Atopic bronchial asthma (synonym: non-infectious allergic bronchial asthma) is one of the forms of bronchial asthma, which is based on an allergy to non-infectious allergens. Atopic asthma accounts for up to 15% of varieties of asthma. The etiology of atopic bronchial asthma is due to various exoallergens. The pathogenesis of atopic bronchial asthma is complex , includes immune and non-immunological mechanisms.
Clinic of Atopic Bronchial Asthma
Atopic asthma often begins before the age of 10 years, the bulk of patients (up to 70%) get sick in the first twenty years of life. There is a high frequency of allergic predisposition along the lines of father and mother, a large percentage of inheritance in a downward direction. No significant influence of gender was noted, although in childhood boys are most often sick. The history of exudative diathesis in 80% of patients, eczema and atopic dermatitis, combined with or preceding atopic asthma, food allergy, drug allergy is characteristic. Often, atopic bronchial asthma is accompanied by allergic rhinosinusopathy, the symptoms of which (rhinorrhea, sneezing, severe difficulty in nasal breathing) are observed in the pre-entry period. Purulent processes in the sinuses and polyposis of the nose and sinuses are rare.
In half of cases, atopic bronchial asthma begins in connection with respiratory infections, while asthma attacks first occur at the height of the infectious process. Patients are sensitive to superinfection of Aspergillus fumigatus and the development of allergic bronchopulmonary aspergillosis. Atopic bronchial asthma is characterized by clearly defined, typical asthma attacks, most often at night, often with prodromal phenomena (itching in the nose, sneezing, urticaria). Auscultation reveals dry rales of high tone. Attacks stop spontaneously or are quickly stopped by adrenergic drugs; end with a cough with the separation of a small amount of light viscous sputum.
After contact with the antigen, some patients develop late-type bronchospastic allergic reactions (after 4-12 hours), lasting 24-48 hours, despite the use of bronchodilators. A double response to the antigen may be observed, combining allergic reactions of the immediate type and the late type. In the absence of an attack and complications, changes in the lungs are not detected. In the early years of the disease, more or less clear long-term remissions are noted; there is a late development of complications. Upon termination of contact with the allergen, remissions may be prolonged. A more severe course with short remissions is characteristic of a polyvalent allergy. At a certain stage, a bacterial allergy may join.
Depending on the leading etiological factor, various forms of atopic bronchial asthma are distinguished: household (dust), pollen, epidermal, fungal, nutritional (food).
Household atopic asthma (dust)
Household bronchial stma (dust) is the most common form of the disease. Its etiological factor is house dust. The disease begins, usually in the heating season, exacerbations are typical in winter, when the dustiness of the premises is highest. Due to the complex composition of house dust antigen, year-round symptoms may occur. For atopic bronchial asthma, household is characterized by the effect of elimination – remission when leaving home, which is especially pronounced in the early years of the disease. Upon returning home, asthma attacks resume. The course with periodic remissions and exacerbations compared with pollen atopic asthma is more severe, the relapses are longer, which is associated with the different nature of the immunological reactions to dust antigens. Often, simultaneously with or before the onset of the clinical period, clinical signs of bronchitis are observed, which are often allergic in nature. This leads to significant diagnostic difficulties, since bacterial and immunological inflammations have a number of identical signs: low-grade fever, cough with mucous or mucopurulent sputum, intoxication symptoms.
At puberty, a significant portion of patients suffering from atopic bronchial asthma since childhood have observed spontaneous remissions of the disease – the disappearance of symptoms for a year or two or more. However, during this period hyperresponsiveness of the respiratory tract persists, which is manifested by increased sensitivity to vagotonic agents (methacholine), various non-specific irritants, and professional allergens. Patients household b. but. they feel bad in the conditions of a subtropical humid climate (Black Sea coast of the Caucasus – Sochi, Sukhumi).
Fungal atopic bronchial asthma
Fungal atopic bronchial asthma may be seasonal or year-round in nature, depending on the characteristics of the spore formation of the fungi. The highest reproduction activity of Cladosporium, Alternaria, Hormodendrum is July – September (exacerbation of atopic bronchial asthma, respectively, in the summer-autumn period); Aspergillus and Candida – from September to March; Penicillium – throughout the year. The concentration of spores of these fungi (except for Candida and Penicillium) increases in the afternoon, so attacks of fungal atopic bronchial asthma, as a rule, occur at night or in the morning. Deterioration in damp weather is observed. Seasonal spore formation ceases with snow falling, in patients there is a significant relief. The “post-frost effect” is characteristic – exacerbation of the disease during the thaw after the first frost, which is associated with activation of the reproduction of mushrooms. Patients often cannot tolerate products containing yeast. Persons allergic to Penicillium may form severe allergic reactions to penicillin administration.
Nutritional atopic bronchial asthma (food)
Nutritional atopic bronchial asthma (food) is not well understood. It is believed that food allergens as the primary etiological factor are of greater importance in childhood. As a provocateur of asthma attacks in adults, food allergies occur in 25-55% of cases. However, some authors recognize its primary role. According to the clinical manifestations of atopic bronchial asthma, nutritive is similar to bronchial infectious-allergic asthma. Food allergy is relatively rarely the only cause of atopic bronchial asthma, most often it is combined with other types of allergies, in particular drug allergies. In certain cases, it causes allergic rhinosinusopathy in patients with atopic bronchial asthma, urticaria, dermatitis, without causing asthma attacks.
Clinical symptoms of food allergies develop predominantly as late bronchospastic reactions (4-12 hours after eating an allergenic food product). The severity of seizures due to food allergies varies from sporadic, mild to severe, prolonged exacerbations, a constantly recurring course with the development of asthma bronchial steroid-dependent. In some patients, in the absence of typical asthma attacks, breathing is constantly difficult, which may be a manifestation of allergic bronchitis. Usually food allergy is observed in patients with a relapsing course of the disease. In these cases, polyvalent food sensitization and frequent use of allergenic products are detected. Attacks of atopic bronchial asthma of food genesis in most patients begin with an aura – runny nose, nasal congestion, sensation of swelling in the throat, dry cough, tightness in the chest. Expiratory dyspnea is combined with inspiratory, the latter prevails in a number of patients. It is suggested that a feature of bronchial obstructive syndrome in atopic bronchial asthma nutritive is the predominance of edema of the bronchial mucosa. Along with asthma attacks, there are other manifestations of food allergies – rhinosinusopathy, migraine, urticaria. Often secondary infectious and inflammatory processes of the respiratory tract join them.
Atopic pollen asthma
Pollen atopic bronchial asthma most often begins at the height of the polling season following the symptoms of pollen rhinitis and conjunctivitis with a significant concentration of pollen in the air. It is easy, severe course is rare (about 7% of cases). More often combined with other manifestations of hay fever. The onset of hay fever with isolated pollen atopic asthma is rare. In addition to severe seasonal attacks of pollen atopic bronchial asthma, some patients may experience mild year-round symptoms due to the general antigenic properties of pollen and seeds, plant fruits when they are consumed. In particular, the year-round symptoms of atopic bronchial asthma in people allergic to hazel pollen can be caused by eating nuts, sunflower pollen and ragweed – sunflower seeds and their products, and cereal grass pollen – flour products.
Epidermal atopic bronchial asthma
Epidermal atopic bronchial asthma, the etiological factor of which is the particles of wool and the epidermis of animals, is rare, mainly as an occupational disease of livestock breeders, workers in experimental laboratories, and hunting farms. Of the pets, the most common cause of sensitization is cats, whose fur, down and saliva are second in terms of allergenic activity after ragweed. This type of atopic bronchial asthma can be combined with household atopic bronchial asthma. There is a clear link between disease and contact with relevant animals. A characteristic beginning is with allergic rhinoconjunctival syndrome, after which asthma attacks quickly develop.
A high frequency of sensitization (up to 80% of cases) is observed in contact with daphnia. Such a disease is characterized by a high degree of skin and bronchial sensitivity, concomitant allergic conjunctivitis is often observed, and often a food allergy to crustaceans (crayfish, crab, shrimp).
Diagnosis of atopic bronchial asthma
Diagnosis of atopic bronchial asthma includes the following methods: allergological history; Allergological diagnostic tests for skin scarification;
allergological diagnostic tests provocative inhalation according to indications with antigens detected during skin testing;
determination of the level of total immunoglobulin E and antibodies related to immunoglobulins E in blood serum (a high level of immunoglobulin E is characteristic, antibodies against allergens are detected in a high titer, which correlates with the results of skin tests and provocative tests);
examination of peripheral blood, nasal and bronchial secrets (eosinophilia is detected), bronchial washings, or bronchoalveolar lavage (an increase of more than 15% in the number of eosinophils and lymphocytes, a decrease in the number of alveolar macrophages). In vitro allergological diagnostic methods are used to confirm sensitization to certain antigens; PPN, RBTL, RTML, histamine release from leukocytes under the influence of specific allergens, which correlates with the activity of clinical manifestations. It should be borne in mind that with the differences in the mechanisms of bronchospasm caused by certain antigens, the clinical features of the atopic bronchial asthma of different etiologies may be associated. When conducting provocative inhalation tests, it is necessary to take into account the possibility of the formation of various types of allergic reactions. The development of allergic reactions of the late type indicates a severe course of atopic bronchial asthma. There is a correlation between their severity and the degree of increased sensitivity of the bronchi to histamine. Due to the complex nature of dust antigens (allergens of down, feather, wool, human and domestic epidermis, ticks, fungi, mold, germs), there are certain difficulties in detecting dust allergies. The diagnosis of food allergies in atopic asthma is particularly difficult. A history of food intolerance is not a reliable criterion. The examination scheme includes: maintaining a food diary and the appointment of elimination diets; carrying out unloading and dietary therapy (therapeutic fasting) for 3, 5, 7 days with a differential diagnostic purpose; provocative tests with suspected products under the control of leukopenic tests and changes in lung function; skin tests with food allergens; determination of specific antibodies in blood serum; X-ray registration of reactions of the stomach and intestines to the accepted food allergen. It is necessary to take into account the intolerance of ordinary products (bread, beef, milk, eggs, potatoes). The criteria for the significance of food allergies in the pathogenesis of asthma attacks are: the relationship of exacerbations of atopic bronchial asthma with certain foods; improving the state and function of breathing during fasting; detection of specific antibodies; positive leukopenic tests; violation of patency of the bronchi during provocative tests. The accompanying chronic diseases of the gastrointestinal tract, allergic reactions to food products in history are significant. It is necessary to examine patients to identify food allergies in connection with its effect on the occurrence of asthma attacks, the similarity of food atopic bronchial asthma with bronchial infectious-allergic asthma.