Bronchial asthma: a brief overview

Bronchial asthma is a chronic inflammatory disease of the airways, in which symptoms can wax and wane. Wheezing, shortness of breath, chest tightness, and cough are typical symptoms. The main clinical feature of asthma is the variability of symptoms and variable limitation of airflow during exhalation. [1]

The modern understanding of asthma has evolved far from the old paradigm, which considered the disease to be merely episodic bronchospasm. Today, asthma is considered a heterogeneous condition with different phenotypes and biological mechanisms. Some patients experience predominantly allergic inflammation, while others have eosinophilic, non-allergic, neutrophilic, or mixed inflammation, and this is why the course and response to treatment can vary greatly. [2]

The disease is widespread and remains a significant cause of decreased quality of life, missed work and school visits, emergency room visits, and hospitalizations. The World Health Organization notes that asthma is one of the most common chronic diseases in children, and severe exacerbations can lead to death, especially in areas where there is underdiagnosis and insufficient access to inhaled medications. [3]

It's important to understand that even rare symptoms don't mean a "safe" form of the disease. A person with rare episodes of coughing or wheezing can still experience a severe exacerbation. This is why current recommendations emphasize not only rapid symptom relief but also ongoing monitoring of airway inflammation. [4]

In practice, asthma is a disease that can be well managed in most cases. With proper diagnosis, selection of inhalation therapy, training in inhalation technique, risk factor management, and regular monitoring, many patients live without frequent attacks, maintain normal physical activity, and avoid serious complications. [5]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, 10th revision, asthma is classified under the heading J45. Within this category, the following are distinguished: allergic asthma J45.0, non-allergic asthma J45.1, mixed asthma J45.8, and asthma unspecified J45.9. A separate category is asthmatic status J46, which clinically corresponds to a severe, potentially life-threatening exacerbation. [6]

In the International Classification of Diseases, 11th revision, asthma is classified in block CA23. The 2025-01 structure distinguishes between allergic asthma CA23.0, non-allergic asthma CA23.1, other specified forms of asthma or bronchospasm CA23.2, and unspecified asthma CA23.3. To clarify the severity, the International Classification of Diseases, 11th revision uses expansion codes, which makes the system more flexible and clinically oriented. [7]

Table 1. Codes for bronchial asthma according to the International Classification of Diseases [8]

System	Code	Formulation
ICD 10	J45	Asthma
ICD 10	J45.0	Predominantly allergic asthma
ICD 10	J45.1	Non-allergic asthma
ICD 10	J45.8	Mixed asthma
ICD 10	J45.9	Asthma, unspecified
ICD 10	J46	Status asthmaticus
ICD 11	CA23	Asthma
ICD 11	CA23.0	Allergic asthma
ICD 11	CA23.1	Non-allergic asthma
ICD 11	CA23.2	Other specified forms of asthma or bronchospasm
ICD 11	CA23.3	Unspecified asthma

Epidemiology

According to the World Health Organization, asthma affected approximately 262 million people and was associated with 455,000 deaths in 2019. It is one of the most common chronic non-communicable respiratory diseases worldwide, with a significant proportion of deaths occurring in low- and lower-middle-income countries, where the problem is often associated not only with the disease itself but also with insufficient access to basic inhalation therapy. [9]

A more recent global estimate from the Global Burden of Disease 2021 study showed approximately 260 million cases of asthma in 2021. The difference compared to the World Health Organization data is explained by the calculation methodology and the time frames used, but both estimates confirm the same thing: a colossal burden on the global health system. [10]

The Global Burden of Disease 2021 study also found that the age-standardized prevalence of asthma globally has declined since 1990, but the absolute number of patients is again increasing and is likely to continue to rise by 2050 due to population growth. This means that even with some improvement in population indicators, the burden on outpatient care, hospitals, and medications will remain high. [11]

In the United States, the latest national data show that current asthma would affect 8.6% of adults and 6.5% of children in 2024. These figures are important not because they are directly applicable to the rest of the world, but because they demonstrate that asthma remains a very common diagnosis even in countries with advanced diagnostic systems and access to inhaled therapy. [12]

The epidemiology of asthma is heterogeneous. Prevalence and severity depend on age, gender, living conditions, air pollution, smoking, obesity, occupational exposures, and access to healthcare. Countries where inhaled anti-inflammatory drugs are unavailable are particularly significant: they have a higher risk of severe exacerbations and preventable mortality. [13]

Table 2. Key epidemiological indicators of bronchial asthma [14]

Indicator	Meaning	Source
The number of people with asthma worldwide in 2019	262 million	World Health Organization
Asthma-related deaths in 2019	455,000	World Health Organization
The number of people with asthma worldwide in 2021	260 million	Global Burden of Disease 2021
Projected number of cases by 2050	275 million	Global Burden of Disease 2021
Current asthma prevalence in US adults in 2024	8.6%	Centers for Disease Control and Prevention
Current Asthma in US Children in 2024	6.5%	Centers for Disease Control and Prevention

Reasons

There is no single, universal cause of bronchial asthma. In most cases, the disease develops through a combination of genetic predisposition and environmental factors. In some people, atopy, a predisposition of the immune system to allergic reactions, plays a leading role; in others, it's repeated viral infections, occupational aerosols, air pollution, or tobacco smoke. [15]

In allergic asthma, the immune system overreacts to inhaled allergens: house dust mites, animal dander, pollen, cockroach particles, and mold. Inflammation in the bronchial mucosa becomes chronic, even if symptoms don't occur daily. Therefore, the absence of complaints between attacks does not mean the disease is absent. [16]

Non-allergic asthma can be triggered by viral infections, cold air, physical exertion, strong odors, irritating chemicals, medications, and occupational factors. In some patients, the clinical picture develops in adulthood, especially due to work with dyes, flour, latex, isocyanates, metals, or other respiratory sensitizers. [17]

Medications and other associated mechanisms play an additional role. In some patients, symptoms worsen after taking aspirin and some other nonsteroidal anti-inflammatory drugs. Symptoms can also be triggered by beta-blockers, severe rhinitis, chronic rhinosinusitis, obesity, and gastroesophageal reflux, although asymptomatic reflux itself is not considered a common cause of poor control. [18]

From a practical standpoint, it's more accurate to speak not of a singular "cause," but of a set of causal and aggravating factors. For one patient, the key factor may be an allergen; for another, obesity and poor inhalation technique; for a third, occupational exposure and a late diagnosis. This is why effective asthma therapy is always personalized. [19]

Risk factors

Current data show that a significant proportion of the global asthma burden is associated with modifiable risk factors. In the Global Burden of Disease 2021 analysis, approximately 29.9% of the global asthma burden, measured by years of life with health loss, was attributed to four main factors: high body mass index, occupational asthmatics, smoking, and nitrogen dioxide air pollution. [20]

In clinical practice, risk factors for exacerbations include poor symptom control, lack of or insufficient use of inhaled glucocorticosteroid, improper inhalation technique, abuse of short-acting bronchodilators, exposure to allergens in the presence of sensitization, smoking, vaping, air pollution, obesity, chronic rhinosinusitis, and previous severe exacerbations.[21]

Prematurity, low birth weight, rapid weight gain in infancy, frequent productive cough, lack of anti-inflammatory therapy in patients with severe exacerbations, tobacco smoke, and low baseline lung function are all associated with the risk of persistent decline in lung function. These factors do not always directly cause the disease, but can aggravate its course and accelerate bronchial wall remodeling. [22]

Risk factors for poor treatment response are worth highlighting separately. These include concomitant upper respiratory diseases, depression, anxiety, obstructive sleep apnea, social difficulties, poor treatment adherence, and inhalation technique errors. These factors often create a picture of "severe asthma," although disease control improves significantly after their correction. [23]

Finally, there are factors that increase the risk of drug-related complications: frequent courses of systemic glucocorticosteroids, long-term use of high doses of inhaled glucocorticosteroids, combination with drugs that affect hepatic metabolism, and advanced age. Modern treatment strategies aim to minimize these risks by transitioning the patient to a safer and more biologically sound regimen. [24]

Table 3. Main risk factors for bronchial asthma and its exacerbations [25]

Group of factors	Examples	Why is this important?
Hereditary	Family history of asthma and allergies	Increase the likelihood of developing the disease
Allergic	Pollen, house dust mites, animal dander, mold	Supports inflammation and symptoms
Behavioral	Smoking, vaping, poor treatment adherence	Increase the risk of poor control and exacerbations
Metabolic	Obesity	Complicates asthma control and increases disease burden
Ecological	Air pollution, nitrogen dioxide	They contribute to new cases and worsen the course of the disease.
Professional	Isocyanates, flour, latex, chemical aerosols	May cause asthma in adults
Clinical	Previous severe exacerbations, low lung function	Markers of high risk of new seizures

Pathogenesis

Bronchial asthma is caused by chronic inflammation of the airway walls. This inflammation makes the bronchi overly sensitive to irritants. In response to an allergen, virus, physical exertion, cold air, or chemical irritant, bronchospasm, swelling of the mucous membrane, and increased mucus production occur, making it difficult for a person to exhale. [26]

A significant proportion of patients experience what's known as type 2 inflammation. It's associated with interleukins 4, 5, and 13, increased eosinophils, immunoglobulin E, and nitric oxide in exhaled air. This variant of asthma has been best studied and has become the basis for the development of targeted biological agents. [27]

However, asthma is not limited to eosinophilic inflammation. There are variants with neutrophilic or paucigranulocyte inflammation, in which classic anti-inflammatory regimens may be less effective. This partly explains why two patients with similar symptoms may respond differently to the same therapy. [28]

If inflammation persists for years, structural changes develop in the bronchi, collectively termed "airway remodeling." These include thickening of the basement membrane, increased smooth muscle mass, goblet cell hyperplasia, subepithelial fibrosis, and more persistent narrowing of the bronchial lumen. Remodeling is associated with deterioration in lung function, a more severe course, and less reversibility of obstruction. [29]

Modern therapy effectively suppresses inflammation and reduces the risk of attacks, but it does not always completely reverse existing structural changes. Therefore, early diagnosis and early initiation of anti-inflammatory treatment are crucial: the sooner the disease is brought under control, the greater the chance of preserving lung function and avoiding the development of persistent airflow limitation. [30]

Symptoms

Classic symptoms of asthma include wheezing, shortness of breath, chest tightness, and cough. A particularly characteristic feature of asthma is that symptoms fluctuate in frequency and intensity: some days they are virtually absent, while on others they intensify sharply. For the physician, this variability is an important diagnostic clue. [31]

In many patients, symptoms worsen at night, early in the morning, with physical exertion, in the cold, after laughing, exposure to allergens, or during a viral infection. In some people, cough may be the only symptom, especially with cough-variant asthma. This often delays diagnosis, as the cough is mistaken for residual symptoms of infection, reflux, or upper respiratory disease. [32]

During an attack, a person may experience shortness of breath, the need to sit supported by their arms, an inability to exhale deeply, anxiety, and increasing weakness. In severe cases, speech becomes short, tachycardia develops, the accessory muscles of respiration become involved, and oxygen saturation drops. Such symptoms require immediate medical attention rather than home observation. [33]

It should be noted that physical examination may be normal between episodes. The absence of wheezing during a routine examination does not rule out asthma. Therefore, the patient's complaints, their recurrence, triggers, spirometry data, and response to therapy are more important for diagnosis than a single "normal" auscultation of the lungs. [34]

Asthma symptoms can mimic other conditions, especially in children, elderly patients, and smokers. In these groups, a more thorough diagnostic evaluation is often required to distinguish asthma from chronic obstructive pulmonary disease, heart failure, laryngeal dysfunction, eosinophilic bronchitis, and other conditions. [35]

Classification, forms and stages

Bronchial asthma can be classified in several ways, and this is important not only academically but also for the selection of therapy. The first level is etiologic: allergic, non-allergic, mixed, and unspecified asthma in the International Classification of Diseases, 10th revision, and allergic, non-allergic, other specified forms, and unspecified asthma in the International Classification of Diseases, 11th revision. [36]

The second level is phenotypic. In clinical practice, the following phenotypes are distinguished: allergic asthma, cough variant, asthma with exercise as the primary trigger, asthma in adults with late onset, asthma associated with obesity, and severe asthma with eosinophilic inflammation. These phenotypes do not always correspond to International Classification of Diseases codes, but they help physicians choose treatment strategies. [37]

The third level is assessment by control and severity. Control is determined by the frequency of daytime symptoms, nighttime awakenings, activity limitation, and the need for a rapid-acting bronchodilator. Asthma severity is usually assessed retrospectively, that is, by the amount of treatment required to achieve control. If control is achieved with a low dose of background therapy, asthma is considered mild. If high doses of combination therapy are required or the disease remains uncontrolled, it is considered severe asthma. [38]

A distinction is made between difficult-to-treat asthma and severe asthma. Difficult-to-treat asthma is not necessarily truly "resistant" disease. It often reflects poor inhalation technique, poor adherence, continued smoking, comorbidities, or even misdiagnosis. Severe asthma is defined as asthma that remains uncontrolled despite good adherence to high-intensity therapy and correction of modifiable factors, or that requires such therapy to maintain control. [39]

From a clinical perspective, it is also useful to talk about stages of the current condition: symptom remission, controlled course, partially controlled course, uncontrolled course, exacerbation, severe exacerbation, and life-threatening exacerbation. This working classification better reflects actual practice than a formal division based solely on the code. [40]

Table 4. Practical classification of bronchial asthma [41]

Basis of classification	Options	Practical significance
According to the International Classification of Diseases	Allergic, non-allergic, mixed, unspecified	Needed for coding and documentation
By phenotype	Allergic, eosinophilic, cough, late-onset asthma, asthma in obesity	Helps choose targeting tactics
By level of control	Controlled, partially controlled, uncontrolled	Determines the need to intensify therapy
By severity	Light, medium, heavy	It is assessed by the volume of therapy required for control
As of the current state	Stable course, exacerbation, severe exacerbation, life-threatening exacerbation	Affects the urgency of assistance

Complications and consequences

The main acute complication of asthma is a severe exacerbation, which can lead to respiratory failure, hospitalization, intensive care unit treatment, and death. The danger of asthma is often underestimated precisely because between attacks, patients may feel almost healthy. However, a severe exacerbation can also develop in people with rare symptoms, especially if they are not receiving anti-inflammatory treatment. [42]

Long-term uncontrolled asthma promotes airway remodeling and a gradual decline in lung function. This can lead to the development of more persistent airflow limitation, which is less responsive to bronchodilators. The more frequent the exacerbations and the longer the patient remains without basic therapy, the higher the risk of this scenario. [43]

No less significant are the long-term consequences for a person's life: chronic fatigue, limited physical activity, decreased sleep quality, anxiety in anticipation of an attack, missed work and school time, and, in children, an impact on daily activities and development. For patients with severe asthma, the toxicity of repeated courses of systemic glucocorticosteroids is also significant. The more frequent such courses are required, the higher the risk of systemic side effects. [44]

Comorbid conditions can also exacerbate the effects of asthma. Rhinitis, chronic rhinosinusitis, nasal polyps, obesity, anxiety, depression, gastroesophageal reflux, and obstructive sleep apnea not only worsen well-being but also hinder control. As a result, patients may progress to higher levels of treatment more quickly than would be necessary with timely correction of these underlying conditions. [45]

When to see a doctor

A routine visit to the doctor is necessary for recurrent coughing, episodes of wheezing, shortness of breath, chest tightness, nighttime awakenings due to breathing, and any repeated association of symptoms with physical activity, allergens, cold, or viral infections. Even if episodes seem rare, the diagnosis should be confirmed objectively and not assumed "by eye." [46]

Urgent consultation is necessary if conventional medications are less effective, symptoms become more frequent, worsen at night, there is a need for repeated inhalations of a bronchodilator, exercise tolerance has decreased, or there have been one or more exacerbations in a year. These symptoms indicate not just discomfort, but an increased risk of a subsequent, possibly more severe attack. [47]

Emergency care is required for severe shortness of breath, inability to speak in long sentences, forced sitting with a forward lean, respiratory rate greater than 30 breaths per minute, oxygen saturation less than 90% on air, peak expiratory flow rate less than 50% of predicted or better, as well as drowsiness, confusion, or a "quiet" chest. These signs have been described as markers of a severe or life-threatening exacerbation. [48]

After any exacerbation, a follow-up visit is also necessary, even if things have improved. International guidelines recommend an early follow-up visit because the risk of further deterioration is highest immediately after an attack. It's also the most convenient time to check inhalation technique, adjust basic therapy, and provide a clear, written action plan. [49]

Diagnostics

The diagnosis of bronchial asthma is based on two pillars: typical variable respiratory symptoms and objective confirmation of variable airflow limitation during exhalation. Symptoms alone are important, but they are not sufficient. International guidelines explicitly emphasize that the diagnosis must be confirmed and documented in medical records based on objective data. [50]

The first step is a detailed interview and examination. The doctor determines the specific symptoms, their frequency, whether there are nocturnal episodes, whether they are triggered by physical activity, laughter, cold air, allergens, or viral infections, and whether there are any associated allergies or family history. At this stage, it is already possible to determine how typical the symptoms are for asthma and whether they resemble other conditions. [51]

The second step is a respiratory function test, primarily spirometry with a bronchodilator test. In adults, an increase in forced expiratory volume in 1 second or forced vital capacity by 12% and 200 ml or more after inhalation of a bronchodilator is considered diagnostically significant. In children, an increase in forced expiratory volume in 1 second by 12% of the predicted value is considered diagnostic. If spirometry is unavailable, peak flowmetry is used, although it is less reliable. [52]

The third step is to confirm variability. If reversibility is not detected on the first test, this does not rule out asthma. Guidelines suggest repeating the test during the symptomatic period, after temporarily discontinuing certain bronchodilators, assessing peak expiratory flow rate variability over 1-2 weeks, performing a bronchial provocation test, or evaluating the response to 4 weeks of inhaled glucocorticosteroid therapy. For adults, assessing fluctuations between visits is also helpful. [53]

The fourth step is additional markers of inflammation. With typical symptoms, elevated exhaled nitric oxide (more than 50 ppb) in adults and adolescents or more than 35 ppb in children, as well as elevated blood eosinophils, may support a diagnosis of type 2 asthma. However, this is merely supportive of the diagnosis, not absolute confirmation, as these levels can also be elevated in other conditions. Normal values do not rule out asthma. [54]

The fifth step is reassessment of the existing diagnosis. In primary care, 25-35% of patients with a previously established asthma diagnosis lack objective confirmation. Therefore, in the presence of a questionable history, poor response to treatment, or atypical clinical presentation, the diagnosis should be reconsidered rather than indefinitely escalating therapy. This is especially important in the elderly, smokers, and patients with persistent obstruction, in whom asthma must be distinguished from chronic obstructive pulmonary disease and its mixed variant. [55]

Table 5. Step-by-step diagnosis of bronchial asthma [56]

Stage	What is being assessed?	What is considered significant
1	Complaints and anamnesis	Variable cough, wheezing, shortness of breath, chest tightness
2	Connection with provocateurs	Night, physical activity, cold, allergens, viral infections
3	Spirometry with a bronchodilator drug	In adults, the increase is 12% and 200 ml or more
4	Peak flowmetry	Daily variability is more than 10% in adults and more than 13% in children
5	Response to trial therapy	Improvement in lung function after 4 weeks of anti-inflammatory treatment
6	Type 2 biomarkers	Elevated exhaled nitric oxide and blood eosinophils
7	Elimination of alternatives	Chronic obstructive pulmonary disease, laryngeal diseases, heart failure and other causes

Differential diagnosis

The differential diagnosis of bronchial asthma begins with a simple question: is this truly a variable bronchial disease, or are the symptoms explained by something else? The most common alternatives are chronic obstructive pulmonary disease, induced laryngeal obstruction, chronic rhinosinusitis with mucus retention syndrome, gastroesophageal reflux, eosinophilic bronchitis, heart failure, an airway foreign body, and pulmonary embolism in acute dyspnea. [57]

In elderly patients and smokers, the main difficulty is distinguishing between asthma and chronic obstructive pulmonary disease, and sometimes recognizing their combination. If obstruction persists and responds poorly to bronchodilator testing, international guidelines recommend reviewing the patient's medical history, the nature of symptoms, and previous records, and, if uncertain, referring the patient to a specialist. In patients with chronic obstructive pulmonary disease and asthmatic features, inhaled glucocorticosteroids should be included in the treatment regimen, as bronchodilator therapy alone is associated with worse outcomes in this group. [58]

If a patient has a predominant cough without obvious wheezing or shortness of breath, it's important to consider not only cough-variant asthma, but also postnasal drip, sinusitis, reflux, angiotensin-converting enzyme inhibitor use, and eosinophilic bronchitis. In such cases, the physician's clinical intuition alone is often insufficient—functional testing, sometimes provocative studies, and an assessment of the response to anti-inflammatory therapy are necessary. [59]

In acute, severe dyspnea, it is important not to miss conditions that masquerade as an asthma attack but require a different approach: heart failure, anaphylaxis, upper respiratory obstruction, foreign body aspiration, and pulmonary embolism. Therefore, in the case of severe deterioration, it is always important to evaluate not only whether it "looks like asthma," but also whether there is a more dangerous alternative. [60]

Treatment

Modern asthma treatment is built around a basic principle: every patient requires therapy containing an inhaled glucocorticosteroid. The 2025 international guidelines emphasize that all adults, adolescents, and children aged 6–11 years should be treated with this class of drugs, as it significantly reduces the frequency and severity of symptoms, the risk of exacerbations, and the risk of asthma-related death. [61]

The basic logic of treatment is not only to rapidly dilate the bronchi but also to suppress chronic inflammation. Therefore, a strategy based solely on a rapid-acting bronchodilator without an anti-inflammatory component is no longer considered optimal. For adults and adolescents, a low-dose combination of an inhaled glucocorticosteroid with formoterol as needed is the preferred option at the initial stages of treatment. In clinical studies, this approach reduced the risk of emergency department visits or hospitalizations by approximately 65% compared with therapy with a rapid-acting bronchodilator alone and by 37% compared with a daily inhaled glucocorticosteroid plus an as-needed rapid-acting bronchodilator. [62]

If symptoms persist, a stepwise intensification of therapy is used. At subsequent steps, a regular maintenance combination of an inhaled glucocorticosteroid and a long-acting beta2-agonist is added. For some patients, a regimen in which the same combination with formoterol is used as both a baseline treatment and a symptomatic reliever is preferable. This regimen simplifies treatment and provides better protection against exacerbations than options with a single, rapid-acting agent. [63]

Inhalation technique and adherence are crucial. In practice, a significant proportion of ineffectiveness is not due to the "weakness" of the drug, but to the patient inhaling incorrectly, not coordinating aspiration and inhalation, not rinsing the mouth after certain medications, using the inhaler inconsistently, or discontinuing basic therapy as soon as they feel better. Therefore, patient education is not an adjunct to treatment, but rather an integral part of the treatment itself. [64]

If control is inadequate, before intensifying the regimen, it is imperative to seek out the underlying causes: persistent smoking, obesity, rhinitis, chronic rhinosinusitis, symptomatic gastroesophageal reflux, anxiety, depression, allergens, and occupational exposures. This approach avoids unnecessary transition to high doses and excessive use of systemic glucocorticosteroids. In obese patients, even a 5-10% weight loss can improve asthma control. [65]

If control remains incomplete with combination therapy, the addition of a long-acting muscarinic antagonist is considered. International guidelines indicate that this class slightly improves lung function and slightly reduces the risk of exacerbations, but generally does not produce a significant impact on symptoms and quality of life. Therefore, the addition of a long-acting muscarinic antagonist is not a universal solution, but a reasonable next step for some patients after optimization of their primary regimens. [66]

In patients with severe asthma, phenotyping and biomarker assessment are key. This is where the greatest progress has occurred in recent years. At stage 5 for adults and adolescents, international guidelines recommend considering targeted biological agents: anti-immunoglobulin E, anti-interleukin 5 or interleukin 5 receptor, anti-interleukin 4 alpha receptor, and anti-thymic stromal lymphopoietin. Not all targets are available for children, and age-specific indications are not uniform in all countries, but the logic of personalized choice has already become firmly established in practice. [67]

Biological therapy has transformed the prognosis of severe asthma. Recent reviews show that it reduces the number of exacerbations, hospitalizations, and the need for maintenance systemic glucocorticosteroids, while also improving quality of life. In school-aged children, a review by Leonard B. Bakari demonstrated that approved biologic agents in phenotype-matched patients reduce exacerbation rates by 27–59% compared with placebo. Drug selection should be based on allergic sensitization, immunoglobulin E levels, blood eosinophils, exhaled nitric oxide, and the patient's clinical profile. [68]

New treatment approaches are associated not so much with the emergence of a single "miracle technology" as with the transition to precision medicine. These include the early use of anti-inflammatory inhalation therapy, single-combination regimens for symptom control and relief, biomarker-guided selection of biological agents, more cautious use of systemic glucocorticosteroids, and the pursuit of clinical remission in at least some patients with severe asthma. International guidelines already note that clinical remission is achievable in some patients with biological therapy. [69]

During an exacerbation, the management depends on the severity. In primary and emergency care, dyspnea, respiratory rate, pulse rate, oxygen saturation, and pulmonary function are assessed. In severe exacerbations, repeated inhalations of a rapid-acting bronchodilator, inhaled ipratropium, oxygen, and systemic glucocorticosteroids are immediately administered. If the response is insufficient, intravenous magnesium sulfate may be considered. Antibiotics, sedatives, and unnecessary chest x-rays are not routinely recommended. [70]

An essential part of treatment is a written asthma action plan. All patients should receive one. The plan outlines routine medications, guidelines for increasing inhalation therapy, criteria for initiating systemic glucocorticosteroids in the event of a worsening condition, and signs that require urgent medical attention. Such a plan makes treatment more manageable and reduces the risk of a delayed response to a worsening condition. [71]

Table 6. Stepwise treatment of bronchial asthma in adults and adolescents [72]

Step	The main idea of treatment	Comment
1	Low dose combination of inhaled glucocorticosteroid with formoterol as needed	Preferred strategy in adults and adolescents
2	Low dose diffusible inhaled glucocorticosteroid or on-demand strategy with an anti-inflammatory component	Suitable for more frequent symptoms
3	Low dose combination of inhaled glucocorticosteroid and long-acting beta2-agonist	Often a single inhaler is used for control and relief.
4	Average dose of a combination of an inhaled glucocorticosteroid and a long-acting beta2-agonist	For insufficient control at the previous stage
5	Phenotype assessment, possible addition of a long-acting muscarinic antagonist, biological agents, sometimes high-dose testing	For severe asthma after optimization of the previous steps

Table 7. Biological therapy for severe bronchial asthma [73]

Target	Examples of drugs	For which phenotype
Immunoglobulin E	Omalizumab	Severe allergic asthma
Interleukin 5	Mepolizumab	Severe eosinophilic asthma
Interleukin 5 receptor	Benralizumab	Severe eosinophilic asthma
Interleukin 4 alpha receptor	Dupilumab	Type 2 asthma, including those with eosinophilia or elevated exhaled nitric oxide
Thymic stromal lymphopoietin	Tezepelumab	Severe asthma with broad applicability across phenotypes

Prevention

Primary prevention of bronchial asthma as a completely guaranteed strategy is not yet possible, as the disease is multifactorial. However, reducing tobacco smoke, controlling air pollution, reducing occupational inhalation exposure, and correcting obesity can reduce the risk of developing the disease and its severe course. The World Health Organization specifically emphasizes the importance of combating tobacco smoke and air pollution for both preventing new cases and controlling existing asthma. [74]

Secondary prevention, that is, preventing exacerbations in an already ill person, is much more realistic. The main measures include regular anti-inflammatory inhalation therapy, proper inhalation technique, cessation of smoking and vaping, control of exposure to allergens in sensitized patients, treatment of rhinitis and chronic rhinosinusitis, weight management, and adequate physical activity. [75]

For some patients with clinically significant sensitization to house dust mites and inadequate control with inhalation therapy, sublingual allergen-specific immunotherapy may be considered, but not in those with significantly reduced lung function. This is not a universal method or a replacement for background therapy, but an additional tool in appropriately selected patients. [76]

Vaccinations and a written action plan play a special role. Recommendations emphasize the need for up-to-date respiratory vaccinations and a mandatory written plan, which helps patients recognize deterioration early and take appropriate measures. Simply having such a plan often reduces the likelihood of late presentation and a severe, advanced attack. [77]

Monitoring is also prevention. Even when feeling well, asthma status should be assessed regularly, and especially closely after an exacerbation. At each visit, it is advisable to reassess symptom control, frequency of use of quick-relief medications, inhaler technique, adherence, and the presence of new risk factors. [78]

Table 8. Practical measures for the prevention of exacerbations of bronchial asthma [79]

Measure	What does it give?
Regular anti-inflammatory inhalation therapy	Reduces the risk of severe attacks and death
Correct inhalation technique	Increases the actual effectiveness of drugs
Quitting smoking and vaping	Reduces inflammation and flare-ups
Control of rhinitis and rhinosinusitis	Helps to better control symptoms
Weight loss in obesity	May improve asthma control
Written action plan	Allows you to react earlier to deterioration
Regular follow-up visits	They help to adjust treatment in time

Forecast

The prognosis for asthma depends largely on how early the diagnosis is confirmed and how consistently anti-inflammatory treatment is administered. With the right regimen, many patients achieve good symptom control, lead normal lives, exercise, and rarely experience severe attacks. [80]

Early initiation of low-dose inhaled glucocorticosteroids is associated with better lung function compared with treatment initiated 2–4 years after symptom onset. Furthermore, patients who experienced a severe exacerbation without such therapy have, on average, worse long-term lung function than those who initiated anti-inflammatory treatment earlier.[81]

The worst prognosis is observed with late diagnosis, smoking, frequent exacerbations, obesity, poor adherence, constant exposure to allergens or occupational irritants, and severe asthma requiring advanced therapy. However, even in some patients with severe asthma, modern biological drugs can already achieve long-term control and clinical remission. [82]

Therefore, the prognosis for asthma cannot be summed up simply as "the disease is permanent" or "the disease is completely curable." It is more accurate to say this: it is a chronic disease, but in most cases it is well controlled, and some patients may experience long-term clinical remission with appropriate therapy and the patient's active participation in treatment. [83]

FAQ

Is it possible to completely cure bronchial asthma?
In the classic sense, complete "disappearance of the disease forever" cannot be guaranteed, as asthma is a chronic disease with various biological mechanisms. However, good symptom control, the absence of severe exacerbations, and even clinical remission are quite achievable in some patients. [84]

Is it dangerous to use only a drug for rapid symptom relief?
Yes, this approach is considered insufficient. Current international recommendations emphasize that treatment should include an anti-inflammatory component and not be limited to rapid bronchodilation alone. [85]

Is asthma always associated with allergies?
No. Asthma can be allergic or non-allergic, and has different phenotypes and endotypes. In some patients, allergens play a leading role, while in others, viruses, occupational irritants, obesity, or other mechanisms play a role. [86]

Is it possible to exercise?
Yes, with good asthma control, physical activity is not contraindicated and may even be beneficial. It is important to have adequately selected background therapy and know how to prevent exercise-induced bronchospasm. [87]

Does all patients require spirometry?
Spirometry is the primary method for objectively confirming the diagnosis in most patients. If it is unavailable, peak flowmetry can be used, but it is less accurate. If in doubt, functional confirmation of the diagnosis is still advisable. [88]

What is severe asthma?
It is asthma that remains uncontrolled despite good adherence to high-intensity therapy and correction of modifiable factors, or that requires such therapy to maintain control. Severe asthma is not simply a common complaint, but a unique clinical situation requiring expert assessment. [89]

When are biologics needed?
Typically, when asthma remains poorly controlled with advanced levels of standard treatment, and the appropriate phenotype is confirmed: allergic, eosinophilic, or another variant of type 2 asthma. The choice depends on biomarkers and the clinical picture. [90]

Is a written action plan necessary?
Yes, it is recommended for all patients. A plan helps recognize deterioration early, determine when to increase inhalation therapy, when to start systemic glucocorticosteroids, and when to seek urgent medical attention. [91]

Key points from experts

Helen K. Reddel, MBBS, PhD, Chair of the Scientific Committee of the Global Initiative for Asthma, Macquarie University and the University of Sydney.
A key current thesis emerging from the work of this expert community is that asthma should be treated with anti-inflammatory interventions from the outset, not just symptomatically. This is the basis for the 2025 strategy: all adults, adolescents, and children aged 6–11 years should receive treatment with an inhaled glucocorticosteroid, as this reduces the risk of severe outcomes and improves long-term control. [92]

Guy Brusselle, MD, PhD, FERS, Chairman of the Board of Directors of the Global Initiative for Asthma, Ghent University and Ghent University Hospital.
The current clinical message, which reflects the international strategy, is that severe asthma cannot be considered a single disease. Phenotyping, searching for comorbid conditions, testing of inhalation technique, and personalized selection of adjunctive therapy are needed, including a long-acting muscarinic antagonist and biologics targeting immunoglobulin E, interleukin 5, interleukin 4 receptor alpha, and thymic stromal lymphopoietin. [93]

Leonard B. Bacharier, MD, professor of pediatrics, Monroe Carell Jr Children's Hospital at Vanderbilt University Medical Center.
For school-age children with severe asthma, the central thesis is that biologic therapy should be tailored not "by overall severity," but by phenotype and biomarkers. His 2025 review showed that current biologic agents significantly reduce exacerbation rates and improve clinical outcomes in appropriate children, and the decision should be based on blood eosinophils, exhaled nitric oxide, allergic sensitization, and immunoglobulin E levels. [94]

A practical conclusion from current expert opinions:
Bronchial asthma today is not a disease to be "tolerated between attacks," but a condition that can and should be actively managed. The key pillars of a good outcome are an objectively confirmed diagnosis, early anti-inflammatory inhalation therapy, regular reassessment of control, a written action plan, and personalized treatment intensification in patients with severe asthma. [95]