Asthma Medications

Function

Understanding asthma pharmacotherapy requires a solid grasp of the underlying physiology and pathophysiology. Asthma is a chronic, heterogeneous inflammatory disorder with multiple phenotypes and endotypes, driven by a dysregulated immune response to environmental and nonenvironmental triggers.

Asthma pathogenesis begins with antigen uptake by airway dendritic cells and presentation to naïve CD4 T lymphocytes (Th0). Th0 cells then initiate 1 of 2 immune pathways—Th1 or Th2—depending primarily on the local cytokine environment, particularly interleukin-12 (IL-12).[5] Th1 cells develop when IL-12 is present, promoting CD8 cell–mediated immunity and neutrophil-driven cytotoxic inflammation, including the release of tumor necrosis factor and interferon gamma. A Th2 response predominates when IL-12 is absent, triggering a complex cascade of cytokine release from CD4 cells, including IL-3, IL-4, IL-5, IL-9, and IL-13.

Asthma has been classically recognized as a type 2–high inflammatory disease, although non–type 2 mechanisms also contribute to pathogenesis in some patients. IL-4 and IL-13 stimulate IgE production, while IL-4 and IL-9 promote mast cell activity. IL-3 activates basophils, and IL-5 primarily drives eosinophil activity, with additional contributions from IL-3 and granulocyte-macrophage colony-stimulating factor. Initial allergen exposure results in IgE binding to high-affinity receptors on mast cells and basophils. Subsequent re-exposure cross-links IgE, triggering degranulation of histamine, prostaglandins, leukotrienes, and other mediators, as well as the synthesis of lipid mediators. These processes contribute to smooth muscle contraction, airway edema, and airflow limitation.[6]

IL-5 is produced by Th2 cells and is necessary for eosinophil production, maturation, accumulation, activation, and survival. In humans, IL-5 primarily promotes the proliferation of eosinophils in the bone marrow and their accumulation in pulmonary tissue. Activated eosinophils release cytotoxic granule proteins and additional cytokines that perpetuate inflammation and contribute to airway remodeling. In addition to adaptive Th2 pathways, epithelial alarmins such as IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) released from injured airway epithelium activate type 2 innate lymphoid cells and dendritic cells, amplifying type 2 inflammation.[6][7][8][9][10]

Tezepelumab is a human IgG2 monoclonal antibody that blocks TSLP by preventing its interaction with the TSLP receptor. As an epithelial-derived cytokine positioned high in the inflammatory cascade, TSLP contributes to the airway and mucosal inflammation central to asthma pathogenesis. Patients with asthma have increased airway expression of TSLP. By inhibiting TSLP, tezepelumab reduces key inflammatory biomarkers and cytokines, including blood and airway eosinophils, IgE, fractional exhaled nitric oxide (FeNO), and type 2 cytokines such as IL-5 and IL-13.[11]

Biomarkers are increasingly used to phenotype asthma, guide treatment selection, and predict response to targeted therapies, particularly in type 2–high asthma. Commonly assessed biomarkers include blood eosinophil count, total and allergen-specific IgE, and FeNO, all of which reflect underlying airway inflammation.[12] Elevated blood eosinophils and FeNO are associated with increased exacerbation risk and enhanced responsiveness to inhaled corticosteroids and biologic therapies targeting IL-5 or IL-4/IL-13 pathways. Higher eosinophil counts predict favorable responses to agents directed at IL-5 or the IL-5 receptor, whereas elevated FeNO identifies patients likely to benefit from therapies targeting IL-4/IL-13. Similarly, total and allergen-specific IgE levels can help identify patients with allergic asthma who may benefit from anti-IgE therapy.[13][14]

Issues of Concern

Asthma is a major public health concern impacting over 260 million individuals worldwide and causing more than 450,000 deaths annually. In the United States, approximately 27 million people are affected, including 1 in 12 children, and asthma remains a leading cause of emergency department visits, hospitalizations, and missed time at school and work. Despite advances in guideline-directed therapy, many patients experience suboptimal disease control, contributing to substantial morbidity, health care utilization, and economic burden. Persistent disparities in access to care, environmental exposures, and adherence further exacerbate asthma-related outcomes globally.[15][16][17][18][19]

Clinical Significance

The primary goals of asthma management are to achieve optimal symptom control, prevent exacerbations, preserve lung function, and minimize medication-related adverse effects. Effective management requires a stepwise, patient-centered approach guided by symptom control. Current National Heart, Lung, and Blood Institute (NHLBI) and Global Initiative for Asthma (GINA) guidelines emphasize early and consistent use of anti-inflammatory therapy and advise against bronchodilator monotherapy, as well as the identification and control of triggers.[18][20] 

A. PHARMACOTHERAPY

1. Short- and Long-Acting Inhaled Beta-2 Agonists

Short-acting beta-2 agonists, most commonly albuterol (salbutamol), provide rapid bronchodilation by stimulating beta-2 adrenergic receptors on airway smooth muscle. Activation of these receptors increases intracellular cyclic adenosine monophosphate via adenylyl cyclase, resulting in reduced intracellular calcium concentrations, activation of protein kinase A, inactivation of myosin light-chain kinase, and smooth muscle relaxation. The associated calcium efflux also activates calcium-dependent potassium channels in the cell membrane, leading to hyperpolarization of smooth muscle cells and inhibition of further contraction. The net effect is decreased airway smooth muscle contractility and reduced responsiveness to bronchoconstrictive stimuli. While SABAs remain effective for acute symptom relief, current guidelines recommend against SABA-only therapy due to an increased risk of exacerbations and asthma-related mortality when used without inhaled corticosteroids (ICS).[21][22]

Long-acting beta agonists, including salmeterol and formoterol, share the same molecular mechanism as SABAs but have longer half-lives, resulting in prolonged receptor binding and an extended bronchodilator effect. Long-acting beta agonists should never be used as monotherapy because of the risk for severe asthma exacerbations, including asthma-related death. When combined with inhaled corticosteroids, LABAs substantially improve symptom control and lung function and reduce exacerbations without increasing the risk of serious adverse events.[23]

Common adverse effects of beta-2 agonists include tremor, nervousness, insomnia, nausea, headache, heart palpitations, and tachycardia. These generally are dose-dependent. Excessive reliance on SABAs may indicate poor symptom control or impaired symptom perception and should prompt reassessment of controller therapy rather than dose escalation.

2. Inhaled Short- and Long-Acting Muscarinic Antagonists

Anticholinergic medications may be short-acting, such as ipratropium bromide, or long-acting, such as tiotropium, aclidinium, glycopyrronium, and umeclidinium. These agents bind to and inhibit parasympathetic muscarinic receptors M1, M2, and M3. M3 receptors are expressed on airway smooth muscle cells, mucosal glands, and vascular endothelium. Blockade of M3 receptors reduces bronchoconstriction, mucus secretion, and mucosal edema. Although the inhibition is not receptor subtype–specific, the primary therapeutic effect in asthma is mediated through antagonism of M3 receptors. Receptor blockade decreases cyclic guanosine monophosphate levels in smooth muscle cells, thereby reducing intracellular calcium, activating protein kinase, inactivating myosin light-chain kinase, and activating myosin light-chain phosphatase, resulting in smooth muscle relaxation. Reduced intracellular calcium also contributes to decreased glandular mucus secretion. M1/M2 receptor blockade may modulate neural signaling but minimally contributes to bronchodilation.[24][25] Inhaled SAMAs are generally reserved for as-needed acute relief, particularly in emergency settings. Combination therapy with SAMAs and SABAs provides synergistic bronchodilation and is recommended for acute exacerbations or select step-up therapy.[26] 

Adverse effects are typically related to systemic anticholinergic activity and may include dry mouth, headache, dizziness, urinary retention, and lower urinary tract symptoms, particularly in elderly males. Other potential adverse effects include bronchitis, exacerbation of chronic obstructive pulmonary disease (COPD), sinusitis, dyspnea, flu-like symptoms, back pain, cough, dyspepsia, and nausea.

3. Inhaled Corticosteroids

Inhaled corticosteroids, including beclomethasone, budesonide, flunisolide, fluticasone, and mometasone, remain first-line controller therapy for both children and adults. Inhaled corticosteroids reduce airway inflammation by modulating gene transcription through glucocorticoid receptors, increasing the synthesis of anti-inflammatory proteins such as annexin A1, secretory leukoprotease inhibitor, and IL-10. They decrease production of proinflammatory cytokines, chemokines, and adhesion molecules and promote apoptosis of eosinophils, T lymphocytes, mast cells, and dendritic cells. These effects reduce airway hyperresponsiveness, mucus hypersecretion, and structural remodeling, addressing the underlying inflammatory pathology of asthma.

Inhaled corticosteroids are recommended as daily maintenance therapy for all patients with persistent asthma. Treatment typically begins with low- to medium-dose ICSs and is escalated only if control is insufficient. Once control is achieved, therapy should be tapered to the lowest effective dose to minimize long-term adverse effects. Inhaled corticosteroids are often combined with LABAs in patients whose asthma is not controlled with ICSs alone. Preferred combinations include fluticasone/salmeterol, budesonide/formoterol, mometasone/formoterol, and fluticasone/vilanterol. Monotherapy with ICSs is favored when possible, as it addresses the underlying inflammation rather than providing only symptomatic relief. Early initiation reduces the risk of exacerbations and preserves lung function.[27]

Inhaled corticosteroids are generally safe, but possible adverse effects include oropharyngeal candidiasis, dysphonia, throat irritation, cough, nasopharyngitis, headache, and sinusitis, with minor systemic effects at higher doses. Proper inhaler technique and use of a spacer can reduce oropharyngeal adverse effects. Inhaled corticosteroids may slightly reduce growth velocity in children, particularly at higher doses, but final adult height is generally not substantially affected when patients are appropriately monitored.[28] Systemic corticosteroids carry a higher risk of hypothalamic-pituitary-adrenal axis suppression, osteoporosis, and oropharyngeal candidiasis.[29] The Global Initiative for Asthma 2023 guidelines and the National Heart, Lung, and Blood Institute 2020 guidelines recommend adding a LAMA as step-up therapy after an ICS-LABA combination for patients aged 12 years and older, particularly for those with a history of exacerbations, persistent airflow limitation, or features of asthma-COPD overlap.

4. Leukotriene Receptor Antagonists

Leukotriene receptor antagonists (LTRAs), including montelukast and zafirlukast, are oral controller medications.[30] They selectively block cysteinyl leukotriene receptors, thereby preventing the leukotriene-mediated bronchoconstriction, increased vascular permeability, eosinophilic inflammation, and mucus production that contribute to asthma symptoms and exacerbations. These agents are anti-inflammatory rather than bronchodilators and are not indicated for the treatment of acute exacerbations.[31]

Current guidelines recognize LTRAs as alternative or add-on maintenance therapy in selected patients, particularly those with mild persistent asthma, exercise-induced bronchoconstriction, or aspirin-exacerbated respiratory disease, as well as in individuals who cannot tolerate ICSs. However, LTRAs are generally less effective than daily ICSs in improving asthma control and reducing exacerbations. LTRAs are also less effective than ICS-LABA combinations when used as add-on therapy. Montelukast, administered once daily (usually at bedtime), is most commonly used. Zafirlukast, administered twice daily and best absorbed on an empty stomach, has similar indications but is less commonly used due to limited pediatric formulations and the potential for hepatic adverse effects.

Leukotriene receptor antagonists are generally well tolerated. Common adverse effects include headache, gastrointestinal symptoms (eg, abdominal pain, nausea, dyspepsia), upper respiratory symptoms (eg, pharyngitis, sinusitis, otitis), and cough. Rare but serious adverse reactions include elevated liver enzymes and hepatitis (more commonly associated with zafirlukast) and eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome). Neuropsychiatric events, including agitation, depression, anxiety, sleep disturbances, and suicidal ideation, have also been reported. Montelukast carries a boxed warning for these effects, and this risk should be discussed with patients or caregivers when initiating therapy.

5. Monoclonal Antibody Immune-Modulating Drugs

Monoclonal antibody immune-modulating drugs, known as biologics, are indicated for patients with severe asthma that remains uncontrolled despite optimized therapy with ICSs and other controller medications. These agents target specific inflammatory pathways involved in type 2–high asthma (eosinophilic or allergic phenotypes). Treatment response is typically assessed after a 3- to 6-month trial and is reflected by improved symptom control, reduced exacerbation frequency, improved lung function, and decreased reliance on oral glucocorticoids. In cases of suboptimal response, switching to a biologic with a different molecular target may be beneficial. Biologics are generally well tolerated, although rare serious adverse effects, including anaphylaxis, have been reported with omalizumab and reslizumab. Many biologics are now available in autoinjector formulations, allowing for patient self-administration at home.[10][32][33]

     5. a. Anti-IgE therapy: Omalizumab

Omalizumab is indicated as an add-on therapy for patients aged 6 or older with moderate-to-severe allergic asthma who have positive skin test results or in vitro reactivity to perennial aeroallergens, or elevated IgE levels. Although it reduces exacerbation risk and has extensive long-term safety data, anaphylaxis is a rare but serious risk that requires monitoring. Omalizumab binds circulating IgE, thereby reducing its ability to trigger downstream T-helper 2–mediated responses, including eosinophilia and mast cell activation.

Baseline IgE levels are not predictive of treatment response but are required for patient selection and dose determination. The dose and frequency of administration (every 2 or 4 weeks) are based on baseline total IgE levels (30-700 IU/mL) and body weight. Patients should be observed after injections (particularly early in therapy), educated on the signs and symptoms of anaphylaxis, and prescribed epinephrine for self-administration if indicated. Other approved indications for omalizumab include chronic spontaneous urticaria, IgE–mediated food allergies, and chronic rhinosinusitis with nasal polyps. Common adverse effects of omalizumab include injection-site reactions (eg, pain, swelling, erythema, pruritus), headache, upper respiratory tract infections, sinusitis, nasopharyngitis, fatigue, arthralgia, myalgia, abdominal pain, and nausea. Rare but serious adverse effects include anaphylaxis and serum sickness–like reactions.

   5. b. Anti–IL-5 Therapies: Mepolizumab, Reslizumab, Dupilumab, Depemokimab

   (i) Mepolizumab

Mepolizumab is an add-on therapy indicated for patients aged 6 and older with severe eosinophilic asthma (absolute eosinophil count ≥150 cells/µL) and has demonstrated efficacy in reducing exacerbations and dependence on oral corticosteroids. It is administered subcutaneously once every 4 weeks at an age-dependent dose (typically 100 mg in adults). Mepolizumab binds IL-5, thereby inhibiting its signaling and reducing eosinophil proliferation and survival.[34][35] Mepolizumab is generally well tolerated, but patients should be monitored for hypersensitivity reactions and infections. Other approved indications for mepolizumab include eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, chronic rhinosinusitis with nasal polyps, and COPD with an eosinophilic phenotype.

Common adverse effects of mepolizumab include headache, injection-site reactions (eg, pain, erythema, swelling, pruritus), back pain, fatigue, upper respiratory tract infections, nasopharyngitis, and influenza-like symptoms. Rare but serious adverse reactions include hypersensitivity reactions and herpes zoster reactivation. Vaccination should be considered before initiating therapy but should be undertaken with caution, as immunocompromised patients are at risk for disseminated varicella-zoster infection.

   (ii) Reslizumab

Reslizumab is an add-on therapy for patients aged 18 and older with severe asthma and eosinophilia and has been shown to reduce exacerbations. As described above, reslizumab binds IL-5, thereby inhibiting its signaling and reducing eosinophil proliferation and survival. The recommended dosage is 3 mg/kg administered by intravenous infusion every 4 weeks. Patients should be monitored during and after infusions for signs and symptoms of anaphylaxis, and facilities administering the drug must be equipped to manage severe hypersensitivity reactions. Common adverse reactions include oropharyngeal pain, headache, myalgia, fatigue, and upper respiratory tract infections. Elevated creatine phosphokinase levels may occur. Rare but serious adverse reactions include anaphylaxis.

   (iii) Benralizumab

Benralizumab is indicated as add-on therapy for patients aged 6 and older with severe eosinophilic asthma, improving exacerbation rates and lung function. It binds IL-5Rα on eosinophils, triggering antibody-dependent cell-mediated cytotoxicity and near-complete eosinophil depletion. For patients aged 12 and older, it is administered as a 30-mg subcutaneous injection every 4 weeks for 3 months, then every 8 weeks. For younger patients, dosing is weight-based. Benralizumab is generally well tolerated, but patients should be monitored for hypersensitivity reactions, particularly after initial doses. Benralizumab is also approved for eosinophilic granulomatosis with polyangiitis. Common adverse effects include headache, pharyngitis, pyrexia, and injection-site reactions.

   (iv) Depemokimab

Depemokimab is a recently approved biologic for severe eosinophilic asthma, indicated as add-on maintenance therapy for patients aged 12 years and older with an absolute eosinophil count greater than 300 cells/µL in the prior 12 months or 150 cells/µL or higher at screening. Depemokimab is an ultra–long-acting monoclonal antibody that targets IL-5, preventing its binding to eosinophil IL-5 receptors and thereby inhibiting eosinophil maturation, activation, recruitment, and survival. The recommended dose is 100 mcg subcutaneously every 6 months.

Reported adverse effects include injection-site reactions, headache, nasopharyngitis, upper respiratory tract infections, and hypersensitivity reactions. As with other anti–IL-5 agents, patients should be evaluated and treated for helminthic infections before initiation. Ongoing postmarketing surveillance will continue to inform the long-term safety profile and detection of rare adverse effects.

    5.c. Anti-IL-4 antibody: Dupilumab  

Dupilumab is a human monoclonal antibody approved as an add-on maintenance therapy for patients aged 6 and older with moderate-to-severe asthma characterized by eosinophilic inflammation and/or dependence on oral corticosteroids. It targets IL-4Rα, blocking both IL-4 and IL-13 signaling—two central cytokines driving type 2 inflammation in asthma. By inhibiting this shared receptor, dupilumab reduces IgE production, eosinophilic airway inflammation, mucus hypersecretion, and airway hyperresponsiveness. Dupilumab is administered subcutaneously every 2 weeks with weight- and age-based dosing, following an initial loading dose. Dupilumab is also approved for atopic dermatitis, eosinophilic esophagitis, chronic rhinosinusitis with nasal polyps, and prurigo nodularis, making it a suitable option for patients with multiple atopic conditions.

Common adverse effects include injection-site reactions, nasopharyngitis, upper respiratory tract infections, headache, and transient eosinophilia. Ocular adverse effects (eg, conjunctivitis, blepharitis, dry eyes) are more frequent in patients treated for atopic dermatitis than for asthma. Other adverse effects include rash, arthralgia, and oropharyngeal pain. Rare but serious adverse effects include hypersensitivity reactions and eosinophilic conditions.

    5. d. Anti–TSLP Antibody: Tezepelumab

Tezepelumab is a human IgG2 monoclonal antibody targeting TSLP. The US Food and Drug Administration has approved tezepelumab as an add-on maintenance therapy for severe asthma in adults and adolescents aged 12 years and older. Tezepelumab is also approved for the management of inadequately controlled chronic rhinosinusitis with nasal polyps.

Common adverse effects include pharyngitis, arthralgia, and back pain. Hypersensitivity reactions and allergic conjunctivitis have been reported. Rare cases of anaphylaxis have occurred, and these patients should receive immediate treatment as indicated. Systemic corticosteroids should not be discontinued abruptly upon initiation of tezepelumab; instead, taper corticosteroids gradually if appropriate. Pre-existing helminth or parasitic infections should be screened and treated before therapy. If patients develop helminthic infections while receiving tezepelumab and do not respond to appropriate treatment, tezepelumab should be discontinued until the infection resolves.[36]

6. Systemic Corticosteroids

Systemic corticosteroids are used in asthma primarily for the management of acute exacerbations and, less commonly, as maintenance therapy in severe refractory disease when other controller options, including biologics, are insufficient or unavailable. According to guidelines from the Global Initiative for Asthma and the National Heart, Lung, and Blood Institute, short courses of systemic corticosteroids are recommended for moderate-to-severe asthma exacerbations to shorten recovery time, prevent relapse, and reduce the risk of hospitalization. Early initiation is preferred, and tapering is generally unnecessary for short courses. While systemic corticosteroids remain life-saving in acute asthma exacerbations, contemporary asthma management emphasizes minimizing systemic steroid exposure through optimized inhaled therapy and early use of targeted biologics to reduce long-term morbidity. Short-term systemic corticosteroid use may cause hyperglycemia, mood changes, insomnia, increased appetite, fluid retention, hypertension, and gastrointestinal irritation. Long-term or repeated exposure is associated with osteoporosis, adrenal suppression, weight gain, diabetes, cataracts, glaucoma, hypertension, dyslipidemia, immunosuppression, growth suppression in children, and increased cardiovascular risk.

7. Methylxanthine

Theophylline is a methylxanthine drug with dual mechanisms of action. It reduces the production and release of proinflammatory mediators, including tumor necrosis factor α and leukotrienes, thereby decreasing airway inflammation. It also acts as a nonselective adenosine receptor antagonist, resulting in smooth muscle relaxation and bronchodilation, thereby reducing airway obstruction.[37] 

Adverse effects, although variably reported, can include central nervous system stimulation (eg, headache, insomnia, irritability, restlessness, seizure), gastrointestinal symptoms (eg, nausea, vomiting, diarrhea), diuresis, skeletal muscle tremors, tachycardia, cardiac arrhythmias, hypercalcemia, difficulty urinating, exfoliative dermatitis, and, rarely, acute myocardial infarction. Theophylline has a narrow therapeutic window, requiring close monitoring of serum levels with periodic blood testing to avoid toxicity. Due to these factors and the availability of more effective therapies, theophylline is infrequently used in contemporary asthma management.

8. Cromolyn and Zileuton

Cromolyn is a mast cell stabilizer that reduces mast cell degranulation and the release of proinflammatory mediators, including histamine. Cromolyn is also thought to attenuate neural responses to airway sensory nerve irritation and to decrease the release of cytokines from preformed eosinophils. Possible adverse effects include cough, flushing, palpitations, chest pain, nasal congestion, nausea, fatigue, migraine, sneezing, wheezing, pruritus, dysphagia, esophageal spasm, pancytopenia, polycythemia, tinnitus, pharyngitis, and, rarely, psychosis. Zileuton is a 5-lipoxygenase inhibitor that decreases leukotriene synthesis, thereby reducing airway inflammation. Liver function must be monitored periodically during therapy due to the risk of hepatotoxicity. 

The stepwise pharmacotherapy approach summarized below is based on the most recent NHLBI and GINA guidelines.

Table 1. Initial Treatment Selection: Adults and Adolescents (12+ Years)

For this age group, GINA recommends 2 tracks. Track 1 (Preferred) is prioritized because using a low-dose ICS-formoterol reliever across all steps reduces the risk of severe exacerbations compared to using a SABA reliever.

Table 2. Initial Treatment Selection: Children (6–11 Years)

Treatment for children is focused on preventing exacerbations while managing symptoms with the lowest effective dose

Table 3. Add-on Biologic Therapies for Severe Asthma as Step 5

Step 5 is reserved for patients with "Difficult-to-Treat" or "Severe Asthma" who remain uncontrolled despite optimized Step 4 therapy

B. NON PHARMACOLOGICAL MEASURES

1. Environmental and Lifestyle changes

Identification and mitigation of environmental and occupational triggers, including allergens, tobacco smoke, air pollution, and respiratory infections, remain essential components of long-term asthma control. Nonpharmacologic strategies include smoking cessation, pulmonary rehabilitation, vaccinations, weight reduction[38][39], and allergen immunotherapy (eg, house dust mite sublingual immunotherapy in selected patients).[40]

Table 4. Environmental and Lifestyle changes*

 *These interventions are recommended to supplement medication for improved symptom control and risk reduction [20][18]

2. Bronchial Thermoplasty

For patients with severe persistent asthma that is poorly controlled or nonresponsive to medical therapy, bronchial thermoplasty offers a nonpharmacologic option. The procedure delivers controlled radiofrequency energy to the airway wall, heating and ablating bronchial tissue. The epithelium, blood vessels, mucosa, and nerves regenerate over time; however, airway smooth muscle does not regenerate and is replaced with connective tissue. The net effect is reduced bronchoconstriction due to decreased airway smooth muscle mass.

Patient selection and timing are critical, as the procedure can trigger postprocedural bronchospasm. Bronchial thermoplasty should be avoided in patients with ongoing exacerbations or chronic structural airway changes such as interstitial disease or bronchiectasis. Clinical trials generally excluded patients with 3 or more exacerbations per year, forced expiratory volume in 1 second (FEV1) less than 60%, and chronic rhinosinusitis.[9][41] The Global Initiative for Asthma 2025 guidelines emphasize a structured, personalized approach to asthma management in adults and adolescents aged 12 years and older. The core principle is continuous, individualized care using a cyclical process of assessment, treatment adjustment, and regular review.

Other Issues

The American College of Chest Physicians 2026 guidelines recommend either omalizumab or dupilumab for adult patients with moderate to severe allergic asthma and a history of 1 or more exacerbations per year requiring oral corticosteroids. For patients with more severe quality-of-life impairment and more than 2 exacerbations per year, omalizumab is preferred over dupilumab. For patients with greater lung function impairment, defined as FEV1 less than 70% of the predicted value, dupilumab is recommended over omalizumab.

In steroid-dependent adults with severe asthma, either anti–IL-5/IL-5Rα therapy or dupilumab may be used. For patients who have not responded to omalizumab after 4 to 6 months, anti–IL-5/IL-5Rα therapy or dupilumab is suggested. Those who do not respond to anti–IL-5/IL-5Rα therapy may transition to dupilumab or tezepelumab, with dupilumab preferred in steroid-dependent patients. In patients who do not respond to dupilumab after 4 to 6 months, anti–IL-5/IL-5Rα therapy or tezepelumab is recommended, with anti–IL-5/IL-5Rα therapy preferred in steroid-dependent patients. For patients who have not responded to anti–IL-5/IL-5Rα therapy after 4 to 6 months, a posttreatment FeNO level of 25 ppb or higher may guide a switch to dupilumab.[42][43] Across all scenarios, recommendations are based on conditional or low-certainty evidence, and care should center on individual patient phenotype, shared decision-making, regular reassessment of response, minimization of systemic corticosteroid exposure, and alignment with patient goals and safety.[44]

Enhancing Healthcare Team Outcomes

Asthma is a widespread condition affecting individuals across all age groups, and even well-controlled cases can abruptly worsen into severe, life-threatening attacks. Optimal management relies on a collaborative interprofessional approach. Accurate diagnosis involves physicians and advanced practice providers who confirm variable airflow limitation using spirometry and clinical evaluation while ruling out other conditions.

Pharmacists optimize inhaled corticosteroid therapy, ensure correct dosing, monitor for drug interactions, and promote proper inhaler technique and adherence. Nurses provide patient education, reinforce written action plans, monitor symptoms, and offer vaccination guidance. Specialists such as pulmonologists and immunologists tailor treatment to asthma phenotypes and escalate therapy to biologics when indicated, particularly in type 2 inflammatory asthma. Pharmacists and respiratory therapists support ongoing symptom monitoring, acute care, and long-term management, with evidence showing that pharmacist-led interventions improve adherence.[45][46]

During severe exacerbations, emergency physicians and critical care teams coordinate urgent interventions, including bronchodilation, systemic corticosteroids, oxygen therapy, or ventilation, and ensure safe transition to long-term control medications. Effective communication and collaboration among physicians, advanced practice providers, specialists, pharmacists, nurses, and respiratory therapists are essential for minimizing adverse effects and optimizing patient outcomes in asthma pharmacotherapy. Central to improving outcomes is patient education, including trigger avoidance and adherence to prescribed therapies.