Asthma in Older Adults 

Updated: Dec 16, 2019
Author: Praveen Buddiga, MD, FAAAAI; Chief Editor: Michael A Kaliner, MD 

Overview

Background

Asthma is a chronic inflammatory disease characterized by hyperresponsiveness of airways to various stimuli. This condition has evolved rapidly over the past few years into an immunologic condition that is a responsive target for precision medicine. The US Food and Drug Administration (FDA) recently approved three anti-interleukin (IL)-5 agents to treat eosinophilic asthma (reslizumab, benralizumab, and mepolizumab) as well as an anti-IL4Ra biologic agent (dupilumab) for the indication of moderate to severe asthma in patients 12 years and older.

The new standard of care in asthma is to immunologically phenotype the patient, assess the total immunoglobulin (Ig) E level, and obtain a complete blood cell (CBC) count with differential to ascertain the absolute eosinophil count. Based on the elevation of total IgE or the absolute eosinophil count, a targeted precision biologic agent is usually selected.[1, 2, 3, 4]

Asthma is complex disease that affects patients of all ages. Although asthma has an equal incidence across all age groups, asthma in the elderly is often underdiagnosed and undertreated. A case-control cohort study showed that older adults with asthma have a higher rate of allergic sensitization, decreased lung function, and significantly worse quality of life when compared to controls.[5]

Some of the stimuli or triggers may generally be subdivided into allergic (allergens such as pollen, molds and fungi, dust mites, pet dander, and insects) or nonallergic (eg, cold air, infections, diesel exhaust, indoor/outdoor air pollution, perfume, tobacco smoke, and other irritants). See the image below.

Asthma in older adults. Allergic and nonallergic t Asthma in older adults. Allergic and nonallergic triggers.

Medical conditions such as rhinosinusitis, gastroesophageal reflux, and aspirin or nonsteroidal anti-inflammatory drug (NSAID) sensitivity may also trigger or exacerbate asthma.

Elderly patients with asthma face disproportionate morbidity, mortality, and cost when compared with younger patient groups. They represent a higher number of unscheduled outpatient visits, emergency room visits, and asthma-related hospitalizations; once hospitalized, the death rate attributable to asthma for patients older than 65 years is 14 times higher than that of patients aged 18-35 years.[6, 7, 8, 9]

Some of the independent risk factors for asthma in older adults include house dust mite sensitization and maternal smoking.[5]

Normal lung tissue and constricted lung tissue are demonstrated in the image below.

Asthma in older adults. Lung tissue normal versus Asthma in older adults. Lung tissue normal versus constricted.

Pathophysiology

Airway inflammation, smooth muscle contraction, epithelial sloughing, mucous hypersecretion, bronchial hyperresponsiveness, and mucosal edema are some of the common pathophysiologic mechanisms seen in asthma. The chronic persistent inflammation may result in airway remodeling and structural changes of the airway wall. These changes include an epithelial thickening and subepithelial fibrosis; changes of extracellular matrix are linked to deposition of collagen and fibronectin in the subepithelial basement membrane.

Clinical trial data suggest an improved clinical outcome for those older than 12 years with moderate to severe persistent asthma, with important endpoints an objective increased forced expiratory volume in 1 second (FEV1) and subjective decreased exacerbations of asthma, with an improved quality of life and reduced dependency on oral corticosteroids.

These novel immunologic molecules target type 2 T-helper cell (Th2) inflammation by communicating sterically with the interleukin (IL)-5 and IL-4 receptors, as well as modifying IL-13 signaling. Decreased IL-4, IL-5, and IL-13 signaling has had clinical endpoints such as decreased moderate to severe persistent asthma, decreased eczema, and a decreased incidence of chronic rhinosinusitis with nasal polyposis (this latter entity is seen with the use of dupilumab).

These data suggest a bright clinical horizon opening for the discovery of novel agents targeting atopic Th2 inflammation that may consequently mount a pragmatic approach to the reduction of asthma, eczema, or atopic dermatitis, chronic rhinosinusitis with nasal polyposis and, potentially, over the atopic diathesis.[1, 2, 3, 4]

Various stimuli and factors may trigger asthma; this is evident by the recruitment and infiltration of proinflammatory cells within the airways. Cells such as eosinophils, neutrophils, lymphocytes, and degranulated mast cells, lead to occlusion of the bronchial lumen by mucus. See the image below.

Asthma in older adults. Allergic and nonallergic t Asthma in older adults. Allergic and nonallergic triggers.

Etiology

Allergic triggers include the following:

  • Pollen: Trees, grasses, weeds

  • Mold: Fungi

  • Dust mites

  • Animal proteins

Allergic triggers usually cause asthma symptoms by dimerizing or bridging the high-affinity immunoglobulin E (IgE) receptors located on the mast cells in the lungs. See the image below.

Asthma in older adults. Allergic and nonallergic t Asthma in older adults. Allergic and nonallergic triggers.

Non-allergic triggers include the following:

  • Cold air

  • Infections: Influenza, Mycoplasma pneumonia, viruses/upper respiratory infections

  • Tobacco smoke

  • Nonsteroidal anti-inflammatory drugs or aspirin[10]

  • Exercise

  • Irritants: Perfumes, paint

  • Pollutants: Diesel exhaust, industrial chemicals

  • Occupational exposures

Epidemiology

There has been an upward trend in the prevalence of asthma across all age groups.[11]  The prevalence of asthma in adults older than 65 years is similar to that found in other age groups, particularly those aged 20 to 34 years (see the images below).[6, 11]

There has been an upward trend in the prevalence o There has been an upward trend in the prevalence of asthma across all age groups since 2001. Courtesy of the CDC (https://www.cdc.gov/asthma/data-visualizations/prevalence.htm).

 

Asthma prevalence by age, 2017. Courtesy of the CD Asthma prevalence by age, 2017. Courtesy of the CDC (https://www.cdc.gov/asthma/data-visualizations/prevalence.htm).

Asthma prevalence is higher among females (9.8%) compared with males (5.4%).[12]

Prognosis

The asthma death rate is highest among persons aged 65 years and older (30.4 per million) compared with persons aged 0-4 years (1.4 per million), 5-11 years (3.3 per million), 12-17 years (2.5 per million), 18-24 years (4.5 per million), 25-34 years (5.9 per million), and 35-64 years (11.4 per million) and are most common among women and blacks.[12] Nevertheless, asthma deaths are relatively rare event and largely preventable. Increased hospitalizations and emergency department visits are risks for death due to asthma.

Several studies have shown that late-onset eosinophilic asthma is associated with more severe disease than noneosinophilic asthma. High levels of eosinophils in sputum and bronchial biopsies are associated with poor asthma control, more severe asthma and fatal or near-fatal asthma attacks. Patients with eosinophilic inflammation despite systemic corticosteroid treatment have almost 20 times higher odds of being intubated than those without eosinophilic inflammation. In patients who died from asthma, significantly more eosinophils have been found in large and small airways, as compared to biopsies from patients with milder exacerbations.

Patients may suffer from both asthma and COPD, so called asthma-chronic obstructive pulmonary disease (COPD) overlap. It is still an open question whether this overlap syndrome represents the coexistence of two distinct airway diseases or whether there are common underlying pathogenic mechanisms leading to this phenotype. Patients who have asthma-COPD overlap have a more rapid disease progression, a worse health-related quality of life, more frequent respiratory exacerbations, increased co-morbidities and health care utilization than those with either disease alone.[13]  

Patient Education

Adult patients with asthma often stop their medications when they feel well. These patients must be monitored on a regular basis to assess their symptoms and to intervene with appropriate asthma control. Adults generally expect to be treated as adults, with a respect and an appreciation for the skills they bring as they have different educational levels, backgrounds, life experiences, and expectations. Adults have established values, beliefs and opinions that must be identified and respected in order to set goals for management.[14]

 

Presentation

History and Physical Examination

History

The clinical presentation of asthma in older adults usually involves the patient indicating recurrent episodes of wheezing, chest tightness, shortness of breath, persistent coughing or nocturnal coughing, and/or recurrent lower respiratory tract infections. Symptoms may vary over time and often triggered by exercise, cold, dust or exposure to either allergic or nonallergic stimuli.

Childhood or family history of allergies or asthma, history of smoking, or exposure to environmental hazards could help differentiate asthma from COPD.[15]

Physical examination

The physical examination of older adults with asthma may find wheezing, a rapid respiratory rate, or in severe cases, use of accessory respiratory muscles. However, the physical examination findings may be entirely normal.

 

DDx

Diagnostic Considerations

COPD

For diagnosis of COPD, the Global initiative for Obstructive Lung Disease (GOLD) endorses the spirometry criterion of post-BD forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) < 0.70. This fixed cut-off is susceptible to the risk of overdiagnosing a substantial number of older symptomatic individuals as having COPD, which might contribute to the relative underdiagnosis of asthma in the elderly, particularly females. An alternative approach has been proposed to overcome this problem, whereby the cut-off is based on the lower limit of predicted normal. This cut-off assumes the “usual progressive” lung function decline of COPD is greater than the physiological age-related decline of the FEV1/FVC ratio.

Asthma-COPD Overlap

Older patients frequently present with chronic respiratory symptoms with features of both asthma and COPD and are found to have chronic airflow limitation that is not completely reversible with bronchodilation. The Global Initiative for Asthma (GINA) and the Global Initiative for Obstructive Lung Disease (GOLD) guidelines offer the following clinical descriptions to help distinguish asthma, COPD and asthma-COPD overlap[15] :

Asthma - characterized by chronic airway inflammation defined by a history of respiratory symptoms including wheezing, shortness of breath, chest tightness and cough that vary in intensity and over time. Variable expiratory airflow limitation is also present.

COPD - characterized by persistent respiratory symptoms and airflow limitations due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

Asthma-COPD overlap - characterized by persistent respiratory symptoms and airflow limitations with multiple features associated with asthma and multiple features associated with COPD.

Differential Diagnoses

 

Workup

Pulmonary Function Tests

Spirometry

Spirometry measures the maximal expiratory flow and exhaled volume during a forced expiratory vital capacity maneuver. The test is widely available, reproducible, and highly standardized in terms of performance, methodology, and equipment specifications.

Spirometry is a useful measure of severity of airflow limitation in asthma and is predictive of clinical outcomes. Normal standardized values for spirometry are well established for healthy, multiethnic populations. It is a safe and low-risk procedure that can be performed repeatedly for long-term monitoring.

The prebronchodilator response and postbronchodilator response maneuver involves a baseline spirometric value compared to a postbrochodilator spirometric value (ie, a repeat spirometry 15 min after two to four inhalations of albuterol). An improvement of 12% or more in the measurement of forced expiratory volume in 1 second (FEV1) improvement of 12% or greater from baseline represents the presence of reversible airflow obstruction, which usually means that the patient has asthma.[16, 17] See the image below.

Asthma in older adults. Spirometric data plot. Pre Asthma in older adults. Spirometric data plot. Pre-bronchodilator forced expiratory volume-one second (FEV1) = 1.77 L, post-bronchodilator FEV1 = 3.11 L, approximating a 75% change or airway reversibility.

Peak expiratory flow

Peak expiratory flow (PEF) is a measure of maximum instantaneous expiratory flow and is used as an indicator of airway caliber in asthma. The advantage of peak expiratory flow is that the test can be self-administered on a daily basis, and the results can be recorded manually or electronically to attain the day-to-day or intraday variability.[17]

Peak flows may be used to monitor changes in airflow in response to treatment, in relation to exercise or other provocations, or to determine if shortness of breath (or other chest symptoms) is associated with a change in airflow measurement when trying to differentiate the various causes for shortness of breath (ie, cardiac vs pulmonary).

Methacholine challenge

Methacholine inhalation challenge (or, bronchoprovocation test) provides a measure of airway responsiveness and has been used as one indication of whether a patient has asthma. A negative methacholine finding is a strong indicator that the patient does not have asthma, whereas a positive finding does not mean that the patient does have asthma.

Methacholine challenges have proven useful in the evaluation of coughing patients and in the evaluation of vocal cord dysfunction. The challenge is performed by inhalation of increasing concentrations of methacholine, which is a cholinergic agonist, until the forced expiratory volume in 1 second (FEV1) falls by 20% or more.[17]

Mannitol challenge

The mannitol inhalation challenge is a promising method of assessing airway hyperresponsiveness by imposing an osmotic stress on the airways. It may induce bronchoconstriction by the same mechanism as exercise or isocapnic hyperventilation.[17]

Mannitol is used for the same indications as methacholine but is easier to perform and less dangerous for individuals who may have airway overreactivity.

Exercise challenge

An exercise challenge measures airflow limitation after a maximum exercise test. A decline in forced expiratory volume in 1 second (FEV1) of 10% or more is a positive result and highly specific for a diagnosis of asthma in children but less so in adults.[17]

Isocapnic hyperventilation challenge

The isocapnic hyperventilation challenge is conducted via the inhalation of cold, dry air, which induces bronchoconstriction in many people with asthma. However, it is not considered a diagnostic test. Wide application of the test is limited by the lack of standardization.[17]

Imaging Studies

Chest radiography

A chest radiograph may reveal hyperinflation of the lungs for a diagnosis of asthma. This imaging modality may be an important part of the work-up for differential diagnosis of other respiratory diseases.

Sinus computed tomography (CT) scanning

A sinus CT scan may reveal evidence of rhinosinusitis or nasal polyposis, which might help with the diagnosis (eg, Samter triad of asthma, aspirin sensitivity, nasal polyposis).

Other Tests

Allergy skin testing

Adults with asthma often have an allergic trigger; therefore, skin tests are useful to identify the offending triggers. Strategies for allergen avoidance can then be developed, (eg, cat allergy, dust mite allergy).

pH probe evaluation

A a=pH probe evaluation is a procedure that involves placing a pH probe attached to a monitor and then measuring in real-time the amount of stomach acid that is refluxed within the esophagus. This may establish a diagnosis of gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR) disorder as the etiology of chronic cough. GERD is also known to trigger and exacerbate asthma. LPR can cause postnasal drip, throat clearing, cough, and hoarseness.

Lifestyle modifications include weight loss, low-fat diet, decreased caffeine and alcohol intake, raising the head of the bed about 6 inches, and avoiding meals 2-3 hours prior to reclining. Medications that reduce gastric acid secretion may also be helpful. Oral steroids may exacerbate GERD symptoms.[18]

 

Treatment

Approach Considerations

The introduction of omalizumab in 2003 as a novel approach for asthma control was a trailblazer for immunologic intervention for respiratory diseases such as asthma by reducing the necessity for chronic oral corticosteroid use, thereby reducing subsequent side effects (eg, early cataracts, osteoporosis, unwanted weight gain).

After a 13-year gap, innovations toward a solution for improved immunologic agents with a mild side effect profile have resulted in improved asthma control and include four novel biologic agents for subcutaneous (mepolizumab, benralizumab, and dupilumab) or intravenous (reslizumab) administration. These novel biologic agents have also been shown to be clinically important in decreasing overall atopic inflammation in patients with moderate to severe asthma; some of the clinical endpoints also showed reduced atopic dermatitis as well as reduced chronic rhinosinusitis with nasal polyposis, the last particularly with dupilumab.[1, 2, 3, 4]

Asthma symptoms usually persist despite avoidance measures; therefore, medications are often needed. The goal of treatment is to prevent fatalities, hospitalizations, and emergency room encounters. The long-term control of asthma with reduction of symptoms, maintenance of normal activity levels, prevention of exacerbations, and preservation of pulmonary function are the goals of therapy. Comorbidities should be treated and modifiable risk factors reduced (ie, smoking cessation, vaccinations).

Consultations

Consultations with the following are indicated:

  • Allergist

  • Pulmonologist

  • Otolaryngologist

Medical Care

Inhaled corticosteroids (ICS) are the initial first-line therapy for treatment of asthma. For patients with eosinophilic asthma, ICS, even at very high doses, are not sufficient to control the disease. Specific therapeutics targeting components of the inflammatory response have been developed or are currently under investigation.

Omalizumab

Omalizumab is a monoclonal antibody that binds IgE. Although total serum IgE levels do not correlate with the degree of tissue eosinophilia, treatment with anti-IgE therapy has been shown to reduce airway and blood eosinophils and effectively reduce exacerbations. However, there are patients with uncontrolled asthma who do not respond to anti-IgE therapy and show persistent eosinophilic inflammation.[10]

Mepolizumab

Mepolizumab is a humanized monoclonal antibody against interleukin-5 that selectively inhibits eosinophilic inflammation and reduces the number of eosinophils in both sputum and blood. Studies have shown mepolizumab significantly reduces asthma exacerbations and improves markers of asthma control in patients with severe eosinophilic asthma whose asthma is not adequately controlled by standard regimens for asthma treatment.[19, 20]

Dupilumab

Dupilumab is a fully human anti–interleukin-4 receptor α monoclonal antibody that blocks both interleukin-4 and interleukin-13 signaling.[4] Studies have shown that patients taking dupilumab had significantly lower rates of severe asthma exacerbation than those who received placebo, as well as better lung function and asthma control.[4, 21]

Benralizumab

In 2017, both the European Medicines Agency Committee for Medicinal Products for Human Use and the FDA approved benralizumab as adjunctive maintenance treatment for adults and children aged 12 years and older with severe eosinophilic asthma. Benralizumab is an antieosinophil humanized monoclonal antibody that selectively targets the interleukin-5 receptor expressed on the surface of eosinophils. The FDA approved benralizumab based on three phase 3 studies, which demonstrated the following[22, 23] :

  • Up to 51% reduction in the annual asthma exacerbation rate vs placebo

  • Significant improvement in lung function as measured by forced expiratory volume in 1 second of up to 159 mL vs placebo, with differences seen as early as 4 weeks after the first dose

  • A 75% median reduction in daily oral corticosteroid use and discontinuation of oral corticosteroid use in 52% of eligible patients

  • An overall adverse event profile similar to that of placebo

Reslizumab

Reslizumab is a humanized anti-interleukin 5 monoclonal antibody that disrupts eosinophil maturation and promotes programmed cell death. Castro et al conducted parallel multicenter, double-blind phase 3 clinical trials with 1185 patients with inadequately controlled, moderate-to-severe asthma. In both studies, patients receiving reslizumab had a significant reduction in the frequency of asthma exacerbations. The adverse event profile was similar to that of placebo. Two patients were withdrawn from the study because of anaphylactic reactions.[24]

Long-Term Monitoring

Asthma is chronic medical condition that requires ongoing monitoring to assess its control and to detect early signs of undertreatment or poor adherence to treatment. Good control in the adult population directly impacts physical function and quality of life, as well as reduces costs by improving the health of older patients with asthma.

 

Guidelines

Guidelines Summary

Asthma Clinical Practice Guidelines (GINA, 2019)

Guidelines for the management and prevention of asthma were published in 2019 by the Global Initiative for Asthma (GINA).[15] This is a quick summary of the guidelines without analysis or commentary. For more information, go directly to the guidelines.

For safety reasons, treatment with short-acting beta2-agonists (SABA) only is no longer recommended.

To reduce risk of serious exacerbations and to control symptoms, all adults and adolescents with asthma should receive controller treatment containing inhaled corticosteroids (ICS).

For mild asthma, as-needed low-dose ICS and low-dose formoterol are recommended. If formoterol is not available, the patient should take low-dose ICS whenever SABA is taken.

ICS-containing treatment should be initiated as soon as possible after asthma diagnosis.

Asthma medications should be added or deleted as the frequency and severity of the patient's symptoms change, as follows:

  • Step 1: As-needed low-dose ICS-formoterol

  • Step 2: Daily low-dose ICS plus as-needed SABA, or as-needed low-dose ICS-formoterol

  • Step 3: Low-dose ICS-LABA maintenance plus as-needed SABA, or low-dose ICS-formoterol maintenance and reliever therapy

  • Step 4: Low-dose ICS-formoterol as maintenance and reliever therapy, or medium-dose ICS-LABA maintenance plus as-needed SABA

  • Step 5: Refer for expert investigation and add-on treatment

2017 GINA Report, Global Strategy for Asthma Management and Prevention

In 2017, the Global Initiative for Asthma (GINA) and the Global Initiative for Obstructive Lung Disease (GOLD) released updated guidelines for the diagnosis and treatment of asthma, COPD and asthma-COPD overlap (ACO). The main goal of the consensus-based guidelines is to assist nonpulmonary specialists in the identification of chronic airway obstructive disease, distinguish between asthma, COPD and ACO, and determine initial treatment approach.[25]

GINA-GOLD no longer use the term asthma-COPD overlap syndrome (ACOS) as asthma-COPD overlap does not describe a single disease entity. Patients with combined features of both disorders more likely have several different phenotypes of airway disease caused by a variety of mechanisms.

The guidelines suggest a stepwise approach to diagnosis that includes the following steps[25] :

  • Step 1: Identifying patients at risk for chronic airway disease through clinical history, physical examination, radiology and screening questionnaires
  • Step 2: Differentiate asthma, COPD and asthma-COPD overlap based on a comparison of the number of features in favor of each possible diagnosis
  • Step 3: Perform spirometry and peak expiratory flow measurement to confirm of exclude diagnoses

Initial treatment recommendations include[25] :

  • For patients with characteristic features of asthma: adequate controller therapy with inhaled corticosteroids (ICS), but not long-acting bronchodilators as monotherapy
  • For patients with characteristic features of COPD: symptomatic treatment with bronchodilators or combination ICS-bronchodilator therapy, but not ICS monotherapy
  • For patients with characteristics of both asthma and COPD: ICS in a low or moderate dose depending on severity of symptoms; add on treatment with long-acting beta-antagonist (LABA) and/or long-acting muscarinic antagonist (LAMA). Do not treat with LABA monotherapy

For all three diagnoses of chronic airflow limitation, treat comorbidities, reduce modifiable risk factors (ie, smoking cessation, vaccinations), increase physical activity, encourage appropriate self-management strategies and perform regular follow-up. For COPD and asthma-COPD overlap, pulmonary rehabilitation is appropriate.

Referral to a pulmonary specialist is indicated for the following[25] :

  • Symptoms persist and/or exacerbations occur despite treatment
  • If diagnosis is uncertain or alternative diagnoses such as bronchiectasis, post-tuberculous scarring, bronchiolitis, pulmonary fibrosis, pulmonary hypertension need to be excluded
  • Atypical or additional signs and symptoms (eg, hemoptysis, weight loss, night sweats, signs of bronchiectasis or other structural lung disease)
  • Chronic airway disease is suspected but few features of asthma and COPD are present
  • Comorbidities are present that may interfere with assessment and management of airway disease

Resources

Go to Asthma and Chronic Obstructive Pulmonary Disease (COPD) for more information.

For more Clinical Practice Guidelines, go to Guidelines.

 

Medication

Beta2 agonists, rapid-acting

Class Summary

Rapid-acting, inhaled beta2 agonists are indicated for treatment of acute bronchospasm and prevention of exercise-induced asthma. Beta2-receptor activation leads to activation of adenylyl cyclase and increased intracellular cyclic adenosine monophosphate (AMP). This increase in cyclic AMP activates protein kinase A, which in turn inhibits myosin phosphorylation and lowers intracellular ionic calcium concentration, resulting in muscle relaxation.

Albuterol (Proventil HFA, Ventolin HFA, Proair HFA, AccuNeb)

Albuterol sulfate is a racemic salt of albuterol.

Levalbuterol (Xopenex HFA)

Levalbuterol tartrate is the (R)-enantiomer of albuterol.

Corticosteroids, Inhalants

Class Summary

Inhaled corticosteroids are the primary maintenance treatment for persistent asthma. These agents decreased the dose or need for oral corticosteroids. Not indicated for relief of acute bronchospasm.

Beclomethasone, inhaled (Qvar)

Available as an inhaled metered-dose aerosol.

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

Available as a dry powder metered-dose inhaler or suspension for inhalation.

Ciclesonide inhaled (Alvesco)

Nonhalogenated glucocorticoid available as an inhaled metered dose aerosol.

Flunisolide inhaled (Aerospan)

Fluorinated glucocorticoid available as an inhaled metered dose aerosol.

Fluticasone inhaled (Flovent HFA, Flovent Diskus)

Available as a powder for inhalation contained within the Diskus device or an aerosolized metered-dose inhaler.

Mometasone inhaled (Asmanex HFA, Asmanex Twisthaler)

Mometasone is a corticosteroid for inhalation. It is indicated for asthma as prophylactic therapy.

Beta2 agonists, long-acting

Class Summary

These agents may be added to a maintenance treatment regimen of inhaled corticosteroids in patients with moderate-to-severe persistent asthma. This drug regimen may allow for a reduced dose of inhaled corticosteroid.

Salmeterol (Serevent Diskus)

Salmeterol xinafoate is a racemic form of the 1-hydroxy-2-naphthoic acid salt of salmeterol. The active component is salmeterol base. Available as a powder for inhalation contained within the Diskus device.

Respiratory Inhalant Combos

Class Summary

Inhalant combinations consisting of a long-acting beta2 agonist plus a corticosteroid may be considered for moderate-to-severe persistent asthma.

Budesonide/formoterol (Symbicort)

Available as a metered dose aerosol.

Mometasone inhaled/formoterol (Dulera)

Available as a metered dose aerosol.

Salmeterol/fluticasone inhaled (Advair Diskus, Advair HFA)

Available as a powder for inhalation contained within the Diskus device. Also available as an aerosolized inhaler.

Vilanterol/fluticasone furoate inhaled (Breo Ellipta)

Indicated for once-daily treatment of asthma for adults not adequately controlled on a long-term asthma control medication (eg, inhaled corticosteroid), or whose disease severity clearly warrants initiation of treatment with both an inhaled corticosteroid and a long-acting beta agonist (LABA). Use prescribe strength (25 mcg/100 mcg or 25 mcg/200 mcg per actuation) once daily via oral inhalation. Fluticasone furoate is a corticosteroid with anti-inflammatory activity. Vilanterol is a long-acting beta agonist (LABA) that stimulates intracellular adenyl cyclase (catalyzes the conversion of ATP to cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.

Corticosteroids, Oral

Class Summary

Because of severe adverse effects with long-term use with systemic corticosteroids, the lowest possible dose should be used to control asthma, and necessary measures (ie, inhaled corticosteroids, additional medications) should be employed to decrease the dose or discontinue the oral corticosteroid.

Prednisone (Sterapred, Sterapred DS, Rayos)

Oral corticosteroid used for severe asthma and acute flairs.

Leukotriene Receptor Antagonists

Class Summary

These agents are selective and competitive receptor antagonists of leukotrienes, which are components of slow-reacting substance of anaphylaxis (SRSA). Cysteinyl leukotriene production and receptor occupation have been correlated with the pathophysiology of asthma, including airway edema, smooth muscle constriction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma.

Montelukast (Singulair)

Selectively blocks binding of leukotriene D4 at the CysLT1 receptor. It is indicated for prophylaxis and chronic treatment of asthma, and for prevention of exercise-induced bronchoconstriction.

Zafirlukast (Accolate)

Inhibits bronchoconstriction as competitive receptor antagonist of leukotrienes C4, D4, and E4. It is indicated for prophylaxis and chronic treatment of asthma.

5-Lipoxygenase Inhibitors

Class Summary

These agents inhibit 5-lipoxygenase, the enzyme that catalyzes the formation of leukotrienes from arachidonic acid. Leukotrienes, which are components of slow-reacting substance of anaphylaxis (SRSA), are correlated with the pathophysiology of asthma, including airway edema, smooth muscle constriction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma.

Zileuton (Zyflo Filmtab, Zyflo, Zyflo CR)

Inhibits leukotriene B4, C4, D4, and E4 formation. It is indicated for prophylaxis and chronic treatment of asthma.

Monoclonal Antibody

Class Summary

Inhibits IgE binding to mast cells and basophils, thereby limiting the degree of release of allergic mediators.

Omalizumab (Xolair)

Recombinant humanized IgG1-kappa monoclonal antibody. It is indicated for moderate-to-severe persistent asthma in patients with a positive skin test or in vitro reactivity to a perennial aeroallergen and symptoms that are inadequately controlled with inhaled corticosteroids.