Chronic Obstructive Pulmonary Disease (COPD) and Asthma: Similarities and Differences
Updated: July 2015
Originally Posted: July 2009
Updated by: Bradley Chipps, MD
Captial Allergy and Respiratory Disease Center
Folsom, CA, USA
|Raquel Watkins, MD
Assistant Professor, Allergy and Immunology
Wake Forest University School of Medicine
Winston Salem, North Carolina USA
|Diane Laber, MD
Fellow, Allergy and Immunology
Wake Forest University School of Medicine
Winston Salem, North Carolina USA
|Stephen P. Peters, MD, PhD
Professor of Medicine and Pediatrics
Associate Director, Center for Human Genomics
Wake Forest University School of Medicine
Winston Salem, North Carolina USA
Definition of COPD and Asthma
According to the American Thoracic Society (ATS)/ European Respiratory Society (ERS) along with the Global Initiative for Obstructive Lung Disease (GOLD),(1) chronic obstructive pulmonary disease (COPD) is a “preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with abnormal inflammatory response of the lung to noxious particles or gasses.”
Asthma is similarly characterized by airflow obstruction; however, according to the National Asthma Education and Prevention Program (NAEPP) and the Global Initiative for Asthma,(2) asthma is additionally typified by variable and recurring symptoms, bronchial hyperresponsiveness and underlying inflammation of the airways.
The severity of airways obstruction in COPD is best classified with spirometry.(1,3) COPD is diagnosed on the basis of a post-bronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) value of <70. In addition post-bronchodilator FEV1 cutoffs of <80%, 50% and 30% of predicted values are used to further stage disease severity (Table 1).(1)
Asthma severity is determined before treatment with controller medications. Asthma control is determined on the basis of both impairment and risk.(2) Impairment is a function of the frequency of daytime and nocturnal symptoms, short-acting β2-agonist (SABA) use, the degree to which normal activity is affected and lung function. Risk is defined by the frequency of exacerbations requiring oral corticosteroid (OCS) use.
Patients are classified as having intermittent or persistent (mild, moderate or severe) asthma depending on the degree of impairment and risk. The severity of asthma is determined on the basis of which of the following factors is the worst: daytime or nocturnal symptoms, rescue SABA use, lung function or exacerbation frequency.
Patients with intermittent asthma have minimal impairment and risk. They experience daytime symptoms ≤2 days/week and nocturnal awakenings ≤2 times/month, and these symptoms do not interfere with normal activity. The frequency of SABA use is ≤2 days/week. Lung function is preserved, FEV1 is >80% of predicted and normal between exacerbations, and FEV1/FVC is normal. These patients typically have no exacerbations or only one exacerbation per year that requires OCS use.
Mild persistent asthma is characterized by >2 daytime symptoms/week, but not daily, and night time symptoms 3-4 times/month. SABA use occurs >2 times/week, but not daily, and not more than once on any day. Patients with mild persistent asthma report minor limitations in activity, have an FEV1 >80% of predicted and have a normal FEV1/FVC.
Patients with moderate persistent asthma experience daytime symptoms daily and nocturnal symptoms more than once a week, but not nightly. They use a SABA daily and express some limitation in exercise tolerance. FEV1 is >60%, but <80% of predicted, and FEV1/FVC is reduced by > 5% below normal.
Patients with severe persistent asthma experience daytime and nighttime symptoms daily. They use a SABA several times per day, and their activity is extremely limited. FEV1 is <60% of predicted, and FEV1/FVC is reduced by >5% below normal. All patients with persistent asthma are at high risk of need for hospitalization, emergency department (ED) visits or to experience fatal or near fatal episodes of asthma, and generally report ≥2 exacerbations per year that require OCS use.
Asthma control is evaluated by assessment of impairment and risk domain with equal weight (2). Step up and step down therapy is guided by the most involved domain (2). It is important to use a validated control instrument for accurate assessment (20). Very poorly controlled asthma and recent exacerbations are major predictors of future exacerbations (21).
Symptoms and Signs of COPD and Asthma
COPD symptoms differ on the basis of disease severity (Table 1). Most patients with COPD usually first develop a chronic productive cough. However, dyspnea is the hallmark symptom of COPD and usually prompts patients to seek medical care. As disease severity progresses, cough and dyspnea result in decreased exercise tolerance and increased disability. COPD mainly affects the lungs; however, notable systemic effects are also associated with COPD. Patients with COPD often experience changes in their metabolism and in caloric intake. Indeed, 50% of patients with severe disease experience weight loss, which is associated with a poorer prognosis.3 Patients with COPD also develop decreased strength, decreased exercise capacity and a reduced quality of life.3 COPD is associated with an increased risk of cardiovascular disease, respiratory infections, osteoporosis and glaucoma.(3)
Physiologic changes associated with asthma include bronchoconstriction, airway hyperresponsiveness and airway inflammation. Therefore, patients with asthma typically develop wheezing, shortness of breath and cough. Because asthma is also characterized by reversible airway obstruction, its symptoms are intermittent and cover a spectrum from mild-to-severe disease.(4)
Several symptoms overlap in patients with COPD and asthma. Nevertheless, a history of wheezing strongly suggests a diagnosis of asthma, whereas chronic cough productive of sputum is more indicative of COPD.
Causes of COPD and Asthma
Risk factors for both COPD and asthma can be categorized as host and environmental factors. The genetic risk factor that has been most closely linked to COPD is a rare deficiency of α1-antitrypsin.(1) Because only 15% of smokers go on to develop COPD, genetics and other susceptibility factors are thought to play an important role. Polymorphisms in genes related to proteases, antioxidants and inflammation have been found to relate to some of the features characteristic of COPD. Polymorphisms in any of three classes of proteases, the serine proteases, cysteine proteases, and matrix metalloproteinases may lead to development of COPD.15 Antioxidant enzymes known to be present in the airways include glutathione-S-transferase, superoxide dismutase and catalase. Cigarettes smoke causes a large number of free radicals, and alterations in these enzymes may also raise susceptibility to COPD.(15) Many pro- and anti-inflammatory mediators, including TNF-a, IL-1, IL6 and TGF-ß are also felt to be important in the development of COPD.(15) A candidate gene—the promoter polymorphism-1111 in the interleukin-13 gene(5)—was identified in populations with either COPD or asthma. This finding provides additional evidence in support of a genetic susceptibility to COPD and asthma.
Host factors for asthma are not as well delineated, and the genetics of asthma continue to be investigated. However, one theory is that overexpression of T-helper 2 lymphocyte (Th2) allergic cells or underexpression of Th1 non-allergic cells contribute to atopy and asthma. The “hygiene hypothesis” has also been postulated, i.e., that particular infections early in life, exposure to siblings or other children through childcare, decreased use of antibiotics, and “country living” (exposure to farming and anthroposophic lifestyles) are associated with a Th1 response and a decreased incidence of asthma.(2) Obesity, family history, atopy (including food sensitization), exposure to heavy traveled roads, environmental tobacco exposure and male sex are also risk factors for asthma in children. Infection with RSV in childhood has also been shown to have a clear relationship to asthma, but it is unclear if RSV infection leads to asthma, or if children with asthma are more susceptible to RSV infection.(16)
Infection with rhinovirus especially in children who have a persistent allergic diathesis is the more common infection to lead to airway hyperactivity (22).
Once the components of control (impairment and risk) are assessed, asthma can be classified as well controlled, not well controlled or very poorly controlled. Patients with well controlled asthma experience daytime symptoms ≤2days/week, experience nocturnal awakenings ≤2 times/month, use SABAs <2 days/week, have peak flow measurements >80% of the predicted personal best and have scores >20 on ACT. Well controlled asthmatics generally have at least one exacerbation per year. Patients with well controlled asthma should be maintained on their current regimen and undergo a reduction in treatment if they can maintain their level of control for ≥3 months. Patients with not well controlled asthma experience daytime symptoms >2days/week, experience nocturnal awakenings 1-3 times/week, use SABAs >2 days/week, have peak flow measurements 60-80% of the predicted personal best and have ACT score of 16-19. Normal activity is limited in these patients. Treatment involves a one-step increase in pharmacotherapy (see Tables 2 and 3) and revaluation in 2-6 weeks. Patients with very poorly controlled asthma experience daytime symptoms daily, experience nocturnal awakening ?4 times/week, use SABAs several times per day, have peak flow measurements <60% of predicted personal best, and have ACT scores ≤15. Activity is extremely limited in these patients. Therapy involves a one- to two-step increase, consideration of a short course of OCS and reevaluation in 2 weeks. Both not well controlled and very poorly controlled asthmatics usually have ≥2 exacerbations that require OCS use per year. Loss of lung function should be monitored long-term at all levels of control, and side effects associated with medication use can vary from none to significant and should be assessed at every visit.
Environmental factors that serve as risk factors for COPD include inhalation exposures to cigarette smoke, occupational dusts and chemicals and indoor and outdoor pollution. A history of severe respiratory infection during childhood is associated with reduced lung function in adulthood. Additionally, a lower socioeconomic status (SES) is associated with the development of COPD; however, it is not clear whether this association is due to SES or to confounders and exposures commonly linked to lower SES, such as a crowded living environment or poor nutrition.(1)
Two environmental factors have been consistently associated with the development of asthma: sensitization to indoor and outdoor aeroallergens and a history of viral respiratory infections, in particular, rhinovirus infections.(6) Other potential environmental irritants include tobacco smoke and air pollution. Maternal smoking during pregnancy is also a risk factor for the development of asthma. Many children of mothers who smoked during pregnancy wheeze during the first 2-3 years of life but have only a few episodes of wheezing or do not wheeze after age 3 years (transient wheezers). Risk factors for transient wheezing are maternal smoking during pregnancy, younger mothers and smaller airways.6 Other risk factors for the development of asthma are included in the Asthma Predictive Index, which is described in the Tucson Children’s Respiratory Study.6 Having either a parent with asthma or a personal history of atopic dermatitis or two of the following conditions—peripheral blood eosinophilia, physician-diagnosed allergic rhinitis, or wheezing for reasons other than a cold—is associated with more persistent asthma symptoms through the age of 13 years. Further analysis of this patient population indicates that onset of symptoms at 6 years of age, persistent wheezing in early life, sensitization to A. alternata, low airway function at 6 years, and bronchial hyperresponsiveness at 6 years are risk factors for persistence of asthma at age 22. Asthma remittance at age 22 was more common in men than in women, and age at diagnosis was linearly related to FEV1 to FVC ratio at age 22.(17)
Prevention of COPD and Asthma
COPD is a preventable disease. Although primary prevention hinges on tobacco cessation strategies, secondary prevention of COPD centers on early diagnosis, risk factor modification and treatment. However, early diagnosis of COPD is often delayed. In 2002, the third National Health and Nutrition Examination Survey (NHANES III)7 reported that approximately 24 million adults in the USA have evidence of impaired lung function on spirometry; however, only about 50% of these patients have physician-diagnosed COPD, most of which is moderately advanced disease. At this late stage of disease, only tertiary prevention, aimed at preventing the complications of COPD, is effective. Therefore, primary and secondary prevention strategies need to be improved.
Better prevention of COPD can be achieved through compliance with guidelines. Numerous guidelines exist to assist physicians in early diagnosis, prevention of disease progression and management of COPD, including those of GOLD,(1) the American Thoracic Society,(8) the National Collaborating Center for Chronic Conditions and the Canadian Thoracic Society.(10)
Tobacco cessation is of paramount importance for preventing COPD and limiting its progression. GOLD reports that tobacco cessation is the single most clinically effective and cost-effective intervention in COPD.(1) Use of the 5 A’s Strategy—“ask, assess, advise, assist and arrange”—in conjunction with the use of nicotine patches, bupropion, varenicline and telephone follow-up have been shown to be effective in tobacco cessation. Both the influenza and pneumococcal vaccines are recommended for patients with COPD.
Identifying and reducing exposure to risk factors is critical in asthma prevention. Measures should include the prevention of allergic sensitization during the perinatal period.(11) For example, exclusive breast-feeding during the prenatal period has been associated with lower asthma rates in childhood,(11) and exposure to tobacco smoke prenatally and postnatally is associated with deleterious effects on lung development and wheezing in early childhood.
After allergic sensitization has occurred in the setting of asthma, prevention of exposure to known triggers can prevent exacerbations. Common indoor triggers include tobacco smoke, dust mites, furry animals, cockroaches and fungi. Outdoor triggers include aeroallergens and air pollutants. Occupational exposures should also be minimized. Allergen-specific immunotherapy may play a role in preventing the development of asthma in atopic children.(12)
Asthmatics with a history of nasal polyps and aspirin or nonsteroidal anti-inflammatory drug sensitivity should be counseled regarding the risk of severe, fatal exacerbations from the use of these drugs and in certain cases, desensitization may be beneficial. Co-morbidities, such as allergic bronchopulmonary aspergillosis, rhinosinusitis and gastroesophageal reflux, should be considered and treated in patients with poorly controlled asthma. The Centers for Disease Control and Prevention recommend inactivated influenza vaccine for patients (aged 6 months to adult) who have asthma.
Numerous guidelines are also available to aid physicians and other healthcare professionals to better prevent and manage asthma. Two frequently referenced guidelines are those of the NAEPP(2) and the Global Initiative for Asthma (GINA).(11)
Treatment of COPD and Asthma
Treatment of COPD encompasses the use of various medications (in the form of glucocorticoids, β2-agonists, anticholinergics and methylxanthines, used either singly or in combination). Non-pharmacological interventions include health education on managing chronic illnesses, pulmonary rehabilitation with focus on physical and dietary measures, patient education, and smoking cessation intervention programs.
Treatment varies depending on symptoms and disease severity. All patients, regardless of disease severity, should be offered the yearly influenza vaccine. Pneumococcal vaccines should be offered to patients with COPD who are 65 years and older and to patients with COPD younger than 65 who have an FEV1 of <40%. As needed, short-acting bronchodilators can also be used during any stage of illness (from mild to very severe) to improve symptoms. However, regular treatment with one or more long-acting bronchodilator (when needed) should be considered in patients with moderate-to-very-severe disease. In patients with severe COPD and frequent exacerbations, inhaled corticosteroids can reduce exacerbations. The Towards a Revolution in COPD Health (TORCH) trial(13) was a randomized, double-blinded trial involving >6000 patients with COPD in which the effectiveness of combination therapy with salmeterol (50 μg) plus fluticasone propionate (500 μg) given twice per day was compared with that of placebo, salmeterol alone or fluticasone propionate alone. TORCH showed a significant reduction in exacerbations and improvements in health status and spirometric measurements in the patients who received combination therapy compared with those who received placebo. TORCH also showed a 17.5% lower risk of death in the COPD patients who received combination therapy than in those who received placebo (P=0.052).
Treatment guidelines are shown in Table 3 Gina Box 7. Equal severity of risk are determined by post bronchodilator FEV1 or exacerbation history, supplemented by a validated symptom such as mMRC tool (Table 4). The role of ICS must be carefully evaluated in patients with COPD. In patients who do not have evidence of Th2 mediated airway inflammation, withdrawal of ICS with persistence of LABA + LAMA may not lead to significant changes in health status, dyspnea or exacerbation (22).
Long term oxygen therapy improves mortality in COPD patients with respiratory failure but has limited effectiveness in less severe patients. It has also shown positive effects on quality of life, but not on COPD exacerbations.(18,19)
GINA(11) proposes five interrelated components of therapy for the management of asthma: 1) a patient-physician partnership (e.g., asthma action plan); 2) identification and reduction of exposure to risk factors; 3) assessment, treatment and follow-up for asthma; 4) management of exacerbations; and 5) individualized care during pregnancy and for rhinosinusitis and nasal polyps, gastroesophageal reflux, aspirin-exacerbated respiratory disease, and anaphylaxis. Pharmacotherapy for asthma is well delineated in the six-step approach recommended by the NAEPP(2) (Table 2) as well as the five step approach recommended by GINA(11). (Table 3 Box 7).
Epidemiology of COPD and Asthma
COPD is the fourth leading cause of death in the USA.(3) In 2001, the World Health Organization reported that COPD was the fifth leading cause of death in high-income countries and the sixth leading cause of death in low- and middle-income countries.
COPD usually presents in middle age, is slowly progressive and is associated with history of cigarette smoking in 80-90% of patients.(3,10) Patients usually present with a chronic productive cough, and atopy is not a frequent finding. Clinical symptoms are slowly progressive, and airflow limitation is only partially reversible after tobacco cessation and with bronchodilator use. T lymphocytes, with macrophages and neutrophils, are the predominant inflammatory cell types.(1,3)
In 2005, an estimated 22.2 million Americans had asthma: 6.5 million children and 15.7 million adults.(14) The public health impact of asthma is significant. In 2003, asthma accounted for 1.4 deaths/100,000 persons in the USA.(14) According to the National Center for Health Statistics,(14) in 2003, children between the ages of 5 and 17 years with a history of at least one asthma attack in the previous year accounted for 12.8 million missed school days, and adults with a history of at least one asthma attack in the previous year accounted for 10.1 million missed workdays.
GINA estimates that the prevalence of asthma is 300 million persons worldwide. The World Health Organization estimates that 1% of the global disease burden, 15 million disability-adjusted life years, is attributable to asthma. Asthma accounts for 250,000 deaths annually worldwide.(11) Mortality does not correlate with prevalence since countries such as Wales and New Zealand have the lowest asthma-related mortality rate, despite a high prevalence of disease.
The epidemiology of asthma differs from that of COPD in that asthma usually presents early in childhood, and atopy is much more prevalent in asthma than in COPD. Asthma is usually not progressive, although exacerbations can be intermittent and variable. Eosinophils and lymphocytes are the major inflammatory cells in asthma. With appropriate therapy, asthma is completely reversible in most patients.(3)
Asthma COPD Overlap Syndrome
The diagnosis of ACOS syndrome has been defined by GINA document published in May 2014. This can be a very problematic diagnosis, particularly in smokers and older adults. ACOS syndrome is identified by features shared by both asthma and COPD. The evaluation requires a thorough history of the patient’s chronic airways disease, pulmonary function testing and also testing to determine if Th2 mediated airway inflammatory pattern is present, which would suggest a response to inhaled steroid. Table 1 defines severity, and in table 2A the usual features of asthma, COPD and the ACOS syndrome are elaborated. Table 3 gives better definition of expected spirometric measures in the three disease states. Table 4 is a stepwise approach to the definition of patients with chronic airflow limitation. Table 5 allows for specialized investigations to be employed to distinguish asthma and COPD.
Table 1: GOLD1 classification of COPD
|Stages of COPD||Spirometry findings||Symptoms|
|Stage 1: Mild||FEV1/FVC <70
FEV1 ≥80% of predicted
|Possible chronic cough and sputum production|
|Stage 2: Moderate||FEV1/FVC <70
50% ≤ FEV1 < 80% of predicted
|Shortness of breath on exertion
Possible chronic cough and sputum production
|Stage 3: Severe||FEV1/FVC <70
30% ≤ FEV1 < 50% of predicted
|Shortness of breath
Reduced exercise tolerance
|Stage IV: Very severe||FEV1/FVC <70
FEV1 <30% of predicted or FEV1 <50% of predicted plus chronic respiratory failure
Elevation of jugular venous pressure
Pitting ankle edema
Abbreviations: COPD, chronic obstructive pulmonary disease; FEV1, forced expiratory volume in one second; FVC, forced vital capacity; GOLD, Global Initiative for Obstructive Lung Disease.
Table 2: NAEPP2-recommended pharmacotherapy for asthma
|Intermittent asthma||Persistent asthma|
|Step 1||Step 2||Step 3||Step 4||Step 5||Step 6|
Short-acting β2- agonist
Low-dose ICS + LABA or medium-dose ICS
Cromolyn, LTRA, nedocromil or theophylline
Low-dose ICS + LABA or medium-dose ICS
Low-dose ICS + LTRA, theophylline or zileuton
Medium-dose ICS + LABA
Medium-dose ICS + LTRA, theophylline or zileuton
High-dose ICS + LABA
Omalizumab for patients with allergies
High-dose ICS + LABA + OCS
Omalizumab for patients with allergies
Consider subcutaneous allergen immunotherapy for patients with allergic asthma
Abbreviations: ICS, inhaled corticosteroids; LABA, long-acting ?2-agonists; LTRA, leukotriene receptor antagonists; NAEPP, National Asthma Education and Prevention Program; OCS, oral corticosteroids.
Table 3: Box 7. Stepwise Approach to Asthma Treatment 2
Table 4. Global Strategy for the Management of COPD 23
Table 5. Asthma, COPD and Asthma-COPD Overlap Syndrome 24
Current definitions of asthma and COPD, and clinical description of ACOS
AsthmaAsthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symtpoms such as sheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation [GINA2014]
COPDCOPD is a common preventable and treatable disease, characterized by persistant airflow limitation that is usually progressive and associated with enhanced chronic inflammatory responses in the airways and the lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in the individual patients [GOLD2014]21
Asthma-CPOD Overlap Syndrome (ACOS) - a description for clinical useAsthma-CPOD Overlap Syndrome (ACOS) is characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with CPOD. ACOS is therefore identified by the features that it shares with both asthma and CPOD.
Usual features of asthma, COPD and ACOS
|Table 2a. Usual features of ashtma, COPD and ACOS||Table 2b. Features that favor asthma or COPD|
|Feature||Asthma||COPD||ACOS||Favors Asthma||Favors COPD|
|Age of onset||Usually childhood onset but can commence at any age.||Usually > 40 years of age||Usually age ≥ 40 years, but may have had symptoms in childhood or early adulthood||
|Pattern of respiratory symptoms||Symptoms may vary over time (day to day, or over longer periods), often limiting activity. Often triggered by exercise, emotions including laughter, dust or exposure to allergens.||Chronic usually continuous symptoms, particularly during exercise, with 'better' and 'worse' days||Respiratory sympstoms including exertional dyspnea are persistent but variability may be prominent||
|Lung function||Current and/or historical variable airflow limitation, e.g. BD reversibility, AHR||FEV1 may be improved by therapy, but post-BD FEV1/FVC < 0.7 persists||Airflow limitation not fully reversible, but often with current or historical variability||
|Lung function between symptoms||May be normal between symptoms||Persistent airflow limitation||Persistent airflow limitation||
|Past history or family history||Many patients have allergies and a personal history of asthma in childhood, and/or family history of asthma||History of exposure to noxious particles and gases (mainly tobacco smoking and biomass fuels)||Frequently a history of doctor-diagnosed asthma (current or previous), allergies and a family history of asthma, and/or a history of noxious exposures|
|Time course||Often improves spontaneously or with treatment, but may result in fixed airflow limitation||Generally, slowly progressive over years despite treatment||Symptoms are partly but significantly reduced by treatment. Progression is usual and treatment needs are high||
|Chest x-ray||Usually normal||Severe hyperinflation & other changes of COPD||Similar to COPD||
|Exacerbations||Exacerbations occur, but the risk of exacerbations can be considerably reduced by treatment||Exacerbations can be reduced by treatment. If present, comorbidities contribute to impairment||Exacerbations may be more common in COPD but are reduced by treatment. Comorbidities can contribute to impairment.||*Syndromic diagnosis of airways disease: how to use Table 2b
Shaded columns list features that, when present, best distinguish between asthma and COPD. For a patient, count the number of check boses in each column. If three or more boxes are checked for either asthma or COPD, that disgnosis is suggested. If there are similiar numbers of checked boxes in each column, the diagnosis of ACOS should be considered. See Step 2 for more details.
|Typical airway inflammation||Eosinophils and/or neutrophils||Neutrophils in sputum, lymphocytes in airways, may have systemic inflammation||Eosinophils and/or neutrophils in sputum.|
Spirometric measures in asthma, COPD and ACOS
|Normal FEV1/FVC pre- or post BD||Compatible with diagnosis||Not compatible with diagnosis||Not compatible unless other evidence of chronic airflow limitation|
|Post-BD FEV1/FVC <0.7||Indicates airflow limitation but may improve spontaneously or on treatment||Required for diagnosis (GOLD)||Usually present|
|FEV1 ≥80% predicted||Compatible with diagnosis (good asthma control or interval between symptoms)||Compatible with GOLD classification of mild airflow limitation (categories A or B) if post-BD FEV1/FVC <0.7||Compatible with diagnosis of mild ACOS|
|FEV1 <80% predicted||Compatible with diagnosis. Risk factor for asthma exacerbations||An indicator of severity of airflow limitation and risk of future events (e.g. morality and COPD exacerbations)||An indicator of severity of airflow limitation and risk of future events (e.g. mortality and exacerbations)|
|Post-BD increase in FEV1 >12% and 200 ml from baseline (reversible airflow limitation)||Usual at some time in course of asthma, but may not be present when well-controlled or on controllers||Common and more likely with FEV1, is low, but ACOS should also be considered||Common and more likely when FEV1 is low, but ACOS should also be considered|
|Post-BD increase in FEV1 >12% and 400ml from baseline (marked reversibility)||High probablility of asthma||Unusual in COPD. Consider ACOS||Compatible with diagnosis of ACOS|
Summary of syndromic approach to diseases of chronic airflow limitation
Specialized investigations sometimes used in distinguishing asthma and COPD
|Lung function tests|
|DLCO||Normal (or slightly elevated).||Often reduced.|
|Arterial blood gasses||Normal between exacerbations||May be chroncially abnormal between exacerbations in more severe forms of COPD|
|Airway hyperresponsiveness (AHR)||Not useful on its own in distinguishing asthma from COPD, but high levels of AHR favor asthma|
|High resolution CT Scan||Usually normal but air trapping and increased bronchial wall thickness may be observed||Low attenuation areas denoting either air trapping or emphysematous change can be quantitated; bronchial wall thickening and features of pulmonary hypertension may be seen.|
|Test for atopy (specific IgE and/or skin prick tests)||Modestly increases probability of asthma; not essential for diagnosis||Conforms to background prevalence; does not rule out COPD|
|FENO||A high level (>50 ppb) in non-smokers supports a diagnosis of eosinophilic airway inflammation)||Usually normal.Low in current smokers.|
|Blood eosinophilia||Supports asthma diagnosis||May be present during exacerbations|
|Sputum inflammatory cell analysis||Role in differential diagnosis is not established in large populations|
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