Asthma vs Chronic Obstructive Pulmonary Disease (COPD): Clinical Insights for Differential Management

Updated According to GINA 2025 & GOLD 2026 Guidelines

Asthma and Chronic Obstructive Pulmonary Disease (COPD) are common chronic respiratory conditions characterized by airflow limitation. Although they may share overlapping clinical features, their underlying pathophysiology, disease course, and management strategies differ substantially.^[1] Accurate differentiation between asthma and COPD is crucial to ensure correct diagnosis, appropriate treatment selection, and effective patient education, as misclassification can lead to suboptimal outcomes.

Asthma is a complex, chronic inflammatory disease of the airways, with etiology and onset driven by a multifaceted interplay of genetic predisposition and environmental factors.  Asthma most often begins in childhood, a time when the immune system is still developing. However, some individuals do not experience symptoms until later in life, a condition referred to as adult-onset asthma.^[1][2]

Similar to asthma, COPD is mainly caused by genetic and environmental factors. The main environmental risks include tobacco smoking and exposure to toxic particles. The most common known genetic risk factor for COPD is the mutation in the SERPINA1 gene that leads to α-1 antitrypsin deficiency.  In addition, several other genetic variants have been linked to reduced lung function and increased COPD risk, though their individual effects are generally small.^[3]

Asthma is primarily driven by eosinophilic inflammation in the larger airways, leading to airway hyperresponsiveness and airflow obstruction that is usually reversible, and is commonly associated with allergies. In contrast, COPD is characterized by neutrophilic inflammation affecting the small airways and lung tissue, leading to emphysema and excess mucus production, and it typically develops in older individuals with a history of smoking.^[9] Furthermore, in contrast to asthma, the airway obstruction in COPD is mostly irreversible. The primary distinctions between the two conditions lie in the type of inflammatory cells involved, whether airflow obstruction is reversible, and the dominant triggers, such as allergens in asthma and smoking or pollution in COPD.^[1]

Figure 1: Pathophysiology & Inflammatory Profiles of Asthma, COPD & ACO.^[4]

The cornerstone of asthma treatment remains inhaled corticosteroids (ICS), often combined with a long-acting beta-agonist (LABA).^[8]

• Controller: ICS-LABA combination tailored to severity. Low-dose ICS formoterol must be taken when symptoms occur or before exercise.
• Reliever: Low-dose ICS-formoterol as needed (preferred over SABA alone due to lower exacerbation risk).

Using low-dose ICS-formoterol as-needed reduces exacerbations and improves asthma control (GINA, 2025).

According to the Global Initiative for Asthma (GINA) 2025, two treatment tracks are recommended: Track 1, which uses ICS-formoterol as the preferred reliever, and Track 2, which uses a short-acting β₂-agonist (SABA) reliever together with daily inhaled corticosteroids (ICS).^[6]  

Management now uses the ABE classification rather than the ABCD tool, focusing on symptom burden and exacerbation risk.

• Initial therapy: Long-Acting Muscarinic Antagonists (LAMA) or LABA monotherapy; dual bronchodilation (LABA + LAMA) for persistent symptoms.
• ICS use: Reserved for patients with frequent exacerbations and blood eosinophils of > 300 cells/μL or more.

"ICS should not be used in COPD unless the patient has a history of exacerbations and blood eosinophils more than or equal to >300 cells/μL" (GOLD, 2026).

The use of inhaled corticosteroids (ICS) in COPD should be individualized based on exacerbation history and blood eosinophil count, as recommended by the GOLD guidelines.  Patients with eosinophil counts ≥300 cells/μL are most likely to benefit; those with 100–300 cells/μL may be considered for ICS based on exacerbation frequency, and those with <100 cells/μL are unlikely to benefit.^[7]

Asthma-COPD Overlap (ACO) refers to patients presenting with persistent airflow limitation and clinical features characteristic of both asthma and COPD. While not classified as a separate disease entity, GINA 2025 emphasizes the importance of recognizing ACO to tailor therapy and reduce treatment-related risks.^[6]

Start treatment with inhaled corticosteroids (ICS) due to the asthma component, especially if the patient has a history of asthma, atopy, or elevated eosinophils (≥300 cells/μL), as recommended in GINA 2025 and GOLD 2026.

Add long-acting bronchodilators (LABA and/or LAMA) based on symptom severity, airflow limitation, and exacerbation risk, as outlined in both GINA and GOLD.^[6][7]

In addition, blood eosinophil count is a useful biomarker to guide ICS use—patients with eosinophils ≥300 cells/μL are more likely to benefit, while those with <100 cells/μL may not.^[7]

Asthma:

• Educate on allergen avoidance, adherence to ICS, and correct inhaler use.^[6]
• Periodic assessment with spirometry and symptom control tools.
• Spirometry Assessments:

1. At Diagnosis: Perform spirometry to confirm the diagnosis and establish baseline lung function.
2. Post-Treatment Initiation: Repeat spirometry after 3–6 months of starting or adjusting treatment to determine the patient's personal best lung function.
3. Ongoing Monitoring: Conduct spirometry at least every 1–2 years for most patients. For those at higher risk—such as individuals with frequent exacerbations, persistent symptoms, or severe asthma—more frequent assessments may be necessary.^[8]

COPD:

• Emphasize smoking cessation, vaccination (influenza, pneumococcal), and pulmonary rehabilitation.
• Use tools like CAT or mMRC scores to monitor disease impact (GOLD, 2026).^[7]

COPD Assessment Test (CAT): An 8-item questionnaire evaluating the impact of COPD on a patient's health status. Scores range from 0 to 40, with higher scores indicating a greater impact.

Modified Medical Research Council (mMRC) Dyspnea Scale: A 5-point scale (0–4) assessing the degree of breathlessness during physical activities.

These tools are integral to the ABE assessment framework introduced in GOLD 2026, which categorizes patients based on symptom severity and exacerbation risk.

• Group A: Low symptoms (mMRC 0–1 or CAT <10), low exacerbation risk.
• Group B: High symptoms (mMRC ≥2 or CAT ≥10), low exacerbation risk.
• Group E: Any symptom level with high exacerbation risk (≥2 moderate exacerbations or ≥1 leading to hospitalization).

While asthma and COPD can present with similar respiratory symptoms, their clinical course, inflammatory mechanisms, and treatment paradigms differ substantially. Adhering to GINA 2025 and GOLD 2026 recommendations ensures optimized outcomes, especially in patients with diagnostic ambiguity.

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1. Cukic V, Lovre V, Dragisic D, Ustamujic A. Asthma and Chronic Obstructive Pulmonary Disease (COPD); differences and similarities. Materia Socio Medica [Internet]. 2012 Jan 1;24(2):100. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3633485/

2. Causes and Triggers | NHLBI, NIH [Internet]. NHLBI, NIH. 2024. Available from: https://www.nhlbi.nih.gov/health/asthma/causes

3. Agusti A, Celli BR, Criner G, Halpin D, Montes De Oca M, Ozoh OB, et al. POCKET GUIDE Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease [Internet]. 2026 EDITION. 2026. Available from: https://goldcopd.org/2026-gold-report-and-pocket-guide/

4. Hudler A, Holguin F, Sharma S. Pathophysiology of Asthma-Chronic Obstructive pulmonary Disease overlap. Immunology and Allergy Clinics of North America [Internet]. 2022 Jun 30;42(3):521–32. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10355375/

5. COPD vs. Asthma: What’s the Difference? [Internet]. GoodRx. Available from: https://www.goodrx.com/health-topic/respiratory/copd-vs-asthma-how-are-they-different

6. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention. 2025. Available from: https://ginasthma.org/

7. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for Prevention, Diagnosis and Management of COPD. 2026. Available from: https://goldcopd.org/

8. 2025 GINA Summary Guide - Global Initiative for Asthma - GINA [Internet]. Global Initiative for Asthma - GINA. 2025. Available from: https://ginasthma.org/2025-gina-summary-guide/

9. Fricker M, Lokwani R. COPD: the role of neutrophils in inflammation, pathophysiology, and as drug targets. Clinical Science [Internet]. 2025 Oct 1;139(20):1199–214. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC12687445/

10. Çolak Y, Afzal S, Nordestgaard BG, Lange P. Characteristics and Prognosis of Never-Smokers and Smokers with Asthma in the Copenhagen General Population Study. A Prospective Cohort Study. American Journal of Respiratory and Critical Care Medicine [Internet]. 2015 Apr 27;192(2):172–81. Available from: https://doi.org/10.1164/rccm.201502-0302oc

11. Seretide Prescribing Information Available from:

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Written By

Tasnim Jaman Raisa

Pharmacist

Reviewed By

Dr Jessica Kaur

Doctor