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What causes exogenous allergic alveolitis?
Last reviewed: 19.10.2021
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Causes of exogenous allergic alveolitis
Exogenous allergic alveolitis is caused by the inhalation of organic dust containing various antigens, microorganisms (for example, thermophilic actinomycetes from hay, the so-called easy farmer), aspergillas and penicillas. Animal and fish proteins, insect antigens, aerosols of antibiotics, enzymes and other substances. In children, the most common cause of development of exogenous allergic alveolitis is contact with the feather and litter of birds (the so-called easy lovers of wavy parrots or light blue people) and elevator dust. In adults, the spectrum of allergens is much wider. Such as dust of cotton (babesiosis) or sugar cane (bagasse), sawdust, fungus spores (light mushrooms), fungal dust in the production of cheeses (light cheese), in patients with diabetes insipidus - inhalation drugs of the posterior lobe of the pituitary gland, etc. Repeated inhalation of allergens in 5 % of contacting causes the formation of specific antibodies (precipitin) of the IgG class and immune complexes that damage the lung's interstitium with the development of fibrosis. It is important to emphasize that the presence of atopy in the anamnesis is not a predisposing factor, since the type of allergic reaction in exogenous allergic alveolitis is immunocomplex.
Pathogenesis of exogenous allergic alveolitis. In contrast to atopic bronchial asthma, in which allergic inflammation of the bronchial mucosa is a consequence of the IgE-dependent type I reaction, the development of exogenous allergic alveolitis is formed with the participation of precipitating antibodies belonging to immunoglobulins of classes IgG and IgM. These antibodies, reacting with the antigen, form large-molecule immune complexes that are deposited under the endothelium of the alveolar capillaries. The complement system is being activated, which is fixed on the complexes. In this case, the C1 and C4 complement fractions act as mediators of inflammation.
Morphologically, in the acute phase of the disease, changes are observed that are characteristic of vasculitis.
With repeated and prolonged exposure to the allergen, sensitized lymphocytes synthesize lymphokines, which are powerful mediators of allergic inflammation. Morphologically, granulomas are determined in this phase, which are transformed into fibrous connective tissue structures, interstitial and alveolar fibrosis is formed, that is, the disease acquires a chronic course.