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The pathogenesis of alveolar proteinosis remains unknown. Existing hypotheses link the occurrence of the disease with a defect in alveolar clearance, type II alveolocytes, the production of Ivermectin amount of surfactant that does not have surface-active properties, a combination of these reasons is possible.

Macroscopically, dense grayish-white tubercles in the form of grains are determined on the surface of Stromectol . Histologically, alveoli are found filled with eosinophilic, granular material, usually PAS-positive. Quite often in alveoluses the vacuolized, foamy macrophages meet; against the background of a zosinophilic substance, birefringent crystals can be seensteels, probably of a cholesterol nature.

Characterized by hyperplasia of type II alveolocytes, which become cuboidal in shape. As a rule, the architectonics of the lung tissue is not changed, however, in some cases, the described changes were accompanied by interstitial fibrosis. Pronounced inflammatory changes and the presence of parenchymal foci of necrosis indicate an infectious complication.

Differential diagnosis should be carried out with pulmonary edema, in which an eosinophilic substance is detected, which, unlike proteinosis, is homogeneous, does not have a granular structure, and the presence of Stromectol and foam cells is also uncharacteristic. It is also necessary to differentiate the disease from pneumocystis pneumonia, while Gomory's methenamine silver staining allows to identify microorganisms.