^

Health

A
A
A

Treatment of infection-dependent bronchial asthma

 
, medical expert
Last reviewed: 06.07.2025
 
Fact-checked
х

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.

We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.

If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.

The treatment program includes the following main areas.

Etiological treatment (in the acute phase) - elimination of acute or exacerbation of chronic inflammatory process in the bronchopulmonary system, sanitation of other foci of infection.

In case of bronchial asthma caused by Candida fungi, it is necessary to stop contact with mold fungi at work and at home, use disinfectant fungicidal solutions; limit the consumption of products containing yeast fungi (cheese, beer, wine, yeast dough); sanitize foci of infection with antifungal drugs.

  1. Drug treatment: antibiotics (taking into account the sensitivity of the flora and individual tolerance); prolonged-release sulfonamides; in case of intolerance to antibiotics and sulfonamides - nitrofurans, metronidazole (Trichopolum), antiseptics (dioxidine), phytoncides (chlorophyllipt); antiviral agents.

In case of carriage of Candida fungi, sanitation is carried out with levorin, nystatin for 2 weeks. In case of pronounced clinical manifestations of candidomycosis, treatment is carried out with antimycotic agents of systemic action: amphotericin B, diflucan, nizoral, ancotil. The drug of choice is diflucan (fluconazole), which does not have allergenic and toxic properties.

  1. Bronchopulmonary sanitation - endotracheal sanitation, therapeutic fibrobronchoscopy (especially for purulent bronchitis, bronchiectasis).
  2. Conservative or surgical treatment of foci of infection in the ENT organs and oral cavity.

Desensitization (in the remission phase).

  1. Specific desensitization to bacterial allergens.
  2. Sputum autolysate treatment. Sputum of a patient with bronchial asthma is very heterogeneous in antigen composition, acquires the properties of an autoantigen and plays an important role in the pathogenesis of the disease. Sputum contains various antigens, including bacterial cells, as well as cells of the tracheal and bronchial secretion. Sputum autolysate treatment is a kind of method of specific hyposensitization, most effective in infection-dependent bronchial asthma. Depending on the severity of the disease and the time elapsed since the last exacerbation, autolysate dilutions are made from 1:40,000-1:50,000 to 1:200,000-1:500,000. Sputum autolysate is injected subcutaneously into the outer surface of the shoulder. 3 cycles of 10-13 injections each are carried out with intervals of 2 weeks between them. The full course of treatment includes 30-50 injections. Treatment begins with a dose of 0.1 ml, then in the first cycle 0.2-0.3 ml, in the second cycle - 0.3-0.4 ml, in the third - 0.3 ml. The entire course of treatment takes 3.5-4.5 months, breaks between courses - 3-6 months. Positive treatment results are noted in 80-90% of patients (A. V. Bykova, 1996).

Contraindications to treatment with sputum autolysate:

  • severe exacerbation of bronchial asthma; age over 60 years;
  • glucocorticoid dependence.
  1. Non-specific hyposensitization and the use of Intal and Ketotifen.

Immunomodulatory agents and extracorporeal therapy methods (hemosorption, plasmapheresis, ultraviolet or laser irradiation of blood).

Impact on the pathophysiological stage.

  1. Restoration of bronchial drainage function: bronchodilators, expectorants, postural drainage, chest massage.
  2. Physiotherapy.
  3. Barotherapy.
  4. Sauna therapy. It is recommended to visit the sauna 2-3 times a week. After a hygienic shower and subsequent rubbing with a dry towel, the patient is placed in the sauna cabin twice for 6-10 minutes with a 5-minute interval at a temperature of 85-95 °C and a relative humidity of 15%. Upon exiting, patients take a warm shower and rest for 30 minutes.

The mechanism of action of the sauna: relaxation of the bronchial muscles, increased blood supply to the mucous membrane of the upper respiratory tract, reduction of the elastic resistance of the lung tissue.

Contraindications: pronounced active inflammatory process in the bronchopulmonary system, high arterial hypertension, arrhythmia and pathological changes in the ECG, attack of bronchial asthma and its pronounced exacerbation.

  1. Speleherapy.

Glucocorticoids by inhalation or orally (indications and treatment methods are the same as for atopic asthma). The need for glucocorticoid therapy is observed more often than in atopic bronchial asthma.

Treatment of the dyshormonal variant

Correction of glucocorticoid insufficiency.

  1. Replacement therapy for adrenal glucocorticoid insufficiency - the use of glucocorticoids orally or parenterally with the administration of the drug at the maximum dose in the first half of the day (i.e. taking into account the circadian rhythm of the adrenal glands).
  2. Activation of the adrenal cortex function - treatment with ethimizol, glycyram, use of physiotherapeutic methods (DKV, ultrasound on the adrenal area). In case of absolute glucocorticoid insufficiency, activation is contraindicated.
  3. Use of glucocorticoids by inhalation.
  4. Treatment of complications of glucocorticoid therapy.

Reduction of corticodependence

  1. Extracorporeal treatment methods (hemosorption, plasmapheresis).
  2. Treatment with drugs that prevent mast cell degranulation (Intal, Ketotifen).
  3. Laser irradiation of blood.
  4. Unloading and dietary therapy in combination with acupuncture.
  5. In corticosteroid-resistant bronchial asthma, some authors recommend adding non-hormonal immunosuppressants (cytostatics) to the glucocorticoid therapy: 6-mercaptopurine (initial daily dose - 150-200 mg, maintenance - 50-100 mg), matioprine (initial daily dose - 200-250 mg, maintenance - 100-150 mg), cyclophosphamide (initial dose - 200-250 mg, maintenance - 75-100 mg). The course of treatment is 3-6 months, a repeat course is possible after 3-6 months.

Correction of dysovarian disorders.

Patients with bronchial asthma with dysovarian disorders (insufficient function of the corpus luteum) are treated with synthetic progestins in the second phase of the menstrual cycle. Turinal and Norcolut are most often used (they contain the hormone of the corpus luteum). Treatment with progestins restores the function of beta2-adrenoreceptors, increases their sensitivity to the effects of adrenaline and helps improve bronchial patency. The effectiveness of treatment with progestins increases with the simultaneous administration of vitamins E, C and folic acid, glutamic acid, taking into account the phases of the menstrual cycle.

Scheme of application of synthetic progestins, vitamins and glutamic acid in treatment of patients with bronchial asthma with dysovarian disorders

Phases of the menstrual cycle Days of the menstrual cycle
Phase I 1-15 days
folic acid 0.002 g 3 times a day orally
glutamic acid 0.25 g 3 times a day orally
Phase II 16-28 days
norkolut (turinal) 0.005 g daily for 10 days
ascorbic acid 0.3 g 3 times a day orally
a-tocopherol acetate one capsule daily orally (vitamin E)

The treatment is carried out for 3 months (three menstrual cycles). If the effect is positive, the treatment courses are repeated at intervals of 2-3 months.

Treatment with synthetic progestins is carried out during the period of abating exacerbation of bronchial asthma against the background of basic therapy or in the remission phase.

Contraindications to treatment with synthetic progestins:

  • tumors of any localization;
  • acute diseases of the liver and biliary tract;
  • acute thrombophlebitis with a history of thromboembolic complications;
  • diabetes mellitus (relative contraindication);
  • chronic thrombophlebitis, varicose veins, chronic liver and kidney diseases.

Correction of disturbances in the production of male sex hormones.

Treatment is prescribed to men over 50 years of age with the development of clinical manifestations of androgen deficiency, male menopause, especially in individuals receiving glucocorticoids. The most appropriate is the use of long-acting androgens - sustanon-250 or omnodren 1 ml intramuscularly once every 3-4 weeks.

Bronchodilators, expectorants, massage.

They are used to restore bronchial patency (the methods are the same as for atopic bronchial asthma).

Treatment of autoimmune pathogenetic variant

The treatment program includes the following areas:

  1. Limitation (stoppage) of tissue denaturalization and autosensitization processes, fight against infection, including viral infection.
  2. Treatment of atopy (non-specific hyposensitization, intal, antistamine agents).
  3. Glucocorticoid therapy.
  4. Immunomodulatory therapy (thymomimetic drugs - thymalin, T-activin; antilymphocyte globulin when reducing the pool of T-suppressors)

Antilymphocyte globulin contains antibodies against lymphocytes, blocking their interaction with antigens. When prescribed in small doses, the drug stimulates the suppressor function of T-lymphocytes and helps reduce the synthesis of IgE. Antilymphocyte globulin is administered intravenously by drip at a dose of 0.5-0.7 mg/kg. The positive effect appears 3-5 weeks after administration. The following side effects are possible: increased body temperature, chills, infectious complications. Contraindications to treatment with antilymphocyte globulin: epidermal sensitization, intolerance to protein and serum preparations.

Immunosuppressants, cytostatics

Patients with the autoimmune variant of bronchial asthma almost always develop glucocorticoid dependence and corticosteroid resistance, various complications of systemic glucocorticoid therapy. In connection with the above, it is recommended to include cytostatics in the treatment complex. In this situation, they exhibit the following positive effects:

  • immunosuppressant (suppress the formation of antipulmonary antibodies formed as a result of sensitization of patients to lung tissue antigens); autoimmune asthma is caused by allergic reactions of types III-IV;
  • anti-inflammatory;
  • significantly reduce the dose and number of side effects of glucocorticoids.

The most commonly used immunosuppressants are:

Methotrexate is an antagonist of folic acid, which is necessary for the synthesis of RNA and DNA, suppresses the proliferation of mononuclear cells and fibroblasts, the formation of autoantibodies to the bronchopulmonary system, and reduces the migration of neutrophils to the site of inflammation. It is prescribed at a dose of 7.5-15 mg per week for 6-12 months.

The main side effects of methotrexate are:

  • leukopenia; thrombocytopenia;
  • development of infectious complications;
  • toxic hepatitis;
  • ulcerative stomatitis;
  • pulmonary fibrosis;
  • alopecia.

Contraindications to treatment with methotrexate:

  • leukopenia;
  • thrombocytopenia; liver and kidney diseases; pregnancy;
  • active inflammatory process of any localization; peptic ulcer.

Treatment should be carried out under control of the number of leukocytes and platelets in the peripheral blood (1-2 times a week) and indicators of liver and kidney function.

Cyclosporine A (sandimmune) is a polypeptide cytostatic produced by the fungus Tolypodadium inflatum.

Mechanism of action of cyclosporine:

  • selectively suppresses the function of T-lymphocytes;
  • blocks the transcription of genes responsible for the synthesis of interleukins 2, 3, 4 and 5, which participate in inflammation, therefore, cyclosporine has an anti-inflammatory effect;
  • suppresses degranulation of mast cells and basophils and thus prevents the release of inflammatory and allergy mediators from them.

Cyclosporine A is administered orally at a dose of 5 mg/kg per day for 3-6 months.

The drug may exhibit the following side effects:

  • gingival hyperplasia;
  • hypertrichosis;
  • liver dysfunction;
  • paresthesia;
  • tremor;
  • arterial hypertension;
  • thrombocytopenia;
  • leukopenia.

Treatment is carried out under control of the content of platelets, leukocytes, liver and kidney function in the blood. Contraindications to cyclosporine are the same as for methotrexate.

Monoclonal antibodies against T-lymphocytes and cytokines, and interleukin antagonists are also used as immunosuppressants.

Efferent therapy (hemosorption, plasmapheresis).

Agents that improve microcirculation and prevent thrombus formation (heparin 10-20 thousand IU per day for 4 weeks, curantil up to 300 mg/day).

Bronchodilators, expectorants.

Psychotropic therapy (sedatives, psychotropic drugs, rational psychotherapy, auto-training).

Treatment of adrenergic imbalance

In adrenergic imbalance, the ratio between beta- and alpha-adrenergic receptors is disrupted, with alpha-adrenergic receptors becoming dominant. The activity of beta-adrenergic receptors in this type of bronchial asthma is sharply reduced. Often, the main reason for the development of adrenergic imbalance is an overdose of adrenergic drugs.

The treatment program includes the following areas:

  1. Complete withdrawal of the adrenomimetic until the sensitivity of beta-adrenergic receptors is restored.
  2. Increased activity of beta2-adrenergic receptors, restoration of their sensitivity:
    • glucocorticoids (mainly parenterally in doses corresponding to those for asthmatic status, for example, hydrocortisone hemisuccinate initially at a dose of 7 mg/kg of body weight, then 7 mg/kg every 8 hours for 2 days, then the dose is gradually reduced by 25-30% per day to the minimum maintenance dose);
    • unloading and dietary therapy;
    • barotherapy;
    • correction of hypoxemia (inhalation of an oxygen-air mixture with an oxygen content of 35-40%;
    • relief of metabolic acidosis by intravenous drip administration of sodium bicarbonate under control of plasma pH (usually about 150-200 ml of 4% sodium bicarbonate solution is administered);
  3. Intravenous administration of euphyllin against the background of the use of glucocorticoids (initial dose of 5-6 mg/kg by drip for 20 minutes, and then until improvement at a dose of 0.6-0.9 mg/kg/h, but not more than 2 pts).
  4. Treatment with membrane-stabilizing drugs (Intal, sodium nedocromil), they reduce the need for inhalation of beta2-adrenergic stimulants and glucocorticoids.
  5. Decreased activity of alpha-adrenergic receptors: use of pyrroxane (0.015 g 3 times a day orally for 2 weeks, it is possible to use droperidol - 1-2 times a day intramuscularly 1 ml of 0.25% solution. Treatment with alpha-adrenergic blockers is carried out under careful monitoring of blood pressure and is contraindicated in arterial hypotension, severe organic lesions of the heart and blood vessels.
  6. Decreased activity of cholinergic receptors: treatment with atrovent, troventol, platifschline, atropine, belladonna preparations.
  7. Treatment with antioxidants (vitamin E, autotransfusion of blood irradiated with ultraviolet light, helium-neon laser).
  8. The use of agents that optimize the microviscosity of the lipid matrix of membranes (inhalation of a liposomal preparation of lily, made from natural phosphate-dylcholine; treatment with lipostabil).
  9. Use of beta2-adrenergic stimulants after restoration of sensitivity of beta2-adrenergic receptors to them.

Treatment of the neuropathogenetic variant

  1. Medicinal effects on the central nervous system (carried out in a differentiated manner, taking into account the nature of the disorders of the functional state of the central nervous system):
    • sedatives (elenium - 0.005 g 3 times a day, seduxen - 0.005 g 2-3 times a day, etc.);
    • neuroleptics (chlorpromazine - 0.0125-0.025 g 1-2 times a day); sleeping pills (radedorm 1 tablet before bedtime); antidepressants (amitriptyline - 0.0125 g 2-3 times a day).
  2. Non-drug effects on the central nervous system: psychotherapy (rational, pathogenetic, suggestion in waking and hypnotic states), autogenic training, neurolinguistic programming.
  3. Effect on the autonomic nervous system:
    • acupuncture;
    • electroacupuncture;
    • novocaine blockades (intracutaneous paravertebral, vagosympathetic);
    • point massage.
  4. General strengthening therapy (multivitamin therapy, adaptogens, physiotherapy, spa treatment).

Treatment of exercise-induced asthma

Exercise-induced asthma develops during or after physical activity. As an independent variant of the disease, it is observed in 3-5% of patients with bronchial asthma, in whom only submaximal physical activity causes bronchial obstruction, in the absence of signs of allergy, infection, dysfunction of the endocrine and nervous systems.

The treatment program for exercise-induced asthma includes the following areas:

  1. Use of beta2-adrenergic agonists - 1-2 inhalations 5-10 minutes before physical activity.
  2. Treatment with mast cell stabilizers (Intal, Tailed). Intal is inhaled in a daily dose of 40-166 mg, Tailed - 4-6 mg. These drugs can be used as pathogenetic treatment for bronchial hyperreactivity (course 2-3 months), as well as for preventive purposes 20-30 minutes before physical activity.
  3. Treatment with calcium antagonists (nifedipine). This drug can be used for pathogenetic treatment (30-60 mg/day for 2-3 months) or as a preventive measure 45 minutes before physical activity. Tableted forms of calcium antagonists are chewed, kept in the mouth for 2-3 minutes and swallowed.
  4. Inhalation of magnesium sulfate (single dose - 0.3-0.4 g, course of 10-14 inhalations).
  5. Ergotherapy is the use of a training regimen of increasing intensity physical activity using ergometers (bicycle ergometer, treadmill, stepper, etc.). A two-month course of ergotherapy with 3-4 sessions per week on a bicycle ergometer completely eliminates post-exercise bronchospasm in 43% of patients and reduces its severity in 40% of patients.
  6. Volitional control of breathing at rest and during physical exertion. Breathing in the controlled hypoventilation mode at a respiratory rate of 6-8 per minute for 30-60 minutes 3-4 times a day eliminates or significantly reduces the severity of post-exertional bronchospasm.
  7. Inhalations of anticholinergics berodual and troventol as a course and preventive treatment.
  8. A course of treatment with heparin inhalations.

It has been established that heparin inhalations prevent the development of asthma attacks after physical exertion. Heparin acts as a specific blocker of inositol triphosphate receptors and blocks the release of calcium in mast and other cells.

  1. The use of point massage. It stops obstructive reactions at the level of large bronchi, eliminates hyperventilation in response to physical exertion. The braking method is used, the massage time of one point is 1.5-2 minutes, no more than 6 points are used for the procedure.
  2. Prevention of bronchospasm induced by cold air and physical activity:
    • breathing through a special conditioning mask, which creates a heat and mass exchange zone that equally reduces the loss of heat and moisture from the bronchi;
    • vibration impact on the body as a whole with mechanical vibrations of infra- and low-sound frequencies for 6-8 minutes before physical activity.

The mechanism of action is to reduce the supply of mediators in mast cells.

Treatment of aspirin asthma

Aspirin asthma is a clinical and pathogenetic variant of bronchial asthma associated with intolerance to acetylsalicylic acid (aspirin) and other non-steroidal anti-inflammatory drugs. It is often combined with nasal polyposis and such a syndrome is called the asthmatic triad (asthma + intolerance to acetylsalicylic acid + nasal polyposis).

After taking acetylsalicylic acid and non-steroidal anti-inflammatory drugs, leukotrienes are formed from arachidonic acid in the cell membrane due to activation of the 5-lipoxygenase pathway, causing bronchospasm.

The treatment program for aspirin-induced bronchial asthma includes the following areas:

  1. Eliminate foods containing natural and added salicylates.

Foods Containing Salicylates

Naturally occurring

Containing added salicylates

Fruits

Berries

Vegetables

Mixed group

Apples

Apricots

Grapefruits

Grape

Lemons

Peaches

Melons

Oranges

Plums

Prunes

Blackcurrant

Cherry

Blackberry

Raspberry

Strawberries

Strawberry

Cranberry

Gooseberry

Cucumbers

Pepper

Tomatoes

Potato

Radish

Turnip

Almond nut

Different varieties

Currants

Raisin

Winter greenery

Root Vegetable Drinks

Peppermint Candies

Candies with greenery additives

Confectionery with greenery additives

  1. Exclusion of drugs containing aspirin, as well as non-steroidal anti-inflammatory drugs: citramon, asfen, askofen, novocephalgin, theophedrine, acetylsalicylic acid, in combination with ascorbic acid (various options), indomethacin (methindol), voltaren, brufen, etc.
  2. Exclusion of food substances containing tartrazine. Tartrazine is used as a yellow caloric food additive and is a derivative of coal tar. Cross-intolerance to tartrazine is observed in 30% of patients with aspirin intolerance. That is why products containing tartrazine are excluded from the diet of patients with aspirin asthma: yellow cakes, glaze mixtures, yellow ice cream, yellow candies, soda water, cookies.
  3. Exclusion of medicinal substances containing tartrazine: inderal, dilantin, elixophylline, dental elixir, multivitamins, etc.
  4. Treatment with membrane-stabilizing drugs (Intal, Tayled, Ketotifen).
  5. Desensitization with acetylsalicylic acid to reduce sensitivity to it. For patients with low sensitivity to aspirin (threshold dose - 160 mg and more), one of the following desensitization schemes is recommended:
    • aspirin is taken throughout the day at two-hour intervals in increasing doses of 30, 60, 100, 320 and 650 mg;
    • Aspirin is taken for 2 days at three-hour intervals:
      • on the first day 30, 60, 100 mg;
      • on the second day 150, 320, 650 mg with a transition to a maintenance dose of 320 mg on subsequent days.

For patients with low sensitivity to aspirin (threshold dose less than 160 mg), E. V. Evsyukova (1991) developed a desensitization scheme with small doses of aspirin, with the initial dose being 2 times less than the threshold. Then, during the day, the dose is slightly increased at 3-hour intervals under the control of forced expiratory flow indices. In the following days, the aspirin dose is gradually increased to the threshold dose and taken 3 times a day. After achieving good bronchial patency indices, a transition is made to maintenance administration of one threshold dose of aspirin per day, which is taken for several months.

Patients with very high sensitivity to aspirin (threshold dose 20-40 mg) undergo a course of AUFOK consisting of 5 sessions before desensitization, with the interval between the first three sessions being 3-5 days, and between the rest - 8 days. The function of external respiration is examined 20 minutes before and 20 minutes after AUFOK. After the course of AUFOK, an increase in the threshold of sensitivity to aspirin by 2-3 times is noted.

  1. In very severe cases of aspirin asthma, treatment with glucocorticoids is carried out.

Treatment of cholinergic (vagotonic) bronchial asthma

The cholinergic variant of bronchial asthma is the variant that occurs with a high tone of the vagus nerve.

The treatment program includes the following activities.

  1. Use of peripheral M-anticholinergics (atropine, platifillin, belladonna extract, belloid).
  2. Inhalation use of M-anticholinergics: iprotropium bromide (Atrovent), oxitropium bromide (Oxyvent), glycotropium bromide (Robinul). These drugs are more preferable compared to platyphylline, atropine, belladonna, since they do not penetrate the blood-brain barrier, do not have a negative effect on mucociliary transport. They are used 2 inhalations 4 times a day.
  3. Use of the combination drug berodual, consisting of the beta2-adrenergic stimulant fenoterol and the anticholinergic ipratropium bromide. It is used 2 inhalations 4 times a day.
  4. Acupuncture - reduces the manifestations of vagotonia.

Treatment of food bronchial asthma

  1. Elimination and hypoallergenic diet.

Exclude products that cause attacks of food bronchial asthma in the patient, as well as products that are more likely to cause asthma (fish, citrus fruits, eggs, nuts, honey, chocolate, strawberries). In case of allergy to cereals, exclude rice, wheat, barley, corn. In case of allergy to chicken eggs, it is necessary to exclude chicken meat as well, since there is sensitization to it at the same time.

  1. Unloading and dietary therapy.
  2. Enterosorption.
  3. Mast cell stabilizers (ketotifen).
  4. Extracorporeal treatment methods (hemosorption, plasmapheresis).

Treatment of nocturnal bronchial asthma

Nocturnal bronchial asthma is the occurrence of symptoms of suffocation exclusively or with a clear predominance during the night and early morning hours.

About 74% of patients with bronchial asthma wake up between 1-5 a.m. due to increased bronchospasm, while there are no significant differences between atopic and non-atopic forms of the disease. Often, in the initial phase of bronchial asthma, nocturnal attacks of suffocation are the only sign of the disease, and therefore bronchial asthma is not diagnosed by a doctor when examining a patient during the day.

The main causes of night attacks of bronchial asthma:

  • the presence of circadian rhythms of changes in bronchial patency (even in healthy individuals, maximum bronchial patency is observed from 13:00 to 17:00, minimum - from 3:00 to 5:00 in the morning). In patients with nocturnal bronchial asthma, the presence of a circadian rhythm of bronchial patency is clearly noted, with its deterioration at night;
  • daily fluctuations in barometric pressure, relative humidity and air temperature. The respiratory tract of patients with bronchial asthma is hypersensitive to a decrease in ambient air temperature at night;
  • increased contact of a patient with bronchial asthma with aggressive allergens in the evening and at night (high concentration of spore fungi in the air on warm summer nights; contact with bedding containing allergens - feather pillows, dermatophagoid mites in mattresses, etc.);
  • the influence of the horizontal position (in the horizontal position, mucociliary clearance worsens, the cough reflex decreases, and the tone of the vagus nerve increases);
  • the effect of gastroesophageal reflux, especially when eating before bedtime (bronchospasm is reflexively provoked, especially in people with increased bronchial reactivity; an irritating effect of aspirated acidic contents on the respiratory tract at night is also possible). Such patients are not recommended to take theophedrine in the afternoon (it reduces the tone of the lower esophageal sphincter);
  • the effect of diaphragmatic hernia (this occurs in some patients), similar to the effect of gastroesophageal reflux;
  • increased activity of the vagus nerve, especially in the cholinergic variant of bronchial asthma and increased sensitivity of the bronchi to acetylcholine at night;
  • the highest concentration of histamine in the blood is at night;
  • increased tendency of mast cells and basophils to degranulate at night;
  • decreased concentration of catecholamines and cAMP in the blood at night;
  • circadian rhythm of cortisol secretion with a decrease in its level in the blood at night;
  • circadian rhythms of changes in the number of adrenoreceptors on lymphocytes of patients with bronchial asthma (lymphocytes carry beta-adrenoreceptors of the same type as bronchial smooth muscles), the minimum density of beta-adrenoreceptors is noted in the early morning hours.

Prevention and treatment of nocturnal attacks of bronchial asthma

  1. Maintaining constant comfortable conditions in the bedroom (this is especially important for patients with increased meteotropic sensitivity).
  2. In case of allergy to house mites - their thorough destruction (radical treatment of apartments with the latest acaricidal drugs, replacement of bedding - foam mattresses, pillows, etc.).
  3. Combating dustiness in rooms, using filtration systems that allow removing almost 100% of fungal spores, pollen, house dust and other particles from the air. The systems include an aerosol generator, fans, ionization devices, electrostatically charged filters.
  4. Patients with gastroesophageal reflux are advised not to eat before bed, to take an elevated position in bed, and are prescribed antacids and enveloping agents. In some cases (especially in the presence of a diaphragmatic hernia), surgical treatment is possible.
  5. To improve mucociliary clearance, bromhexine is prescribed, especially before bedtime, 0.008 g 3 times a day and 0.008 g at night, or ambroxol (lasolvan), a metabolite of bromhexine, 30 mg 2 times a day and at night.
  6. Patients with severe hypoxemia are recommended to breathe oxygen during sleep (this helps to increase the saturation of hemoglobin with oxygen and reduces the number of asthma attacks at night. To reduce hypoxemia, long-term use of Vectarion (Almitrine) 0.05 g 2 times a day is also recommended.
  7. Using the principle of chronotherapy. Preliminarily, bronchial patency is measured at different times for three days. Subsequently, it is recommended to take bronchodilators during periods of expected deterioration of respiratory function. Thus, inhalations of beta-adrenergic agonists are prescribed 30-45 minutes before this time, Intal - 15-30 minutes, Beclomet - 30 minutes, taking euphyllin orally - 45-60 minutes. In most patients, chronotherapy reliably prevents night attacks of bronchial asthma.

Self-management programs for patients with bronchial asthma have been developed abroad. Patients monitor bronchial patency during the day using portable spirometers and peak flowmeters; they adjust their beta-adrenergic agonists accordingly, thereby reducing the number of asthma attacks.

  1. Taking prolonged theophylline preparations is the main way to prevent night attacks of bronchial asthma. Traditionally, taking these preparations in equal doses twice a day (morning and evening) results in the concentration of theophylline in the blood being lower at night than during the day, due to the deterioration of its absorption at night. Therefore, if night attacks of suffocation predominate, it is optimal to take one third of the daily dose in the morning or at lunchtime and two thirds of the dose in the evening.

Extended-release second-generation theophyllines are increasingly being used (they act for 24 hours and are taken once a day).

When a daily dose of extended-release second-generation theophyllines is taken in the morning, the highest concentration of theophylline in the serum is observed during the day, and the night concentration is 30% lower than the average for 24 hours, therefore, in case of nocturnal bronchial asthma, extended-release daily theophylline preparations should be taken in the evening.

The drug Unifil, when prescribed in a dose of 400 mg at 8 p.m. to more than 3,000 patients with nocturnal or morning attacks of suffocation, reliably prevented these attacks in 95.5% of patients (Dethlefsen, 1987). The domestic drug Teopec (extended theophylline of the first generation, acts for 12 hours) for nocturnal attacks of suffocation is taken at night in a dose of 0.2-0.3 g.

  1. Taking prolonged β-adrenomimetics. These drugs accumulate in the lung tissue due to their high lipid solubility and thus have a prolonged effect. These are formoterol (prescribed at 12 mcg 2 times a day as a metered aerosol), salmeterol, terbutaline retard in tablets (take 5 mg at 8 a.m. and 10 mg at 8 p.m.), saltos in tablets (take 6 mg 3 times a day.

It has been established that the optimal dose is 1/2 of the daily dose in the morning and 2/3 in the evening.

  1. Taking anticholinergic drugs.

Ipratropium bromide (Atrovent) - inhalations of 10-80 mcg, provides an effect for 6-8 hours.

Oxytropium bromide in inhalations of 400-600 mcg provides a bronchodilatory effect for up to 10 hours.

Treatment with these drugs, inhaled before bedtime, prevents night attacks of bronchial asthma. These drugs are most effective in cholinergic bronchial asthma, and their effect is more pronounced in infection-dependent bronchial asthma than in atonic asthma.

  1. Regular treatment with mast cell stabilizers helps prevent nighttime asthma attacks. Intal, ketotifen, and azelastine, a prolonged-release drug, are used. It delays the release of mediators from mast cells and neutrophils, counteracts the effects of leukotrienes C4 and D4, histamine, and serotonin. Azelastine is taken at 4.4 mg 2 times a day or at a dose of 8.8 mg 1 time per day.
  2. The question of the effectiveness of evening inhalations of glucocorticoids in the prevention of nocturnal bronchial asthma has not been finally resolved.

Clinical examination

Bronchial asthma of mild to moderate severity

Examination by a therapist 2-3 times a year, pulmonologist, ENT doctor, dentist, gynecologist - 1 time per year. General blood test, sputum, spirography 2-3 times a year, ECG - 1 time per year.

Allergological examination - as indicated.

Therapeutic and health-improving measures: dosed fasting - once every 7-10 days; acupuncture, non-specific desensitization twice a year; therapeutic microclimate; psychotherapy; spa treatment; exclusion of contact with the allergen; specific desensitization according to indications; breathing exercises.

Severe bronchial asthma

Examination by a therapist once every 1-2 months, by a pulmonologist, allergist - once a year; examinations are the same as for mild and moderate bronchial asthma, but corticosteroid-dependent patients undergo urine and blood tests for glucose content twice a year.

Therapeutic and health-improving measures: dosed fasting - once every 7-10 days; non-allergenic diet, hyposensitizing therapy, breathing exercises, physiotherapy, psychotherapy, halo- and speleotherapy, massage, herbal medicine, bronchodilators.

In terms of dispensary observation for any form and severity of bronchial asthma, it is necessary to provide for patient education. The patient should know the essence of bronchial asthma, methods for self-stopping an asthma attack, situations when it is necessary to call a doctor, individual asthma triggers that should be avoided, signs of deterioration of the condition and bronchial patency, an individual daily dose of preventive drugs for asthma control.

You are reporting a typo in the following text:
Simply click the "Send typo report" button to complete the report. You can also include a comment.