Asthma-COPD overlap

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Asthma-COPD overlap
Specialty Pulmonology
Symptoms wheezing, coughing, dyspnea, sputum production
Usual onsetAdulthood
DurationLong term
Causes Genetic and environmental factors
Risk factors smoking, air pollution, allergens
Diagnostic method Based on symptoms, response to therapy, spirometry
TreatmentAvoiding triggers, inhaled corticosteroids, bronchodilators

Asthma-Chronic Obstructive Pulmonary Disease (COPD) Overlap (ACO), also known as Asthma-COPD Overlap Syndrome (ACOS), is a chronic inflammatory, obstructive airway disease in which features of both asthma and COPD predominate. Asthma and COPD were once thought of as distinct entities; however, in some, there are clinical features of both asthma and COPD with significant overlap in pathophysiology and symptom profile. It is unclear whether ACO is a separate disease entity or a clinical subtype of asthma and COPD. The pathogenesis of ACO is poorly understood, but it is thought to involve both type 2 inflammation (usually seen in asthma) as well as type 1 inflammation (seen in COPD). The incidence and prevalence of ACO are not well known. The risk factors for ACO are also incompletely understood, but tobacco smoke is known to be a major risk factor.

Contents

Signs and Symptoms

ACO presents with symptoms of both asthma and COPD. [1] ACO presents in adulthood, usually after the age of 40 (after there has been significant tobacco smoke or other toxic fumes exposure), with symptoms of dyspnea (shortness of breath), exercise intolerance, sputum production, cough and episodes of symptomatic worsening known as exacerbations.

Cause

A history of significant and persistent noxious fumes exposure is required for the diagnosis of COPD; therefore, it is also required for the diagnosis of ACO. [2] This can be due to tobacco smoking, indoor air pollution, or outdoor air pollution.

Pathophysiology

ACOS presents with features of both asthma and COPD. Both asthma and COPD (as well as ACO) present with exacerbations, periods where symptoms deteriorate, with marked reductions in airflow. However, in asthma, the airflow limitation usually completely resolves after exacerbations, whereas in COPD it may not. [1] ACO presents with a chronic airflow limitation or obstruction (due to inflammation), with characteristics of both asthma and COPD. Inflammation of the large and medium airways (classically seen with asthma) is seen in ACO. [1] This consists of bronchoconstriction due to smooth muscle spasm as well as smooth muscle hyperresponsiveness (due to allergens or irritants) causing obstruction of airflow. [1] Mucus production and inflammation in the airways can also cause airflow obstruction in asthma. [1]

Features of COPD (which includes the subtypes of chronic bronchitis and COPD) are also seen in ACO. These include the features of chronic bronchitis such as inflammation of the small airways and mucus production or hypersecretion. [1] Peribronchial inflammation may lead to fibrosis (obliterative bronchiolitis) [1] as well as features of emphysema, including inflammation leading to alveolar destruction resulting in lung hyperinflation and air trapping. [1]

Diagnosis

There are no widely accepted diagnostic criteria for ACO. However, the diagnosis requires clinical features of both asthma and COPD. [3] One diagnostic criteria, based on expert consensus, first described in 2016, requires the presence of three major and at least one minor criteria for the diagnosis of ACO. The major criteria are: a persistent airflow limitation (a ratio of forced expiratory volume in 1 second divided by forced vital capacity (FEV1/FVC) of less than 0.7 or below the lower limit of normal), a significant exposure history to tobacco smoke (defined as a greater than 10-pack/year history), or significant exposure to other indoor or outdoor air pollution, and a documented history of asthma or a significant improvement in FEV1 (of greater than 400mL) to an inhaled bronchodilator. [4] The minor criteria include a history of atopy or allergic rhinitis, a more limited response to an inhaled bronchodilator (greater than 200 mL improvement in the FEV1 or a 12% improvement from baseline), and peripheral blood eosinophils greater than 300 cells/μL. Spirometry (documenting obstruction) is required for the diagnosis of ACO. [4]

In those with asthma, some features often seen in COPD that may aid in the diagnosis of ACO include emphysema seen on imaging or a decreased diffusion capacity (DLCO) indicating significant lung tissue damage. In those with COPD, other features often seen in asthma that may aid in the diagnosis of ACO include an increase in the fraction of exhaled nitric oxide (FENO), a marker that is specific to the degree of airway inflammation in those with asthma, or increased levels of IgE (either total IgE or specific to inhaled antigens). [4]

Treatment

Treatment of ACO is based on expert opinion, as there are no universally accepted clinical guidelines. Treatment is usually based on whether clinical features of asthma or COPD predominate. [4] Inhaled corticosteroids are the primary treatment in those with ACOS. [2] [1] [4] Inhaled corticosteroids (ICS) should be continued in those with asthma who develop decreased airway responsiveness to bronchodilators consistent with ACO. [1] Therapy can be escalated to include a long-acting beta-agonist (LABA) and inhaled steroid combination (ICS-LABA) or by adding on a long-acting anti-muscarinic inhaler (LAMA), known as triple therapy, in those with more severe or resistant disease. [4]

Monoclonal antibodies targeting type 2 inflammation (which is predominant in asthma) have been used to treat severe asthma, and may also be used in severe cases of ACO. [4] These monoclonal antibodies include omalizumab (an Anti-IgE antibody), mepolizumab (an anti-IL-5 antibody) and benralizumab (an anti-IL-5 receptor α antibody). [4] People with ACOS and eosinophilia have a better response to ICS, with fewer exacerbations and hospitalizations seen in ACOS treated with long-term ICS. [1] Systemic corticosteroids (intravenous or oral steroids) may be used during exacerbations of ACOS. [1]

Prognosis

The progression of permanent airflow obstruction (as measured by the rate of FEV1 decline) is slower in ACO as compared to COPD, but ACO with late-onset asthma is associated with a more rapid FEV1 decline (a more rapid progression of obstruction) and a worse prognosis. [4] ACO with late-onset asthma is associated with a higher mortality as compared to COPD, asthma or healthy controls. [4] Excluding ACO with late-onset asthma, ACO has better survival (lower mortality) than COPD, but higher mortality compared to asthma. [4] In other studies, ACO was associated with worse dyspnea symptoms, more coughing, wheezing, and sputum production, as well as more frequent and more severe exacerbations as compared to COPD or asthma. [5]

Epidemiology

Due to heterogeneity of diagnostic criteria and a paucity of clinical trials, the prevalence of ACO is not well known. Based on a meta analysis, the prevalence of ACO in the general population is estimated to be 2%, whereas the prevalence of ACO in those with asthma is 26.5% and in those with COPD it is 29.6%. [6]

Related Research Articles

<span class="mw-page-title-main">Asthma</span> Long-term inflammatory disease of the airways of the lungs

Asthma is a long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. These may occur a few times a day or a few times per week. Depending on the person, asthma symptoms may become worse at night or with exercise.

<span class="mw-page-title-main">Bronchiectasis</span> Permanent enlargement of the lung airways

Bronchiectasis is a disease in which there is permanent enlargement of parts of the airways of the lung. Symptoms typically include a chronic cough with mucus production. Other symptoms include shortness of breath, coughing up blood, and chest pain. Wheezing and nail clubbing may also occur. Those with the disease often get lung infections.

<span class="mw-page-title-main">Spirometry</span> Pulmonary function test

Spirometry is the most common of the pulmonary function tests (PFTs). It measures lung function, specifically the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled. Spirometry is helpful in assessing breathing patterns that identify conditions such as asthma, pulmonary fibrosis, cystic fibrosis, and COPD. It is also helpful as part of a system of health surveillance, in which breathing patterns are measured over time.

<span class="mw-page-title-main">Budesonide/formoterol</span> Medication for asthma & chronic obstructive pulmonary disease

Budesonide/formoterol, sold under the brand name Symbicort among others, is a fixed-dose combination medication used in the management of asthma or chronic obstructive pulmonary disease (COPD). It contains budesonide, a steroid; and formoterol, a long-acting β2-agonist (LABA). The product monograph does not support its use for sudden worsening or treatment of active bronchospasm. However, a 2020 review of the literature does support such use. It is used by breathing in the medication.

<span class="mw-page-title-main">Inhaler</span> Medical device used to deliver medicines into lungs

An inhaler is a medical device used for delivering medicines into the lungs through the work of a person's breathing. This allows medicines to be delivered to and absorbed in the lungs, which provides the ability for targeted medical treatment to this specific region of the body, as well as a reduction in the side effects of oral medications. There are a wide variety of inhalers, and they are commonly used to treat numerous medical conditions with asthma and chronic obstructive pulmonary disease (COPD) being among the most notable.

<span class="mw-page-title-main">Bronchoconstriction</span> Constriction of the terminal airways in the lungs

Bronchoconstriction is the constriction of the airways in the lungs due to the tightening of surrounding smooth muscle, with consequent coughing, wheezing, and shortness of breath.

Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. Asthma is caused by multiple genes, some having protective effect, with each gene having its own tendency to be influenced by the environment although a genetic link leading to acute severe asthma is still unknown. Symptoms include chest tightness, rapidly progressive dyspnea, dry cough, use of accessory respiratory muscles, fast and/or labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest. The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses.

Airway obstruction is a blockage of respiration in the airway that hinders the free flow of air. It can be broadly classified into being either in the upper airway (UPA) or lower airway (LOA).

An overlap syndrome is a medical condition which shares features of at least two more widely recognised disorders. Examples of overlap syndromes can be found in many medical specialties such as overlapping connective tissue disorders in rheumatology, and overlapping genetic disorders in cardiology.

<span class="mw-page-title-main">Bronchitis</span> Inflammation of the large airways in the lungs

Bronchitis is inflammation of the bronchi in the lungs that causes coughing. Bronchitis usually begins as an infection in the nose, ears, throat, or sinuses. The infection then makes its way down to the bronchi. Symptoms include coughing up sputum, wheezing, shortness of breath, and chest pain. Bronchitis can be acute or chronic.

<span class="mw-page-title-main">Obstructive lung disease</span> Category of respiratory disease characterized by airway obstruction

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling, and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms, and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

Restrictive lung diseases are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

<span class="mw-page-title-main">Pulmonary function testing</span> Test to evaluate respiratory system

Pulmonary function testing (PFT) is a complete evaluation of the respiratory system including patient history, physical examinations, and tests of pulmonary function. The primary purpose of pulmonary function testing is to identify the severity of pulmonary impairment. Pulmonary function testing has diagnostic and therapeutic roles and helps clinicians answer some general questions about patients with lung disease. PFTs are normally performed by a pulmonary function technologist, respiratory therapist, respiratory physiologist, physiotherapist, pulmonologist, or general practitioner.

<span class="mw-page-title-main">FEV1/FVC ratio</span> Ratio used in the diagnosis of lung disease

The FEV1/FVC ratio, also called modified Tiffeneau-Pinelli index, is a calculated ratio used in the diagnosis of obstructive and restrictive lung disease. It represents the proportion of a person's vital capacity that they are able to expire in the first second of forced expiration (FEV1) to the full, forced vital capacity (FVC). FEV1/FVC ratio was first proposed by E.A. Haensler in 1950. The FEV1/FVC index should not be confused with the FEV1/VC index as they are different, although both are intended for diagnosing airway obstruction. Current recommendations for diagnosing pulmonary function recommend using the modified Tiffeneau-Pinelli index. This index is recommended to be represented as a decimal fraction with two digits after the decimal point.

<span class="mw-page-title-main">Acute exacerbation of chronic obstructive pulmonary disease</span> Medical condition

An acute exacerbation of chronic obstructive pulmonary disease, or acute exacerbations of chronic bronchitis (AECB), is a sudden worsening of chronic obstructive pulmonary disease (COPD) symptoms including shortness of breath, quantity and color of phlegm that typically lasts for several days.

<span class="mw-page-title-main">Chronic obstructive pulmonary disease</span> Lung disease involving long-term poor airflow

Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease characterized by chronic respiratory symptoms and airflow limitation. GOLD 2024 defined COPD as a heterogeneous lung condition characterized by chronic respiratory symptoms due to abnormalities of the airways and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.

<span class="mw-page-title-main">Olodaterol</span> Chemical compound

Olodaterol is an ultra-long-acting β adrenoreceptor agonist (ultra-LABA) used as an inhalation for treating people with chronic obstructive pulmonary disease (COPD). It is manufactured by Boehringer Ingelheim.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is a diffuse parenchymal lung disease which often presents with symptoms of cough and shortness of breath. The pathological definition published by the World Health Organization is “a generalized proliferation of scattered single cells, small nodules, or linear proliferations of pulmonary neuroendocrine (PNE) cells that may be confined to the bronchial and bronchiolar epithelium.” The true prevalence of this disease is not known. To date, just under 200 cases have been reported in the literature. However, with an increase in recognition of this disease by radiologists and pulmonologists, the number of cases has been increasing. DIPNECH predominantly affects middle-aged women with slowly progressive lung obstruction. DIPNECH is usually discovered in one of two ways: 1) as an unexpected finding following a lung surgery; or 2) by evaluation of a patient in a pulmonary clinic with longstanding, unexplained symptoms.

<span class="mw-page-title-main">Beclometasone/formoterol/glycopyrronium bromide</span> Combination drug

Beclometasone/formoterol/glycopyrronium, sold under the brand name Trimbow among others, is an inhalable fixed-dose combination medication for the treatment of chronic obstructive pulmonary disease (COPD) and asthma. It contains beclometasone dipropionate, formoterol fumarate dihydrate, and glycopyrronium bromide.

Fluticasone furoate/umeclidinium bromide/vilanterol, sold under the brand name Trelegy Ellipta among others, is a fixed-dose combination inhaled medication that is used for the maintenance treatment of chronic obstructive pulmonary disease (COPD). The medications work in different ways: fluticasone furoate is an inhaled corticosteroid (ICS), umeclidinium is a long-acting muscarinic antagonist (LAMA), and vilanterol is a long-acting beta-agonist (LABA).

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 Postma, Dirkje S.; Rabe, Klaus F. (24 September 2015). "The Asthma–COPD Overlap Syndrome". New England Journal of Medicine. 373 (13): 1241–9. doi:10.1056/NEJMra1411863. PMID   26398072.
  2. 1 2 Cosio, Borja G.; Soriano, Joan B.; López-Campos, Jose Luis; Calle-Rubio, Myriam; Soler-Cataluna, Juan José; de-Torres, Juan P.; Marín, Jose M.; Martínez-Gonzalez, Cristina; de Lucas, Pilar; Mir, Isabel; Peces-Barba, Germán; Feu-Collado, Nuria; Solanes, Ingrid; Alfageme, Inmaculada; Casanova, Ciro; Calvo Bonachera, José; Lacárcel Bautista, Celia; Domenech, Adolfo; Guzmán, Rosirys; Irigaray, Rosa; Zamora, Meritxell López; Ríos, Angel; Córdova, Rocío; López, Carlos Cabrera; Acosta, Alejandro Sánchez; González, Juan Abreu; Balbin, Ramón Agüero; Balcells, Eva; Campos, Elena Miguel; Marin, Alicia; Casanova, Antonia Llunel; Moreno, Amalia; Márquez Pérez, Francisca Lourdes; Riesco Miranda, Juan Antonio; Rodríguez, Julia Tabara; Gómez, Rafael Golpe; de Miguel Díez, Javier; Río, Francisco García; Lobato, Salvador Díaz; Galdiz Iturri, Juan Bautista; Royo, Margarita Marín; de Diego Damia, Alfredo (January 2016). "Defining the Asthma-COPD Overlap Syndrome in a COPD Cohort". Chest. 149 (1): 45–52. doi:10.1378/chest.15-1055. PMID   26291753.
  3. ↑ "Asthma, COPD, and Asthma-COPD Overlap Syndrome". Global Initiative for Chronic Obstructive Lung Disease - GOLD.
  4. 1 2 3 4 5 6 7 8 9 10 11 Mekov, Evgeni; Nuñez, Alexa; Sin, Don D; Ichinose, Masakazu; Rhee, Chin Kook; Maselli, Diego Jose; Coté, Andréanne; Suppli Ulrik, Charlotte; Maltais, François; Anzueto, Antonio; Miravitlles, Marc (June 2021). "Update on Asthma–COPD Overlap (ACO): A Narrative Review". International Journal of Chronic Obstructive Pulmonary Disease. 16: 1783–99. doi: 10.2147/COPD.S312560 . PMC   8216660 . PMID   34168440.
  5. ↑ Ulrik, Charlotte Suppli; Nielsen, Mia; Bårnes, Camilla Boslev (July 2015). "Clinical characteristics of the asthma–COPD overlap syndrome a systematic review". International Journal of Chronic Obstructive Pulmonary Disease. 10: 1443–1454. doi: 10.2147/COPD.S85363 . PMC   4524387 . PMID   26251584.
  6. ↑ Hosseini, Mostafa; Almasi-Hashiani, Amir; Sepidarkish, Mahdi; Maroufizadeh, Saman (December 2019). "Global prevalence of asthma-COPD overlap (ACO) in the general population: a systematic review and meta-analysis". Respiratory Research. 20 (1): 229. doi: 10.1186/s12931-019-1198-4 . PMC   6813073 . PMID   31647021.
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