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Exogenous allergic alveolites

Exogenous allergic alveolitis (synonym: hypersensitive pneumonitis, interstitial granulomatous alveolitis) is a group of diseases caused by intense and, rarely, prolonged inhalation of antigens of organic and inorganic dusts and are diffuse, unlike pulmonary eosinophilia, damage to alveolar and interstitial structures. The emergence of this group of diseases is associated with the development of immunocomplex (type III) and cell-mediated (type IV) allergic reactions.

Atonic IgE-dependent mechanisms are not characteristic of allergic alveolitis. The inflammatory process is localized in the alveoli and interstitium of the lungs, and not in the air-conducting paths, as in bronchial asthma, although the latter may be a concomitant disease in patients with alveolitis.

Etiological factors that can cause exogenous allergic alveolitis, can be divided into 3 groups:

1) microorganisms (bacteria, fungi, protozoa and their metabolic products (proteins, enzymes, endotoxins, etc.));

2) organic matter of animal and vegetable origin (animal dander, bird feathers, rice dust, etc.);

3) low molecular weight compounds (diisocyanite, salts of heavy metals, including gold), medications (Intal, antibiotics, nitrofurans, antimycotic drugs, antimetabolites). For the emergence of alveolitis requires several conditions:

1) inhalation route of penetration of the antigen (the diameter of the dust particles is not more than 5 microns);

2) high concentrations of antigen in the air we breathe and significant exposure;

3) the antigen must be presented in the corpuscular form (cells) or in the form of an aggregated protein; soluble antigens do not cause the development of alveolitis;

4) the antigen must have the ability to activate the complement system along an alternative path, i.e. without antibodies.

Pathologically allergic alveolitis is characterized by damage to the alveolar and endothelial cells, vasculitis, mononuclear and (or) polynuclear infiltration of the interstitial tissue and alveolar structures of the lungs, the formation of sarcoid-like granulomas, interstitial fibrosis.

The name of the disease most often reflects the etiological factor:

“Milling lung”, “lung cheesemakers”, “poultry farmers lung”, etc.

During the course of the disease there are acute, subacute and chronic stages (forms).

The acute form develops 4-12 hours after the patient contacts the allergen. There is flu-like syndrome: chills, fever, cough, shortness of breath, nausea, myalgia, arthralgia. Other acute forms include pneumonia-like (crepitus and moist rales on auscultation, interstitial infiltrates on X-ray) and bronchotic (dry cough, "scattered wheezing in the lungs) syndromes.
Neutrophilic leukocytosis is observed in the blood. In the study of respiratory function, a mixed type of respiratory failure (obstructive and restrictive) is detected. Radiologically, reticular or modular (0.1–1 cm diameter) infiltrative shadows can be detected:

Frosted glass type changes, indistinguishability of vascular pattern.

The acute form may have a progressive course with severe

the prognosis, but more often the suspension due to illness from work or hospitalization leads to an improvement in the condition. The diagnosis of the acute form of exogenous alveolitis is rarely made, usually diagnosed with influenza, ARVI, acute pneumonia or bronchitis.

Subacute form develops with continued contact with the antigen. In these cases, the “Monday phenomenon” is typical:

acute manifestations are observed in the days after rest, and by the end of the working week they subside.

The chronic form of exogenous allergic alveolitis is observed during long-term contact with an allergen and a long course of the disease. Pathologically, interstitial fibrosis (“fibrosing alveolitis”) underlies this form; therefore, the clinical manifestations of the disease are similar to the clinic of idiopathic fibrosing alveolitis (Hammen-Rich disease). In patients with respiratory failure, accompanied by asthenic syndrome, anorexia, and weight loss. A pulmonary heart develops with appropriate symptoms. An X-ray examination reveals signs of pulmonary fibrosis: diffuse reticular, modular and linear shadows, symptoms of lung defrostation, a “cellular lung” pattern. In the study of respiratory function registered restrictive type of respiratory failure.

DIAGNOSIS of exogenous allergic alveolitis is carried out on the basis of an assessment of the clinic of the disease, a thorough history taking, instrumental methods and an immunological examination. For the detection of specific antibodies, precipitation reactions, passive hemagglutination, enzyme immunoassay are used. The pagpenthelial reaction of lymphocyte blast-transform and inhibition of leukocyte migration with a specific antigen have a diagnostic significance.

Intradermal tests with the dilution of allergen 1:10 have not lost their value. Sometimes a lung biopsy is required.

The differential diagnosis is carried out in the acute stage with acute respiratory viral infections, influenza, acute pneumonia, acute bronchitis. In the chronic stage, the disease is differentiated from idiopathic fibrosing alveolitis and granulomatous processes in the lungs (tuberculosis, sarcoidosis, Wegener's granulomatosis, etc.) -
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Exogenous allergic alveolites

  1. Exogenous allergic alveolitis
    This is a group of diseases caused by inhalation of organic dust, which occur with diffuse granulomatous lesions of the interstitial lung tissue. Unlike other granulomatous lesions of the lungs, such as sarcoidosis and coccidioidomycosis, there are no systemic manifestations in exogenous allergic alveolitis. Inhalation of organic dust leads to the development of exogenous allergic
  2. Allergic rhinitis, allergic conjunctivitis, urticaria, quinck edema
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