Treatment of bronchial asthma: etiologic and pathogenetic treatment

"Bronchial asthma is a chronic inflammatory disease of the respiratory tract, in which many cells participate: mast cells, eosinophils, T-lymphocytes.

In susceptible individuals, this inflammation results in recurrent episodes of wheezing, shortness of breath, chest tightness, and cough, particularly at night and/or in the early morning. These symptoms are usually accompanied by widespread but variable airway obstruction that is at least partially reversible spontaneously or with treatment. The inflammation also causes a concomitant increase in airway responsiveness to a variety of stimuli" (Report "Global Strategy for Asthma Prevention and Treatment", WHO, National Heart, Lung, and Blood Institute, USA, 1993).

Thus, the modern definition of bronchial asthma includes the main provisions reflecting the inflammatory nature of the disease, the main pathophysiological mechanism - bronchial hyperreactivity, and the main clinical manifestations - symptoms of airway obstruction.

The main criterion for prescribing antiasthmatic drugs for bronchial asthma is its severity. When determining the severity of the disease, the following are taken into account:

• clinical signs characterizing the frequency, severity, time of occurrence during the day of episodes of increased symptoms, including attacks of suffocation;
• results of the study of peak expiratory flow rate (PEF), measured using an individual peak flow meter (deviations from the expected values in percentage and the spread of indicators during the day).

Peak expiratory flow (L/min) is the maximum speed at which air can leave the airways during the fastest and deepest exhalation after a full inspiration. PEF values are closely correlated with FEV1 (forced expiratory volume in liters in the first second).

• the nature and extent of therapy required to establish and maintain disease control.

It is also advisable to take into account the phase of the disease: exacerbation, unstable remission, remission and stable remission (more than 2 years).

Step therapy for bronchial asthma

Step	Treatment
Mild and intermittent, episodic course	Long-term therapy with anti-inflammatory drugs is generally not indicated. Prophylactic inhalation of a beta2-agonist or sodium cromoglycan before anticipated exercise or contact with an allergen Short-acting bronchodilators (inhaled beta2-agonists) as needed to control symptoms, no more than once a week
Mild persistent course	Daily long-term preventive use for asthma control: Inhaled corticosteroids at a daily dose of 200-500 mcg or sodium cromoglycate, nedocromil or extended-release theophylline If necessary, the dose of inhaled corticosteroids should be increased. If it was 500 mcg, it should be increased to 800 mcg or prolonged bronchodilators should be added (especially for the control of nocturnal asthma): inhaled (beta-agonists, theophylline or prolonged oral beta2-agonists (in tablets or syrup) To relieve asthma attacks - short-acting bronchodilators - inhaled beta2-agonists no more than 3-4 times a day: inhaled anticholinergics may be used
Asthma persistent, moderate	Daily prophylactic use of anti-inflammatory drugs to establish and maintain asthma control: inhaled corticosteroids at a daily dose of 800-2000 mcg (using an inhaler with a spencer) Long-acting bronchodilators, especially for the relief of nocturnal asthma (beta2-agonists in the form of inhalations, tablets, scrolls or theophylline) To relieve asthma attacks - short-acting bronchodilators - inhaled beta2-agonists no more than 3-4 times a day, it is possible to use inhaled anticholinergics
Severe persistent	Daily intake Inhaled corticosteroids in a daily dose of 800-2000 mcg or more Long-acting bronchodilators, especially in the presence of nighttime asthma attacks (beta2-agonists in the form of inhalations, tablets, syrup m/or theophylline) Glucocorticoids orally To stop or relieve an asthma attack - short-acting bronchodilators, inhaled beta2-agonists (no more than 3-4 times a day). Inhaled anticholinergics may be used.

Notes:

1. Patients should be prescribed treatment (at the appropriate level) taking into account the initial severity of the condition.
2. If asthma symptoms are not controlled sufficiently, it is recommended to move to a higher level. However, it is necessary to first check whether the patient is using medications correctly, following the doctor's advice, and avoiding contact with allergens and other factors that cause exacerbations.
3. If it is possible to control the course of bronchial asthma over the last 3 months, it is possible to gradually reduce the volume of treatment and move to the previous stage.
4. Short courses of oral glucocorticoid therapy are given at any stage if necessary.
5. Patients should avoid contact with triggers or control their exposure to them.
6. Therapy at any stage must include patient education.

In accordance with the severity of the manifestations of bronchial asthma, a step-by-step approach to its treatment is provided. The choice of drugs and the method of their use are determined by the severity of the disease, designated as the corresponding step.

A step therapy for bronchial asthma similar to the above was proposed in 1991 by Vermeire (Belgium). He identifies the following stages of anti-asthmatic therapy:

1. identification of provoking factors and administration of beta-adrenergic agonists by inhalation to relieve an attack of bronchial asthma;
2. addition of sodium cromoglycate or low doses of glucocorticoids inhaled;
3. addition of high doses of glucocorticoids in inhalations;
4. addition of theophylline orally and/or cholinomimetics by inhalation and/or beta2-adrenergic agonists orally and/or increasing the dose of beta2-adrenergic agonists by inhalation;
5. addition of glucocorticoids orally.

The treatment program includes the following areas.

Etiological treatment:

1. Elimination therapy.
2. Allergy-free rooms.
3. Isolation of the patient from surrounding allergens.

Pathogenetic treatment:

1. Impact on the immunological phase of pathogenesis
   1. Specific and non-specific hyposensitization.
      • unloading and dietary therapy - isolated and in combination with enterosorption;
      • treatment with histaglobulin, allergoglobulin;
      • treatment with adaptogens.
   2. Treatment with glucocorticoids.
   3. Treatment with cytostatics.
   4. Immunomodulatory therapy (immunomodulatory agents, extracorporeal immunosorption, monoclonal anti-IgE immunosorption, plasmapheresis, lymphocytapheresis, thrombocytapheresis, laser and ultraviolet irradiation of blood).
2. Impact on the pathochemical stage
   1. Membrane stabilizing therapy.
   2. Extracorporeal immunopharmacotherapy.
   3. Inhibition of mediators of inflammation, allergy, bronchospasm.
   4. Antioxidant therapy.
3. Impact on the pathophysiological stage, use of asthma drugs.
   1. Bronchodilators (bronchodilators).
   2. Expectorants.
   3. Injection of novocaine into the Zakharyin-Ged points.
   4. Physiotherapy.
   5. Naturotherapy (non-drug treatment).
      • Chest massage and postural drainage.
      • Barotherapy (hypobarotherapy and hyperbarotherapy).
      • Normobaric hypoxic therapy.
      • Rational breathing exercises (breathing with resistance, breathing through a dosed respiratory dead space, voluntary elimination of deep breathing, artificial regulation of breathing, stimulation of diaphragmatic breathing).
      • Acupuncture.
      • Su-jok therapy.
      • Mountain climate treatment.
      • Speleotherapy, halotherapy.
      • Aerophytotherapy.
      • UHF therapy.
      • Homeopathic therapy.
      • Thermotherapy.

In the specified treatment program, such sections as etiological treatment and such types of pathogenetic therapy as impact on the immunological phase (except for glucocorticoids), the pathochemical phase, as well as many therapeutic effects aimed at the pathophysiological stage, are carried out in the remission phase of bronchial asthma (i.e. after the relief of the asthma attack).

Variants of intolerance to plant allergens, food products and medicinal plants in hay fever

	Possible cross-allergic reactions to pollen
Etiological factor	Pollen, leaves, stems of plants	Plant-based foods	Medicinal plants
Birch	Hazel, alder, apple	Apples, pears, cherries, cherries, peaches, plums, apricots, carrots, celery, potatoes, eggplants, peppers	Birch leaf (bud, alder cones, belladonna preparations)
Wild weeds (timothy, fescue, orchard grass)	-	Food grains (oats, wheat, barley, rye), sorrel	-
Sagebrush	Dahlias, chamomile, dandelion, sunflower	Citrus fruits, sunflower oil, halva, sunflower seeds, honey	Yarrow, coltsfoot, chamomile, elecampane, thyme, tansy, calendula, succession
Quinoa, ambrosia	Sunflower, dandelion	Beetroot, spinach, melon, bananas, sunflower seeds. sunflower oil	-

Etiological treatment

1. Elimination therapy is a complete and permanent cessation of the patient's contact with the causative allergen, i.e. the allergen or group of allergens that cause an asthma attack. This therapy is carried out after the allergen has been identified using special allergological diagnostics.

Completely stopping contact with the allergen in the early stages of the disease, when there are no complications, can be very effective and often leads to recovery.

In case of hypersensitivity to pet hair, daphnia, professional factors, it is necessary to change living conditions and rational employment (do not have pets or aquariums in the apartment, leave work with professional hazards).

If the patient is allergic to horse dander, anti-tetanus and anti-staphylococcal serums should not be administered, since cross-allergic reactions with horse serum used in the manufacture of these drugs may develop. Clothes made of fur or wool of an animal that is allergenic should not be worn (for example, a sweater made of angora wool or mohair - if allergic to sheep wool).

Cross-allergenic properties of drugs

Allergy causing drug	Medicines that should not be used due to cross-allergy
Euphyllin, diaphyllin, aminophylline	Ethylenediamine derivatives (suprastin, ethambutol)
Aminazine	Phenothiazine derivatives: antihistamines (pipolfen, diprazine); neuroleptics (propazine, tizercin, ztaperazine, mazeptil, sonapax, etc.); antiarrhythmic drugs (ethmozin, etacizin); antidepressants (fluoroacyzine)
Penicillin group drugs	Cephalosporin antibiotics
Novocaine	Local anesthetics (anesthesin, lidocaine, trimecaine, dicaine) and drugs containing them (menovazine, sulfocamphocaine) Sulfonamides Sulfonylurea derivatives - hypoglycemic agents (glibenclamide, gliquidone, glipizide, gliclazide - predian, diabetone, chlorpropamide, etc.) Diuretics - dichlorothiazide, cyclomethiaide, furosemide, bufenox, clopamide, indalamide, diacarb, etc.)
Iodine	Radiopaque iodine-containing agents Inorganic iodides (potassium iodide, Lugol's solution, sodium iodide) Thyroxine, triiodothyronine

In case of hypersensitivity to plant pollen, it is necessary to minimize possible contact with pollen (during the pollination period of plants, do not go to the forest, field, do not work in the garden, refrain from going outside in dry windy weather, during the day and in the evening, i.e. at the time when the concentration of pollen in the air is highest).

Many patients suffering from pollen bronchial asthma may have intolerance to many herbal preparations and food products due to cross-reactions with pollen allergens. This must be taken into account during treatment and the corresponding food products must be excluded from the diet. When consuming the above products, pollen bronchial asthma and other symptoms of hay fever may worsen.

In case of hypersensitivity to house dust, it is necessary to take into account that the main allergens of house dust are mites or fungi. Optimal conditions for the growth of mites are a relative humidity of 80% and a temperature of 25 °C. The number of mites increases in seasons with high humidity. These same conditions are favorable for the development of fungi.

The main places where ticks accumulate are mattresses, upholstered furniture, carpets, pile fabrics, stuffed animals, plush toys, and books. Mattresses should be covered with washable, impermeable plastic and wet-cleaned once a week. It is recommended to remove carpets, plush toys, pile, woolen and wadded blankets from the apartment, place books on glass shelves, change bed linen regularly, wash wallpaper and vacuum the room, irradiate the room with ultraviolet rays: in the summer - with direct sunlight, in the winter - with ultraviolet lamps.

In hospital wards, the number of ticks is less than 2% of their number in apartments, so hospitalization improves the condition of patients.

In case of food-induced bronchial asthma, it is necessary to eliminate from food the allergen that causes an attack of bronchial asthma (elimination diet), as well as "obligate" food allergens.

In drug-induced bronchial asthma, it is necessary to discontinue the drug that causes the disease or its exacerbation, and also not to use drugs that cause cross-allergic reactions.

One of the most important factors in the development of bronchial asthma is air pollution. In this regard, it is advisable to use highly effective air purification systems in the complex treatment of patients with bronchial asthma. Modern air purifiers evenly purify the air in the entire room (ward, apartment), regardless of the place of installation. With the help of special filters, they capture allergens, bacteria, viruses, plant pollen, house dust and other air pollutants, which significantly reduces the severity of exacerbation of bronchial asthma, and sometimes allows you to completely get rid of this disease.

2. Allergy-free wards are used to treat patients with inhalation allergies (usually with severe sensitization to plant pollen). These wards are equipped with a fine air purification system for aerosol mixtures (dust, fog, plant pollen, etc.). The air is purified from all allergens and enters the ward. The exchange rate is 5 times per hour. Polymer fine-fiber filter materials made of perchlorovinyl are used to purify the air.
3. Isolation of the patient from the surrounding allergens (permanent or temporary change of residence, for example, during the flowering period of plants, change of place and working conditions, etc.) is carried out in the event of the impossibility of eliminating the allergen in the case of severe polyvalent allergy.

[ 1 ], [ 2 ], [ 3 ]

Pathogenetic treatment

Therapeutic measures in this phase are aimed at suppressing or significantly reducing and preventing the formation of reagins (IgE) and their combination with antigens.

Treatment with histaglobupin and allergoglobulin

Histaglobulin and allergoglobulin are non-specific desensitization agents. One ampoule (3 ml) of histaglobulin (histaglobin) contains 0.1 mcg of histamine and 6 mg of gamma globulin from human blood.

The mechanism of action is the production of antihistamine antibodies and an increase in the ability of serum to inactivate histamine.

Treatment method: histaglobin is administered subcutaneously - first 1 ml, then after 3 days 2 ml, and then three more injections of 3 ml are given at intervals of 3 days; if necessary, the course is repeated after 1-2 months.

Another method of treatment with histaglobulin can be used: the drug is administered subcutaneously twice a week, starting with 0.5 ml and increasing the dose to 1-2 ml, the course consists of 10-15 injections. Histaglobulin is effective in pollen and food sensitization, atonic bronchial asthma, urticaria, Quincke's edema, allergic rhinitis.

Contraindications to the use of hisgaglobulin: menstruation, high body temperature, treatment with glucocorticoids, exacerbation of bronchial asthma, uterine fibroids.

Antiallergic immunoglobulin is similar in its mechanism of action and effectiveness to allergoglobulin. It contains blocking antibodies - IgG. The drug is administered intramuscularly at 2 ml with an interval of 4 days, a total of 5 injections. Allergoglobulin is placental γ-globulin in combination with gonadotropin. The drug has a high histamine-protective ability. It is available in 0.5 ml ampoules. Allergoglobulin is administered intramuscularly at a dose of 10 ml once every 15 days (a total of 4 injections) or intramuscularly - 2 ml every 2 days (4-5 injections).

It is possible to combine allergoglobulin with its rapid antiallergic effect (blocking free histamine) and histaglobulin (development of "antihistamine immunity" - long-term delayed action) according to the following scheme: once a week, 5 ml of allergoglobulin is administered intramuscularly and 3 ml of histaglobulin subcutaneously. The course is 3 such complexes for 3 weeks. Treatment with histaglobulin and allergoglobulin is carried out only during the remission period, repeated courses are possible after 4-5 months. Since allergoglobulin and antiallergic immunoglobulin contain gonadotropic hormones, they are contraindicated in puberty, with uterine fibroids, mastopathy.

Treatment with adaptogens

Treatment with adaptogens, as a method of non-specific desensitization, leads to an improvement in the function of the local bronchopulmonary defense system, the general immune system, and desensitization.

During the remission phase, the following remedies are usually used for a month:

• Eleutherococcus extract 30 drops 3 times a day;
• saparal (derived from Manchurian aralia) 0.05 g 3 times a day;
• tincture of Chinese magnolia vine, 30 drops 3 times a day;
• ginseng tincture 30 drops 3 times a day;
• tincture of Rhodiola rosea, 30 drops 3 times a day;
• pantocrine 30 drops 3 times a day orally or 1-2 ml intramuscularly 1 time per day;
• rantarin - an extract from the antlers of male reindeer, taken orally 2 tablets 30 minutes before meals 2-3 times a day.

Treatment with glucocorticoids

Glucocorticoid therapy for bronchial asthma is used in the following variants:

1. Treatment with inhaled forms of glucocorticoids ( local glucocorticoid therapy ).
2. Use of glucocorticoids orally or parenterally ( systemic glucocorticoid therapy ).

Treatment with cytostatics (immunosuppressants)

Treatment with cytostatics is currently rarely used.

The mechanism of action of cytostatics is to suppress the production of reagins and have an anti-inflammatory effect. Unlike glucocorticoids, they do not suppress the adrenal glands.

Indications:

• severe form of atopic bronchial asthma that does not respond to treatment with conventional means, including glucocorticoids;
• corticosteroid-dependent corticosteroid-resistant bronchial asthma - in order to reduce corticosteroid dependence;
• autoimmune bronchial asthma.

Immunomodulatory therapy

Immunomodulatory therapy normalizes the immune system. It is prescribed for protracted bronchial asthma that is resistant to conventional therapy, especially when the atopic form is combined with an infection in the bronchopulmonary system.

Treatment with thymalin

Thymalin is a complex of polypeptide fractions obtained from the thymus of cattle. The drug regulates the number and function of B- and T-lymphocytes, stimulates phagocytosis, reparative processes, and normalizes the activity of T-killers. It is produced in vials (ampoules) of 10 mg, dissolved in isotonic NaCl solution. It is administered intramuscularly at 10 mg once a day for 5-7 days. Yu. I. Ziborov and B. M. Uslontsev showed that the therapeutic effect of thymalin is most pronounced in individuals with a short-term illness (2-3 years) with normal or reduced activity of T-lymphocyte suppressors. The immunogenetic marker of a positive effect is the presence of HLA-DR2.

Treatment with T-activin

T-activin is obtained from the thymus of cattle and is a mixture of polypeptides with a molecular weight of 1,500 to 6,000 daltons. It has a normalizing effect on the function of T-lymphocytes. It is produced in ampoules of 1 ml of 0.01% (i.e. 100 mcg). It is administered intramuscularly once a day at a dose of 100 mcg, the course of treatment is 5-7 days. The immunogenetic marker of a positive effect is the presence of HLA-B27.

Treatment with thymoltin

Timoptin is an immunomodulatory drug for the thymus, containing a complex of immunoactive polypeptides, including a-thymosin. The drug normalizes the indices of T- and B-systems of lymphocytes, activates the phagocytic function of neutrophils. It is produced as a lyophilized powder of 100 mcg, before administration it is dissolved in 1 ml of isotonic solution. It is administered subcutaneously at a dose of 70 mcg/m2 (i.e. for adults usually 100 mcg) once every 4 days, the course of treatment is 4-5 injections.

Treatment with sodium nucleinate

Sodium nucleinate is obtained by hydrolysis of yeast, stimulates the function of T- and B-lymphocytes and the phagocytic function of leukocytes, and is prescribed orally at 0.1-0.2 g 3-4 times a day after meals for 2-3 weeks.

Alkimer is an immunomodulatory drug obtained from Greenland shark liver oil. There are reports of its effectiveness in bronchial asthma.

Antilymphocyte globulin

Antilymphocyte globulin is an immunoglobulin fraction isolated from the blood serum of animals immunized with human T-lymphocytes. In small doses, the drug stimulates T-suppressor activity of lymphocytes, which helps reduce the production of IgE (reagins). That is why the drug is used to treat atonic bronchial asthma. B. M. Uslontsev (1985, 1990) recommends using antilymphocyte globulin at a dose of 0.4-0.8 mcg per 1 kg of body weight of the patient intravenously by drip, the course of treatment consists of 3-6 infusions. The clinical effect is observed 2-3 months after the end of treatment and most often occurs in individuals who are carriers of the HLA-B35 antigen.

[ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ]

Laser irradiation and UV irradiation of blood

Laser irradiation and UFO of blood have an immunomodulatory effect and are used in moderate and severe bronchial asthma, especially in the presence of corticosteroid dependence. Laser irradiation of blood reduces the need for glucocorticoids.

Impact on the pathochemical phase of pathogenesis

[ 9 ], [ 10 ]

Inhibition of some mediators of inflammation, allergy, bronchospasm

Some mediators are released from mast cells during their degranulation (histamine; platelet-activating factor; slow-reacting substance, eosinophilic and neutrophil chemotactic factors, proteolytic enzymes), a number of mediators are formed outside mast cells, but with the help of activators released from them (bradykinin, thromboxane, serotonin, etc.).

Of course, it is impossible to inactivate all mediators of bronchospasm and inflammation with one drug or several groups of drugs.

Only a few drugs can be named that inactivate certain mediators.

Antiserotonin agents

Antiserotonin agents block the effects of serotonin. The best-known drug in this group is peritol (cyproheptadine). It has a pronounced antiserotonin effect (reduces the spasmogenic and other effects of serotonin), but at the same time exhibits antihistamine (blocks H1 receptors) and anticholinergic effects. The drug also causes a pronounced sedative effect, increases appetite and reduces migraine symptoms.

It is used in tablets of 4 mg 3-4 times a day. Contraindicated in glaucoma, edema, pregnancy, urinary retention.

[ 11 ], [ 12 ], [ 13 ]

Antikinin agents

Antiquinine agents block the action of quinines, reduce capillary permeability and bronchial edema.

Anginine (prodectin, parmidine, pyridinolcarbamate) - is prescribed at 0.25 g 4 times a day for a month. But treatment with this drug has not become widespread due to its small and questionable effect. The use of the drug is advisable in combination with bronchial asthma and damage to the arteries of the lower extremities (obliterating endarteritis, atherosclerosis).

[ 14 ], [ 15 ]

Inhibition of leukotrienes and PAF

Inhibition of leukotrienes and PAF (suppression of synthesis and blocking of their receptors) is a new direction in the treatment of bronchial asthma.

Leukotrienes play an important role in airway obstruction. They are formed as a result of the action of 5-lipoxygenase enzymes on arachidonic acid and are produced by mast cells, eosinophils, and alveolar macrophages. Leukotrienes cause the development of inflammation in the bronchi and bronchospasm. Inhibitors of leukotriene synthesis reduce the bronchospasm response to the effects of allergens, cold air, physical exertion, and aspirin in patients with bronchial asthma.

Currently, the effectiveness of three-month treatment of patients with mild to moderate bronchial asthma with zileuton, an inhibitor of 5-lipoxygenase and leukotriene synthesis, has been studied. A pronounced bronchodilating effect of zileuton has been established when taken orally at a dose of 600 mg 4 times a day, as well as a significant decrease in the frequency of asthma exacerbations and the frequency of use of inhaled beta2-agonists. Currently, clinical trials of leukotriene receptor antagonists accolote, pranlukast, singulair are underway abroad.

The use of PAF antagonists leads to a decrease in the content of eosinophils in the bronchial wall and a decrease in bronchial reactivity in response to contact with an allergen.

Antioxidant therapy

In the pathochemical stage of the pathogenesis of bronchial asthma, there is also activation of lipid peroxidation and the formation of peroxides and free radicals that support allergic inflammation of the bronchi. In this regard, the use of antioxidant therapy is justified. The use of antioxidants is provided for by the recommendations of the European Society for the Diagnosis and Treatment of Obstructive Lung Diseases, but it should be noted that this therapy has not solved the problem of bronchial asthma, it is prescribed in the interattack period.

Vitamin E (tocopherol acetate) in capsules of 0.2 ml of 5% oil solution (i.e. 0.1 g) 2-3 times a day for a month is used as an antioxidant. Tocopherol acetate can be used at 1 ml of 5% solution (50 mg) or 1 ml of 10% solution (100 mg) or 1 ml of 30% solution (300 mg) intramuscularly once a day. Aevit in capsules (a combination of vitamins A and E) is also recommended; it is prescribed 1 capsule 3 times a day for 30-40 days. Vitamin E also has an immunocorrective effect.

Vitamin C (ascorbic acid) also has an antioxidant effect. A significant amount of it is found in the fluid located on the inner surface of the bronchi and alveoli. Vitamin C protects the cells of the bronchopulmonary system from oxidative damage, reduces bronchial hyperreactivity, and reduces the severity of bronchospasm. Vitamin C is prescribed at 0.5-1.0 g per day. Higher doses can stimulate lipid peroxidation due to the reduction of iron, which is involved in the formation of hydroxyl radicals.

Selenium compounds, which are part of the enzyme glutathione peroxidase, which inactivates peroxides, are also used as antioxidants. Selenium deficiency has been found in patients with bronchial asthma, which helps reduce the activity of glutathione peroxidase, a key enzyme in the antioxidant system. The use of sodium selenite in a daily dose of 100 mcg for 14 weeks significantly reduces the clinical manifestations of bronchial asthma. S. A. Syurin (1995) recommends the combined use of sodium selenite (2-2.5 mcg/kg sublingually), vitamin C (500 mg/day), vitamin E (50 mg/day), which significantly reduces lipid peroxidation.

Acetylcysteine is also an antioxidant. It is an expectorant and can be deacetylated to form cysteine, which is involved in the synthesis of glutathione.

Ultraviolet irradiation of blood reduces lipid peroxidation, normalizes the activity of the antioxidant system, improves the clinical course of bronchial asthma, reduces the severity of bronchial obstruction, and allows for a reduction in the amount of bronchodilators taken.

Indications for the use of antioxidants in bronchial asthma:

• insufficient activity of traditional drug treatment;
• treatment and prevention of acute respiratory infections;
• prevention of seasonal exacerbations of asthma (winter, spring), when there is the greatest deficiency of vitamins and microelements;
• asthmatic triad (in this case, UFO blood is recommended).

[ 16 ], [ 17 ], [ 18 ]

Extracorporeal immunopharmacotherapy

Extracorporeal immunopharmacotherapy involves treating mononuclear cells isolated from patients' blood with drugs (prednisolone, vitamin B12, diucifon), followed by cell reinfusion. As a result of such exposure, the histamine-releasing activity of mononuclear cells decreases and the synthesis of interleukin-2 is stimulated.

Indications for extracorporeal immunopharmacotherapy:

• corticosteroid-dependent atonic bronchial asthma;
• combination of atopic bronchial asthma with atopic dermatitis, allergic rhinoconjunctivitis.

[ 19 ]