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KembaraXtra-Medicine – Asthma–COPD Overlap (ACO)
Asthma–COPD overlap (ACO) is a recognized clinical entity describing patients—often current or former smokers—who have chronic obstructive pulmonary disease (COPD) but also share important inflammatory and clinical features of asthma. Compared with COPD alone, ACO tends to be a more severe phenotype, with greater symptom burden and worse overall outcomes. ACO may be described as asthma with partially reversible airflow obstruction (with or without emphysema or reduced diffusing capacity) or as COPD with emphysema accompanied by reversible or partially reversible airflow obstruction (with or without allergies or reduced diffusing capacity). Because patients present with different patterns—such as COPD with eosinophilia, severe asthma in smokers, neutrophilic-predominant asthma, or asthma that has become largely irreversible due to airway remodeling—the term “ACO” is preferred over the older “ACOS” to reflect this heterogeneity.
ACO is discussed using overlapping ICD-10 codes including asthma (J45), chronic bronchitis (J42), emphysema (J43), COPD (J44, J44.9), and other overlap syndromes (M35.1). Epidemiologically, COPD prevalence varies across regions, and asthma affects tens of millions of people in the U.S. Bronchial hyperresponsiveness is common in COPD and bronchodilator reversibility can also be seen in COPD, which complicates diagnosis. Across studies, patients identified as having ACO generally demonstrate worse lung function, more respiratory symptoms, more frequent exacerbations, higher health-care utilization, and lower quality of life than those with asthma or COPD alone. Reported prevalence of ACO among adults with obstructive airway disease is commonly estimated around 15%–25%, with higher prevalence in older adults and in those with more severe disease. Some data suggest mortality in ACO is similar to COPD and worse than asthma alone.
Risk factors for ACO include cigarette smoking and atopy, along with older age, allergies, higher BMI, childhood asthma history, and respiratory infections such as rhinovirus or influenza. While no definitive genetic basis is established, some research has identified variants (including in GPR65) associated with ACO in certain populations. Clinically, patients may have wheezing, dyspnea, chest tightness, chronic cough (often productive), reduced exercise tolerance, recurrent respiratory infections, and episodic symptoms triggered by allergens, odors, or temperature changes. Physical examination can be normal or may show wheezing or rhonchi; in more severe cases, decreased air entry and accessory muscle use may appear, and signs such as the Hoover sign can suggest hyperinflation.
Diagnosis is considered when a patient demonstrates a mixed pattern of asthma-like and COPD-like features. A practical approach relies on objective confirmation of persistent airflow obstruction plus evidence of reversibility or airway hyperresponsiveness. Patients should have a reduced post-bronchodilator FEV₁/FVC (below the lower limit of normal or <0.7), along with either bronchodilator reversibility (increase in fev₁ or fvc by ≥200 ml and ≥12%) airway hyperresponsiveness demonstrated a positive methacholine challenge. because can occur copd symptoms overlap substantially, aco remains clinical diagnosis supported the pattern of symptoms, smoking history, asthma />llergy features, and pulmonary function testing rather than a single definitive test.
The differential diagnosis includes asthma, COPD, central airway obstruction, bronchiectasis, heart failure, and obliterative bronchiolitis. Workup typically includes spirometry with bronchodilator testing, and sometimes airway provocation testing. Additional supportive testing may include ABG (especially in severe disease), CBC with eosinophils, total IgE, sputum assessment, allergy testing, and peak flow monitoring. Imaging with chest x-ray or chest CT may help evaluate emphysema, alternative diagnoses, or complications, and ECG may be used when cardiac disease is suspected.
Management is challenging because many ACO patients have been excluded from major asthma and COPD drug trials, leaving limited high-quality evidence to guide therapy. A central reason to identify ACO is the potential for different responses to inhaled corticosteroids (ICS), particularly in patients with eosinophilic inflammation. Nonpharmacologic management includes smoking cessation, avoidance of triggers, inhaler technique education, and pulmonary rehabilitation; vaccination and oxygen supplementation may also be appropriate depending on severity. Pharmacologic treatment is generally symptom-directed, with bronchodilators used for dynamic obstruction and hyperinflation, while ICS is often included when asthma-like features or eosinophilia are present. Current guidance discourages using LABA and/or LAMA without ICS when asthma features are present, due to safety concerns and the need to treat underlying airway inflammation. Combination ICS/LABA therapy has evidence of benefit in some ACO populations, and observational data suggest improved outcomes compared with bronchodilator therapy alone in patients with overlapping asthma and COPD histories. Selected patients with allergic features may respond to biologic therapy such as omalizumab, with some observational data showing improvements similar to those seen in asthma without ACO.
Long-term care emphasizes earlier recognition in smokers or former smokers with partially reversible obstruction and progressive exercise intolerance, along with comprehensive management of comorbidities that worsen respiratory symptoms—such as GERD, chronic aspiration, vocal cord dysfunction, and nasal/sinus disease. Cardiovascular evaluation is especially important given higher cardiovascular risk in this population. Referral to a specialist is appropriate when symptoms or exacerbations persist, diagnosis remains uncertain, atypical features appear (e.g., hemoptysis, weight loss, fevers, night sweats, suspected bronchiectasis), comorbidities complicate management, or there is poor response to standard therapy. Prevention strategies focus on smoking cessation and minimizing exposure to triggers and irritants.
Asthma–COPD overlap (ACO) is a recognized clinical entity describing patients—often current or former smokers—who have chronic obstructive pulmonary disease (COPD) but also share important inflammatory and clinical features of asthma. Compared with COPD alone, ACO tends to be a more severe phenotype, with greater symptom burden and worse overall outcomes. ACO may be described as asthma with partially reversible airflow obstruction (with or without emphysema or reduced diffusing capacity) or as COPD with emphysema accompanied by reversible or partially reversible airflow obstruction (with or without allergies or reduced diffusing capacity). Because patients present with different patterns—such as COPD with eosinophilia, severe asthma in smokers, neutrophilic-predominant asthma, or asthma that has become largely irreversible due to airway remodeling—the term “ACO” is preferred over the older “ACOS” to reflect this heterogeneity.
ACO is discussed using overlapping ICD-10 codes including asthma (J45), chronic bronchitis (J42), emphysema (J43), COPD (J44, J44.9), and other overlap syndromes (M35.1). Epidemiologically, COPD prevalence varies across regions, and asthma affects tens of millions of people in the U.S. Bronchial hyperresponsiveness is common in COPD and bronchodilator reversibility can also be seen in COPD, which complicates diagnosis. Across studies, patients identified as having ACO generally demonstrate worse lung function, more respiratory symptoms, more frequent exacerbations, higher health-care utilization, and lower quality of life than those with asthma or COPD alone. Reported prevalence of ACO among adults with obstructive airway disease is commonly estimated around 15%–25%, with higher prevalence in older adults and in those with more severe disease. Some data suggest mortality in ACO is similar to COPD and worse than asthma alone.
Risk factors for ACO include cigarette smoking and atopy, along with older age, allergies, higher BMI, childhood asthma history, and respiratory infections such as rhinovirus or influenza. While no definitive genetic basis is established, some research has identified variants (including in GPR65) associated with ACO in certain populations. Clinically, patients may have wheezing, dyspnea, chest tightness, chronic cough (often productive), reduced exercise tolerance, recurrent respiratory infections, and episodic symptoms triggered by allergens, odors, or temperature changes. Physical examination can be normal or may show wheezing or rhonchi; in more severe cases, decreased air entry and accessory muscle use may appear, and signs such as the Hoover sign can suggest hyperinflation.
Diagnosis is considered when a patient demonstrates a mixed pattern of asthma-like and COPD-like features. A practical approach relies on objective confirmation of persistent airflow obstruction plus evidence of reversibility or airway hyperresponsiveness. Patients should have a reduced post-bronchodilator FEV₁/FVC (below the lower limit of normal or <0.7), along with either bronchodilator reversibility (increase in fev₁ or fvc by ≥200 ml and ≥12%) airway hyperresponsiveness demonstrated a positive methacholine challenge. because can occur copd symptoms overlap substantially, aco remains clinical diagnosis supported the pattern of symptoms, smoking history, asthma />llergy features, and pulmonary function testing rather than a single definitive test.
The differential diagnosis includes asthma, COPD, central airway obstruction, bronchiectasis, heart failure, and obliterative bronchiolitis. Workup typically includes spirometry with bronchodilator testing, and sometimes airway provocation testing. Additional supportive testing may include ABG (especially in severe disease), CBC with eosinophils, total IgE, sputum assessment, allergy testing, and peak flow monitoring. Imaging with chest x-ray or chest CT may help evaluate emphysema, alternative diagnoses, or complications, and ECG may be used when cardiac disease is suspected.
Management is challenging because many ACO patients have been excluded from major asthma and COPD drug trials, leaving limited high-quality evidence to guide therapy. A central reason to identify ACO is the potential for different responses to inhaled corticosteroids (ICS), particularly in patients with eosinophilic inflammation. Nonpharmacologic management includes smoking cessation, avoidance of triggers, inhaler technique education, and pulmonary rehabilitation; vaccination and oxygen supplementation may also be appropriate depending on severity. Pharmacologic treatment is generally symptom-directed, with bronchodilators used for dynamic obstruction and hyperinflation, while ICS is often included when asthma-like features or eosinophilia are present. Current guidance discourages using LABA and/or LAMA without ICS when asthma features are present, due to safety concerns and the need to treat underlying airway inflammation. Combination ICS/LABA therapy has evidence of benefit in some ACO populations, and observational data suggest improved outcomes compared with bronchodilator therapy alone in patients with overlapping asthma and COPD histories. Selected patients with allergic features may respond to biologic therapy such as omalizumab, with some observational data showing improvements similar to those seen in asthma without ACO.
Long-term care emphasizes earlier recognition in smokers or former smokers with partially reversible obstruction and progressive exercise intolerance, along with comprehensive management of comorbidities that worsen respiratory symptoms—such as GERD, chronic aspiration, vocal cord dysfunction, and nasal/sinus disease. Cardiovascular evaluation is especially important given higher cardiovascular risk in this population. Referral to a specialist is appropriate when symptoms or exacerbations persist, diagnosis remains uncertain, atypical features appear (e.g., hemoptysis, weight loss, fevers, night sweats, suspected bronchiectasis), comorbidities complicate management, or there is poor response to standard therapy. Prevention strategies focus on smoking cessation and minimizing exposure to triggers and irritants.
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