Asthma‑COPD Overlap (ACO) is a clinical entity that sits between chronic obstructive pulmonary disease (COPD) and asthma, sharing features of both airway obstruction and inflammation. Recognising ACO matters because patients often experience more frequent exacerbations, a higher symptom burden, and a need for a blended therapeutic approach.
Both COPD and asthma impact airflow, but they arise from different pathways. COPD, a disease most common in adults over 40, is driven largely by smokingthe inhalation of toxic particles that cause irreversible airway narrowing. Asthma, on the other hand, often begins in childhood and is linked to allergen exposuresuch as pollen, dust mites, or pet dander, triggering reversible bronchoconstriction. When a patient shows signs of both-persistent airflow limitation plus a strong eosinophilic response-they may fall into the ACO category.
Inflammation is the common thread. In COPD, neutrophilic inflammationdominates, producing mucus hypersecretion and airway remodeling. Asthma is characterised by eosinophilic inflammationthat leads to airway hyper‑responsiveness. ACO patients often display a mixed pattern: elevated eosinophils alongside neutrophils, making diagnosis trickier but also opening doors to targeted therapies such as inhaled corticosteroids combined with long‑acting bronchodilators.
Because symptoms blur, clinicians rely on objective testing to separate pure COPD, pure asthma, and ACO.
Spirometrymeasures forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) remains the gold standard. A post‑bronchodilator FEV1/FVC ratio below 0.70 confirms airflow obstruction. In asthma, this ratio often improves by >12% after bronchodilator; in COPD, the change is modest. ACO patients show a partial reversal-enough to hint at an asthmatic component.
Blood eosinophil countabove 300 cells/µL suggests steroid‑responsive inflammation and helps guide inhaled corticosteroid (ICS) use. High neutrophil countor C‑reactive protein (CRP) points to COPD‑dominant disease. Chest CT can reveal emphysematous changes typical of COPD, while airway wall thickening aligns with asthma.
Effective treatment blends the pillars of both diseases:
For patients who continue to exacerbate, biologic agents targeting interleukin‑5 (IL‑5) or IgE can be considered, mirroring asthma‑specific therapies.
| Feature | COPD | Asthma | ACO |
|---|---|---|---|
| Typical onset age | ≥40 years | Childhood-early adulthood | Mid‑life, often with prior asthma |
| Primary cause | Smoking / occupational pollutants | Allergen exposure, atopy | Combined smoking and atopy |
| Inflammation type | Neutrophilic | Eosinophilic | Mixed neutrophilic/eosinophilic |
| FEV1/FVC reversibility | ≤12% post‑bronchodilator | >12% post‑bronchodilator | Partial (5‑15%) |
| Core treatment | LAMA ± LABA | ICS+LABA | LAMA+LABA+ICS (if eosinophils high) |
Patients with ACO tend to have a higher rate of hospitalisation compared with those having pure COPD or asthma. Cardiovascular disease, osteoporosis, and anxiety/depression are common companions, driven by chronic systemic inflammation and frequent steroid bursts. Early detection of the overlap phenotype enables clinicians to introduce ICS sooner, which can curb exacerbation frequency and potentially slow lung function decline.
Understanding ACO opens doors to several adjunct topics that deserve a deeper dive:
Readers interested in the broader landscape might explore topics such as "Management of Chronic Respiratory Disease" (a broader cluster) or "Differentiating COPD Phenotypes" (a narrower, more specific article).
Both COPD and asthma cause airflow trouble, but when they intertwine the result is a distinct, often more severe picture. Recognising the Asthma‑COPD overlap enables a more nuanced treatment plan, better symptom control, and a chance to halt rapid lung function loss.
ACO is a clinical syndrome where a patient exhibits features of both chronic obstructive pulmonary disease and asthma, such as persistent airflow limitation with a partial bronchodilator response and mixed inflammatory patterns.
Diagnosis combines spirometry (showing obstructive defect with some reversibility), blood eosinophil counts, smoking history, and symptom patterns. Imaging and response to inhaled corticosteroids also help differentiate ACO from pure COPD or asthma.
Yes. The typical regimen includes a long‑acting bronchodilator (LABA or LAMA) plus an inhaled corticosteroid if eosinophil levels are high. Some may benefit from biologic agents that target eosinophilic inflammation.
Absolutely. Smoking accelerates COPD‑type changes and can worsen the overlap picture. Quitting smoking is a cornerstone of management for any ACO patient.
Prognosis depends on how well the disease is controlled. Regular use of appropriate inhalers, pulmonary rehab, and avoiding triggers can reduce exacerbations and improve survival compared with untreated or misdiagnosed cases.
Emma Rauschkolb
September 25, 2025 AT 17:05Wow, the mechanistic interplay between eosinophilic‑driven bronchial hyper‑reactivity and neutrophil‑mediated airway remodeling is truly fascinating 🤓. The ACO phenotype essentially epitomizes a hybrid immunopathology, blending Th2 cytokine cascades with innate neutrophilic infiltration. Clinicians should therefore calibrate their therapeutic algorithms to target both IL‑5 pathways and mucolytic strategies. Ultimately, precision‑medicine biomarkers will dictate outcomes in this convoluted landscape.