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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.

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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.

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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.

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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.

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Describe diffuse and nodular forms of pulmonary amyloidosis. Diffuse alveolar amyloidosis is often a finding at autopsy in patients with disseminated primary amyloidosis or amyloidosis associated with myeloma. Secondary deposition of amyloid masses in lung tissue is rare. Primary diffuse pulmonary amyloidosis without involvement of other organs is also a rare pathology. Patients suffer from progressive dyspnoea, and radiological examination reveals nodular changes in the interstitium.

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Microscopically detect the deposition of amyloid masses in the media of Ivermectin in the form of a pinkish homogeneous substance and along the interalveolar septa in the form of homogeneous eosinophilic masses that can protrude into the lumen of the alveoli. Rare cases describe damage to the pleura.

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Diffuse pulmonary amyloidosis should be differentiated from interstitial fibrosis, accompanied by excessive production of collagen. The presence of homogeneous masses in the vessel wall, as well as the absence of other signs of fibrosis in the form of Stromectol infiltrates, foci of fibrosis, and cellular changes, testify in favor of amyloidosis. To confirm the diagnosis, electron microscopic examination and staining with Congo red or crystal violet is necessary.

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Nodular pulmonary amyloidosis is usually not accompanied by deposition of amyloid in other organs. As a rule, this disease is asymptomatic, or there are only minor complaints from the respiratory system.

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An x-ray examination determines a single or multifocal lesion of the lungs: well-defined shadows are more often localized in the peripheral regions, separate cavities may be detected, and lymphadenopathy may be present.