, dust mites) to irritants (cold air, exercise). Unlike COPD, asthma’s airflow limitation can often be fully reversed with medication, and lung function may be normal between attacks.
Scientists call the coexistence "asthma‑COPD overlap" (ACO). The overlap occurs because both diseases involve airway inflammation a response that narrows the air passages and makes them more sensitive. However, the inflammatory cells differ: eosinophils dominate in asthma, while neutrophils are more common in COPD. When a patient has a mixed inflammation pattern, they experience features of both conditions.
Key risk factors for ACO include:
Accurate diagnosis hinges on spirometry a breathing test that measures lung volumes and flow rates. Doctors look for two patterns:
If both criteria are met, the patient likely has ACO. Additional tests-fractional exhaled nitric oxide (FeNO) for eosinophilic inflammation or chest CT for emphysema-help refine the picture.
The therapeutic goal is to control symptoms, prevent exacerbations, and slow lung function decline. Because ACO blends traits of both diseases, treatment usually combines strategies from each.
Bronchodilators (short‑acting and long‑acting) keep the airways open. Inhaled corticosteroids (ICS) anti‑inflammatory meds delivered directly to the lungs target eosinophilic components common in asthma. For patients with frequent exacerbations, adding a long‑acting muscarinic antagonist (LAMA) can improve outcomes, especially when emphysema is present.
Vaccinations (influenza, pneumococcal) and pulmonary rehabilitation are also part of the plan. Most importantly, smoking cessation the process of quitting tobacco use dramatically reduces the rate of lung function loss.
Patients with ACO tend to have more frequent exacerbations acute worsening of symptoms that often require steroids or antibiotics than those with COPD or asthma alone. Hospitalization risk is about 30% higher, and quality‑of‑life scores are lower. However, aggressive use of combination inhalers and lifestyle changes can bring the risk down to levels similar to well‑controlled asthma.
Researchers are exploring biomarkers that can pinpoint the exact inflammatory mix in each patient. Blood eosinophil counts, periostin levels, and sputum neutrophil percentages are promising. Personalized medicine-matching therapy to the dominant cell type-could soon replace the one‑size‑fits‑all approach.
Another hot area is the use of biologic agents (e.g., anti‑IL‑5, anti‑IgE) originally approved for severe asthma. Small trials suggest they also shrink exacerbation rates in ACO patients with high eosinophils. Large‑scale studies are expected by 2027.
Feature | COPD | Asthma | Overlap (ACO) |
---|---|---|---|
Typical age of onset | 40‑70years | Childhood‑early adulthood | 40‑65years |
Primary trigger | Smoking, occupational dust | Allergens, exercise, cold air | Combination of smoke & allergens |
Inflammatory cells | Neutrophils | Eosinophils | Mixed neutrophil‑eosinophil |
Reversibility (post‑bronchodilator) | <12% & 200mL | >12% & 200mL | Both criteria met |
Exacerbation frequency | 2‑3yr⁻¹ (moderate‑severe) | 1‑2yr⁻¹ (if uncontrolled) | 3‑4yr⁻¹ (higher risk) |
Preferred inhaler regimen | LABA+LAMA | ICS+SABA | ICS+LABA±LAMA |
Yes. Many long‑term smokers develop COPD but also retain an underlying allergic tendency. When both are present, clinicians label it asthma‑COPD overlap and treat with a combination inhaler.
Patients with ACO face a higher chance of severe flare‑ups and hospitalization. The mortality risk is modestly increased, but aggressive therapy can bring outcomes close to those of well‑controlled asthma.
Usually a single combination inhaler (ICS+LABA) covers the asthma component, while adding a LAMA addresses the COPD side. Your doctor will tailor the regimen.
It’s critical. Quitting stops further lung damage and can improve response to inhaled steroids, lowering exacerbation rates dramatically.
Biologics targeting eosinophils (like mepolizumab) are being tested in ACO trials. Early results show fewer severe attacks, and larger studies are expected in the next two years.
Comments
Mansi Mehra
28 September 2025The article is well‑structured.