A.G. Chuchalin: “Asthma is not a reason to give up even a career as a soloist of the Bolshoi Theater”

Academician of the Russian Academy of Medical Sciences, professor, doctor of medical sciences, director of the Moscow Research Institute of Pulmonology Alexander Grigorievich Chuchalin is an iconic figure in modern therapy. It is he who is rightfully considered the founder of the national school of pulmonology. Therefore, when the editors of the Pharmacy Council received a large number of questions about the treatment of bronchial asthma (BA), we thought: “Who should we ask them if not Alexander Grigorievich?” And we were very glad that the respected scientist, world-famous clinician not only agreed to meet with us, but also gave detailed answers and recommendations for our readers.

Alexander Grigorievich, one of the readers of the “Pharmacy Council”, a pharmacy worker, noticed: people turn to him for drugs to treat bronchial asthma several times a week. Is this disease really that widespread?

Bronchial asthma is a very common disease throughout the world and in our country in particular. The data that I will give differs from the figures of official statistics. The reason for the discrepancies is simple: the Ministry of Health and Social Development takes into account only those patients who go to medical institutions for asthma (as a rule, they call an ambulance and are admitted to a hospital). Recently, the number of such patients has been decreasing. We also have data from epidemiological studies, according to which in the pediatric population, asthma occurs in 7-8%. In the adult population, asthma is somewhat less common; it is detected in only 4-5% of people. The total is about 6 million people, and this, you see, is a lot.

I believe that in recent years we have made significant progress in the fight against asthma due to the introduction of modern clinical guidelines based on documents from the World Health Organization. They give a clear definition of what bronchial asthma is, what are the criteria for making a diagnosis - this is very important for the domestic school of pulmonologists. Previously, there were disagreements, and there was even some ambiguity on important points. For example, it was not entirely clear what was considered bronchial asthma and what was considered another disease. But now, fortunately, we have overcome this and, moreover, have achieved good results in controlling bronchial asthma.

When talking about the treatment of bronchial asthma, this term is often used - control. What does it mean? That the disease cannot be cured, but can be controlled?

Not certainly in that way. To explain the terminology, I'll start from the beginning. Asthma is treated according to severity: mild, moderate or severe. In addition, there are concepts of exacerbation, when attacks occur frequently, and remission, when the patient’s condition remains satisfactory for a long time.

The main symptoms of bronchial asthma are:
an annoying, persistent cough, which has the character of an attack of suffocation (we say “paroxysmal cough”, “paroxysm” translated from Greek means “increase”);

Shortness of breath, or, as patients themselves more often say, suffocation. Shortness of breath can occur both during the daytime and in the middle of the night. By the way, the development of attacks at night indicates a more severe course of asthma;

The appearance of a viscous, or, as they say in textbooks, glassy secretion. After its departure, the patient's condition improves sharply.

Those. If a person comes to you with such complaints, can you say with confidence that he has bronchial asthma?

Complaints alone are, of course, not enough. It is necessary that they be supported by data from functional studies of the respiratory organs. For example, it is necessary to conduct a study of external respiration parameters: measure peak expiratory flow, forced vital capacity in 1 second, etc. Those. there must be a functional diagnosis of bronchial asthma. In addition, we attach great importance to identifying certain biochemical markers of allergies that are associated with increased production of immunoglobulin E. Our institute, the Moscow Research Institute of Pulmonology, where I work and which I direct, is constantly developing new approaches to the diagnosis of bronchial asthma. One of the recently opened directions is the conduct of highly sensitive tests for determining biomarkers, which make it possible to obtain confirmation of the presence of inflammatory processes in the airways in bronchial asthma. Such a marker, in particular, is nitric oxide.

Returning to the examination program, I will say that the doctor should not just listen to the patient, but ask him targeted questions, clarify what the nature of the cough is, what the sputum looks like, etc. Then examine the function of external respiration and conduct an allergological examination. All this allows us to establish the diagnosis of “bronchial asthma”. But this, as they say in specialist circles, is still half the diagnosis.

That is, maybe, in fact, this patient does not have bronchial asthma at all, but some other disease?

No, there are simply many different types of asthma that cause it. One of the most common is asthma associated with flowering plants. However, the disease can be associated with house dust and certain foods. Sometimes asthma is induced by viral or bacterial agents. The doctor is faced with the task of identifying risk factors that lead to the development of bronchial asthma, and thus determining its nature. There is, say, asthma that is caused by taking aspirin - aspirin asthma. There is also asthma associated with exercise.

Are you talking about novice athletes who, having decided to connect their lives with sports, suddenly feel those same attacks of suffocation?

Rather, about professionals - among this category of people, asthma is much more common than in the general population. The leading number of patients with bronchial asthma is found among athletes. This is facilitated by increased stress on the respiratory system, and contact with allergens, such as chlorinated pool water, and much more. And all this must be taken into account when making a diagnosis. One of the first questions that, in my opinion, a doctor should ask a patient with suspected bronchial asthma is: “What do you do?”

Alexander Grigorievich, do pharmacy workers belong to a group at increased risk of developing bronchial asthma?

I would include all people in contact with potential allergens in this conditionally allocated group - after all, bronchial asthma is of an allergic nature. The smell in pharmacies, of course, is specific, but I don’t think that sales floor employees have such close contact with medicinal substances. But employees of the recipe and production departments really belong to a potential risk group. I would recommend that they work only in special masks, despite the inconvenience. This will reduce the likelihood of allergens entering the respiratory tract.

What other preventative measures can you recommend?

Unfortunately, other than minimizing contact with allergens, nothing. For persons with a hereditary factor, we can recommend changing their diet, lifestyle, quitting smoking, sometimes it is necessary to change their place of residence, but this is not always possible. Preventive use of any specific drugs is also not prescribed - bronchial asthma is treated, as they say, based on its presence.

It is known that there is treatment for an attack and there is basic therapy. What's more important? Or is it always necessary to have both?

The main task is to influence the inflammatory process in the respiratory tract. In other words, it is allergic inflammation that needs to be treated - this is what basic anti-inflammatory treatment consists of. If it is not there, it is impossible to achieve good results. In 1995, we introduced local anti-inflammatory therapy into practice - these were inhaled glucocorticosteroids. They are still used today - in modified form, of course.

But for mild asthma, especially in pediatrics, we do not start therapy with inhaled steroids. First, it is advisable to prescribe, for example, leukotriene inhibitors. Therapy consists of several stages, and therefore the doctor sets the time frame for determining the effectiveness of treatment. Let's say, he schedules the next visit in 2 weeks, in 1 month, then in 3 months, and then the doctor will be able to determine whether this treatment regimen is “working” or not.

Moderate severity of bronchial asthma is characterized by daily attacks of suffocation. The therapy described above will not be enough, therefore it is necessary to include inhaled glucocorticosteroids in combination with bronchodilators of two classes: short-acting and long-acting. In this case, asthma should also not be considered as a “disease of one visit to the doctor.”

I am forced to state the fact that our patients are not treated well enough. We have research data in which the incidence of severe bronchial asthma reaches 20%. If asthma is severe - say, the symptoms of the disease significantly disturb the patient’s sleep, lead to a decrease in quality of life, disability - we adhere to treatment regimens for moderate asthma, but strengthen the anti-inflammatory component. For example, as part of basic therapy, in addition to inhaled glucocorticosteroids, we prescribe leukotriene inhibitors.

Psychiatrists and psychotherapists consider bronchial asthma a psychosomatic disease and therefore recommend “treating not the body, but the soul.” How do you feel about psychotherapy as a possible treatment for asthma?

It is recognized throughout the world that psychotherapeutic effects are partly responsible for the placebo effect in any disease. However, I am not aware of studies confirming the reliable effectiveness of psychotherapy for bronchial asthma. Of course, we must have a certain reserve of therapeutic effects and use them in certain situations. In my opinion, such backup methods include not psychotherapy or herbal medicine, but the use of monoclonal antibodies to immunoglobulin E. Today there is only one drug from this group, but I think it will soon have competitors.

) used to assess the tone of the LES and the state of gastric motor function. Currently, computerized measurement of LES tone is used. A manometric sign of GER is a change in the nature of contractions of the esophagus and the contractile complex itself (decreased amplitude, increased duration of contractions, irregular shape of the contractile complex).

An informative diagnostic method is 24-hour monitoring of esophageal pH. This method makes it possible to identify the total number of reflux episodes during the day and their duration (normal pH levels of the esophagus are 5.5–7.0, in the case of reflux less than 4). The presence of GERD is indicated if the total number of episodes of GER during the day is more than 50 or the total duration of the decrease in pH to a level of less than 4 exceeds 1 hour. Comparison of the study results with data from the patient’s diary (registration of periods of food intake, medications, time of onset of pain, heartburn, etc.) allows us to assess the role of the presence and severity of pathological reflux in the occurrence of certain symptoms. The presence of several sensors (3 – 5) makes it possible to identify the duration and height of reflux, which is informative in the case of studying reflux-induced pulmonary pathology.

pH monitoring can be carried out in combination with other research methods, for example, assessment of respiratory function, polysomnography.

Another method for detecting GER is scintigraphy of the esophagus. Technetium sulfate colloid is used for testing. The test is considered sensitive and specific. A delay of more than 10 minutes in the esophagus of the isotope indicates a slowdown in esophageal clearance. In addition, the test is informative for assessing the evacuation of gastric contents. In some cases, the method makes it possible to record reflux-induced microaspiration.

X-ray of the esophagus detects the reflux of contrast agent from the stomach into the lumen of the esophagus, the presence of a hiatal hernia.

Therapy

Timely diagnosis and adequate treatment of GERD can reduce the frequency of asthma attacks and improve the quality of life of patients with asthma.

Basic principles conservative treatment reflux esophagitis include:

– prescription of drugs that suppress gastric secretion (antacids, adsorbents);

– prescription of drugs that stimulate the motor-evacuation function of the digestive tract (prokinetics);

– the use of drugs that have a protective effect on the mucous membrane of the esophagus.

General recommendations for regimen and diet provide for frequent and small meals (5 – 6 times a day), intake of mechanically and chemically gentle food. The last meal should be no later than 3 to 4 hours before bedtime. It is necessary to avoid consuming foods that increase GER (coffee, fats, chocolate, etc.). If reflux is severe, it is recommended to eat while standing and walk for half an hour after eating. An undoubted benefit comes from patients giving up smoking and drinking alcohol, which have an adverse effect on the mucous membrane of the esophagus. Considering that a certain body position contributes to the development of GER, it is recommended to sleep on a bed with the head end raised by 20 cm.

Antisecretory drugs. The goal of antisecretory therapy for GERD is to reduce the damaging effect of acidic gastric contents on the esophageal mucosa. H2 receptor blockers (ranitidine, famotidine) are widely used. Numerous clinical trials have shown that healing of the esophageal mucosa occurs in 65–75% of cases after an 8-week course of therapy. Ranitidine (300 mg) and famotidine (40 mg) are prescribed once in the evening after dinner (no later than 20 hours). Long-term medications are used in half the daily dose to prevent exacerbations of the disease.

The antisecretory effect of the Na+,K+-ATPase blocker omeprazole is superior to other drugs. By inhibiting the proton pump, omeprazole provides pronounced and long-lasting suppression of acidic gastric secretion. The drug has no side effects, since its active form exists only in the parietal cell. Omeprazole is usually prescribed in a daily dose of 30–40 mg for 3–4 weeks.

Antacid therapy aims to reduce the acid-proteolytic aggression of gastric juice. Of the drugs in this group, Maalox and Phosphalugel (1-2 packets 2-3 times a day), as well as Gastal (2 tablets 2-3 times a day) deserve special attention. Typically, medications are taken 40–60 minutes after a meal, when heartburn and retrosternal discomfort most often occur, and at night.

Motor skills correction As one of the most important pathogenetic factors of GERD, it is successfully achieved using prokinetics. This group of drugs includes domperidone, a gastrokinetic agent of the second generation. Domperidone increases the tone of the LES, accelerates the evacuation of gastric contents, has a positive effect on esophageal clearance, and reduces GER. Prescribe the drug 1 tablet (10 mg) 3 times a day 15 – 20 minutes before meals, if necessary 10 mg at night.

A promising drug in the treatment of GERD is cisapride, a gastrointestinal prokinetic agent of a fundamentally new type of action, which is based on enhancing the physiological release of acetylcholine at the level of the myenteric nerve plexus. Cisapride increases LES pressure, increases the amplitude of esophageal contractions and accelerates the evacuation of gastric contents, used in a dose of 10 mg 2–4 times a day.

The choice of treatment method depends on the characteristics of the disease and the cause of GERD. Stopping taking medications immediately after healing of esophageal erosions often leads to relapse of the disease. This circumstance necessitates long-term use of medications (up to 6–12 months) as maintenance therapy. For this purpose, antacids, H2 receptor blockers, omeprazole and cisapride are used. Prescribing Coordinax at a dose of 20 mg at night for 6–12 months prevented the development of relapse of reflux esophagitis in 60–80% of patients.

Literature:

1. Goodall RJR, Earis JE, et al. Relationship between asthma and gastroesophageal reflux. Thorax 1981;36:116–21.
2. Benjamin Stanley B, Kern Deschner. Exstraesophageal manifestations of gastroesophageal reflux. Am J Gastroenterol 1989;84(1):1–5.
3. Ekstrom T, Tibbling L. Esophageal acid perfusion airway function, and symptoms in asthmatic patients with marked bronchial hyperreactivity. Chest 1989;96(5):963.
4. Chuchalin A.G. “Bronchial asthma,” T. 2. – M., – 1997. – P. 40–63.
5. Allen CJ, et al. Gastroesophageal reflux and chronic respiratory disease. In Baum G. L., Wolinski E., eds, Textbook of Pulmonary Diseae, vol 2. Boston: Little, Brown 1989:1471.
6. Allen ML, Robinson MG. Gastroesophageal reflux and cough. Am J Gastroenterol 1989;84(6):689.
7. Amberson J.B. Aspiration bronchopneumonia. Int Anesthesiol Clin 1937;3:1281.
8. Grigoriev P.Ya., Yakovenko E.P. Diagnosis and treatment of diseases of the digestive system. M., 1996. – P. 7–31.
9. Kalinin A.V. Gastroesophageal reflux disease. Ter. archive. – 1996. – No. 8. – P. 16–20.
10. Nebel OT, et al. Symptomatic gastro-esophageal reflux incidence and precipitating factors. Dig Dis Sci 1976;21:955.
11. The story of oesophagitis. Janssen series on the quintessence of everyday gastro-esophageal pathology 1992;1:1–40.
12. Sheptulin A.A. Modern ideas about the pathogenesis, diagnosis and treatment of reflux esophagitis. // News of medicine and pharmacy. – 1994. – No. 4. – P. 14–19.
13. Castell DO. Diet and the lower esophageal sphincter. Am J Clin Nutr 1975;28:1296.
14. Global Initiative on Asthma. Joint report of the National Heart, Lung and Blood Institute and WHO // Pulmonology, 1995. Appendix, 1996. – pp. 48–59.
15. Verlinden M. Ibid 1–6.
16. Meirh. Kryger. Thomas Roth. Principles and practice of sleep medicine. Philadelphia 1993;P2:622–31, 596–7.
17. Chernow B, Johnson LF, Jauowitz WR, Castell DO. Pulmonary aspiration as a consequence of gastroesophageal reflux. Dig Dis Sci 1979;24:839–44.
18. De Meester TR, et al. Technique, implications and clinical use of 24 hour esophageal pH monitoring. J Thorac Cardiovasc Surg 1980;79:656.
19. Bremner RM, Hoeft SF, Costantini M, et al. Pharyngeal swallowing. The major factor in clearance of oesophageal reflux episodes. Ann Surg 1993;218:364–9.
20. Blum A, Badli F and the Eurocis Study Group. J Drug Dev 1993;5(suppl. 2):7–13.

Gratitude

The author of the article and the editors of the Russian Medical Journal express gratitude to the Moscow representative office of Glaxo Wellcome for providing comprehensive information support provided to the author in the preparation of this publication.

Reflux-induced bronchial asthma.

THEM. Beytuganova - Research Institute of Pulmonology, Ministry of Health, Moscow.

A.G. Chuchalin - academician, director of the Research Institute of Pulmonology of the Ministry of Health, Moscow.

RMJ, Volume 6, No. 17, 1998.

The mechanism of occurrence of gastroesophageal reflux and its role in the development of gastroesophageal reflux disease and exacerbations of bronchial asthma are discussed in detail. Recommendations for diagnosis and treatment are given.

81 - M.: Medicine, 1985. 160 p., ill. 50 k. - 100,000 copies.

The book comprehensively covers all aspects of bronchial asthma. The development factors, immunopathology of asthma, clinical picture of the disease, drug and climatic treatment of patients, intensive care during the attack period are described. The clinical pharmacology of drugs used in the treatment of bronchial asthma is described in detail.

The book is intended for therapists.

Preface

The last 20-30 years have been characterized by an increase in the incidence and severity of bronchial asthma. In terms of social significance, bronchial asthma takes one of the first places among respiratory diseases.

Thanks to active scientific research, medical practice is enriched with new data that relate to such aspects as epidemiology and immunopathology of bronchial asthma. Fundamentally new methods for studying the function of external respiration are emerging. The study of the clinical picture of bronchial asthma has been supplemented with new data. Thus, in recent years, issues such as prostaglandin metabolism in patients with bronchial asthma and intolerance to non-steroidal anti-inflammatory drugs, features of physical exertion asthma, and food-related asthma have been highlighted. Therapeutic options have expanded. An assessment of traditional medications from a modern perspective, the role and place of those that have appeared recently are important issues of practical medicine that require regular coverage. "

In this book, the author, summarizing his many years of work experience, the results of scientific observations and research at the Department of Internal Medicine of the II Moscow State Medical Institute named after. N.I. Pirogov and literature data, sought to answer questions that arise in everyday clinical practice.

Corresponding Member of the USSR Academy of Medical Sciences, Head. Department of Internal Medicine

II MOLGMI named after. N. I. Pirogova

A. G. CHUCHALIN

Publishing house "Medicine", 1985

LIST OF ABBREVIATIONS

Definition and classification

BP - blood pressure

BALT - bronchus-associated lymphoid tissue VGO - intrathoracic gas volume

VIP - vasoactive intestinal peptide

Vital capacity - vital capacity of the lungs

IgG, IgM - immunoglobulins COMT - catechol-o-methyltransferase LHF - lipid chemotactic factor

MVL - maximum ventilation

MRS-A - slow reacting substance of anaphylaxis

NSAIDs - non-steroidal anti-inflammatory drugs

NHF - high molecular weight neutrophil chemotactic factor OPG - general plethysmography

FEV - forced expiratory volume

PGE, PGF - prostaglandins

PSDV - air speed indicator

PAF - platelet activating factor

FVD - function of external respiration

FVC - forced vital capacity cAMP - cyclic adenosine monophosphate cGMP - cyclic guanosine monophosphate

ECP - eosinophilic chemotactic peptide

ECHFA - eosinophilic chemotactic factor of anaphylaxis

Most currently existing definitions of bronchial asthma use predominantly clinical signs as criteria. They emphasize the generality and reversibility of bronchial obstruction disorders, increased sensitivity of the trachea and bronchi to physical or chemical irritants, and the presence of nocturnal attacks of suffocation.

In our country, the definition of disease given by G. B. Fedoseev (1982) is most widespread. According to this definition, bronchial asthma is an independent chronic, recurrent disease, the main and obligatory pathogenetic mechanism of which is altered bronchial reactivity, caused by specific immunological (sensitization and allergy) or nonspecific mechanisms, and the main (obligatory) clinical sign is an attack of suffocation due to bronchospasm, hypersecretion and swelling of the bronchial mucosa.

This definition highlights the main signs of bronchial asthma: bronchial hyperreactivity, manifested by spasm of smooth muscles, edema and hypersecretion, and the development of suffocation. G. B. Fedoseev rightly emphasizes that the existing hyperreactivity of the bronchi can be caused by factors that have both immunological and non-immunological mechanisms.

The factors that provoke the development of asthma are so numerous and varied, and the course options are so dissimilar, that there is an assumption about the existence of several diseases, different in pathogenesis, which are united by the term “bronchial asthma”.

The classification of individual forms of bronchial asthma throughout the history of its study has been the subject of extensive discussion. In the middle of the last century, the neurogenic mechanisms of asthma and those patients in whom the neurogenic factor was dominant were intensively studied. The next important step was the study of allergic reactions, their role in the occurrence and development of bronchial asthma! At the beginning of the century, the anaphylactic theory of bronchial asthma arose, which in the 20s was transformed into the identification of an atonic (allergic) form of asthma [Co-" A. F. J., Cooke R. A., 1923].

Further study of the mechanisms of the disease, as well as a thorough analysis of the clinical manifestations and features of the course of asthma, made it possible to establish such a variety of forms that could not be explained from the standpoint of one theory or another. As a result, generalizing works appear in which they try to justify the identification of a hereditary form of the disease, toxic, psychopathic, reflex.

The classification proposed by Rackeman (1944) has received practical application and the most widespread classification, according to which exogenous (extrinsic) and endogenous (intrinsic) forms of bronchial asthma are distinguished.

In the exogenous form, it is possible to establish hypersensitivity using an allergological examination, identify an allergen or group of allergens, and thus prove the allergic nature of the disease. If the allergen cannot be identified and the nature of the disease remains unclear, asthma can be considered endogenous. SJ In our country, the classification of P.K. Bulatov and A.D. Ado (1968) was more often used, according to which allergic (atonic) and infectious-allergic forms of the disease are distinguished. This classification reflects an attempt to consider the frequent combination of asthma with chronic bacterial bronchitis as natural.

In the last 20 years, aspirin (prostaglandin) asthma has been studied in more detail, which is based not on allergic reactions, but on a perverted reaction of prostaglandins to non-steroidal anti-inflammatory drugs (NSAIDs). Exercise-induced asthma has been identified, which in some patients may be a feature of the course of the disease, and in others it is the main syndrome. There has been renewed interest in neurogenic factors that may contribute to the onset and progression of the disease. Hormonal disorders in patients with bronchial asthma have not been sufficiently studied. Clinical observations indicate a non-random combination of some endocrinopathies with asthma.V

Achievements of the last 20-30 years have made it possible to specify the genetic forms of the disease. Particular attention is paid to forms in which the balance in the functional activity of adrenergic and cholinergic receptors is disturbed. The great importance of meteorological factors, as well as infectious processes in the respiratory tract, is still emphasized .

As a result of numerous observations and special examinations of patients with asthma, it can be assumed that the mechanisms of development of the disease are different, and in the same person one can observe hypersensitivity to pollen allergens and exacerbation of asthma provoked by a viral infection of the respiratory tract, clinical features of exercise asthma and hormonal disorders, increased sensitivity to non-steroidal anti-inflammatory drugs and meteorological factors, significant psycho-emotional lability.

It is fundamentally important to recognize bronchial asthma as an independent nosological unit, taking into account the existence of clinical forms with a predominance of various pathogenetic mechanisms/

The classification of bronchial asthma by G. B. Fedoseev (1982) is currently generally accepted. The author identifies the stages of disease development, forms of bronchial asthma, pathogenetic mechanisms, severity of bronchial asthma, phases of bronchial asthma and complications.

Classification of bronchial asthma [according to Fedoseev G.B., 1982] I. Stages of development of bronchial asthma

1. State of pre-asthma. This term refers to conditions that pose a risk of bronchial asthma. These include acute and chronic bronchitis, acute and chronic pneumonia with elements of bronchospasm, combined with vasomotor rhinitis, urticaria, vasomotor edema, migraine and neurodermatitis in the presence of eosinophilia in the blood and an increased content of eosinophils in the sputum, caused by immunological or non-immunological mechanisms of pathogenesis.

2. Clinically defined bronchial asthma - after the first attack or status of bronchial asthma

P. Forms of bronchial asthma

1. Immunological form

2. Non-immunological form

III. Pathogenetic mechanisms of bronchial asthma

1. Atonic - indicating the allergenic allergen or allergens

2. Infectious-dependent - indicating the infectious agents and the nature of the infectious dependence, which can manifest itself as stimulation of the atopic reaction, infectious allergies and the formation of primary altered bronchial reactivity

3. Autoimmune

4. Dyshormonal - indicating the endocrine organ whose function is altered and the nature of the dishormonal changes

5. Neuropsychic with indication of variants of neuropsychic changes

6. Adrenergic imbalance

7. Primary altered bronchial reactivity, which is formed without the participation of altered reactions of the immune, endocrine and nervous systems, can be congenital, manifests itself under the influence of chemical, physical and mechanical irritants and infectious agents and is characterized by attacks of suffocation during physical exertion, exposure to cold air, medications and etc.

Note. Various combinations of mechanisms are possible, and by the time of the examination one of the mechanisms is the main one. A patient may have one pathogenetic mechanism of bronchial asthma. During the development of bronchial asthma, a change in the primary and secondary mechanisms may occur.

IV. Severity of bronchial asthma

1. Mild course

2. Moderate course

3. Severe course

V. Phases of bronchial asthma

1. Exacerbation

2. Fading exacerbation

3. Remission

VI. Complications

1. Pulmonary: emphysema, pulmonary failure, atelectasis, pneumothorax, etc.

2. Extrapulmonary: myocardial dystrophy, cor pulmonale, heart failure, etc.

The classification of G. B. Fedoseev is one of the most complete at present. The selection will be of great practical importance. When assessing this condition, one should take into account not only background diseases that can transform into bronchial asthma, but also increased bronchial reactivity, which should be considered a mandatory sign.

It is important to distinguish not only the immunological forms of the disease, but also the clinical ones. The modern clinic has accumulated specific experience in the management of patients with allergic, infectious forms of bronchial asthma. There are aspirin (prostaglandin) forms of the disease, physical exertion asthma, neurogenic and mixed forms of the disease. In clinical practice, a steroid-dependent form of the disease is often identified.

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