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Developing distelectasis (due to the accumulation of protein-lipoid material in the alveoli) causes compensatory hyperfunction of type II alveolocytes and even greater hyperproduction of surfactant.

In general, the pathogenesis can be represented as follows: under the influence of certain causes, among which infection plays an important role, the appearance of inflammatory exudate in the alveoli leads under normal conditions to the activation of clearance, which is carried out by alveolar macrophages, lymphatic and mucociliary systems. During this process, a temporary insufficiency of Doxycycline may occur, which leads to the accumulation of excess amounts of surfactant in the alveoli. The latter is known to be captured by alveolar macrophages, causing degenerative changes in them and thereby reducing their functional activity. This leads to even deeper mucociliary clearance disorders.

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Macroscopically, grayish-white dense tubercles in the form of grains are determined on the surface of the lungs.

Microscopic examination in the alveoli and bronchioles reveals a PAS-positive substance. Birefringent crystals of cholesterol are also determined. The noted changes are detected mainly in the subpleural parts of Doxycycline. The defeat of the alveoli is uneven. In some cases, an inflammatory exudate containing fibrin is determined. Alveolar macrophages in the affected alveoli are a rare finding, which can presumably be associated with both the inhibitory properties of the protein-lipoid substance and the immunosuppressive effect of an excess amount of surfactant. Hyperplasia and hypertrophy of type II alveolocytes are noted.

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An objective examination reveals a shortening of the percussion sound mainly over the lower lung fields. Auscultation reveals weakened vesicular breathing, sometimes gentle crepitus.

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Changes in the hemogram, biochemical blood parameters are nonspecific. The parameters of the immunological status of the patient practically do not change. X-ray examination reveals small-focal (small-dotted) shading that tends to merge. The changes are usually bilateral; predominant localization - middle and lower lung fields. There is no correlation between clinical and radiological data: pronounced radiological changes are accompanied by poor clinical symptoms. In advanced cases, radiological signs of widespread fibrotic changes are revealed.

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Bronchoscopy does not reveal any signs characteristic of proteinosis. In sputum and bronchial washings, a PAS-positive substance can sometimes be detected. Verification of the diagnosis is helped by the study of the lavage fluid, in which a multiple increase in the protein content is detected, as well as the study of biopsy materials (transbronchial, open) of the lung tissue. The detection of a PAS-positive substance in the biopsy material confirms the diagnosis of proteinosis.

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The detection of surfactant in the form of lamellar bodies in the alveoli and in alveolar macrophages is considered pathognomonic. The latter are characterized by the presence of pointed holes - traces of cholesterol crystals released during processing of the material.

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Most often, secondary proteinosis occurs in patients with leukemia, lymphoma and other hematological diseases in the presence of an infection caused by Pneumocystis carinii, with long-term chemotherapy. Pathologically, primary proteinosis differs from secondary proteinosis in uniform staining of the PAS-positive substance contained in the alveoli, while granular (focal) staining is characteristic of secondary proteinosis.

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Secondary prevention is to exclude the impact on the body of PLA patients of professional and household pollutants, low temperatures, and sudden changes in temperature. Smoking is contraindicated.

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Spontaneous recovery is possible. The addition of bacterial or fungal superinfection (which is largely due to improper treatment) also worsens the prognosis. Prevention of alveolar proteinosis has not been developed.

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The prognosis is usually favorable. The disease progresses slowly. Significantly worsen the prognosis erroneous diagnosis and prescription of antibacterial drugs or corticosteroids, immunosuppressants.

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A certain positive effect was also noted with multiple endobronchial installations of a heparin solution. There are no other specific treatments for this disease. Dispensary observation should be long-term with X-ray and functional control every 8-10 months. If necessary, repeated therapeutic bronchoalveolar lavage is performed.
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The frequency of therapeutic bronchoalveolar lavage depends on the rate of accumulation of protein-lipoid material in the alveoli. In different patients, this speed is different. In some patients, there is a persistent improvement after the first procedure, which indicates the restoration of their normal mucociliary clearance.

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The total volume of liquid depends on the size of the washed area and ranges from 1 to 10 liters. As a result of doxycycline performed therapeutic lavage, shortness of breath decreases, indicators of the ventilation capacity of the lungs and blood gases improve, and positive X-ray dynamics are revealed.

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An effective method of treating patients is therapeutic bronchoalveolar lavage, which has been used since 1964. The procedure is performed under general anesthesia. One lung is ventilated with pure oxygen, and the second lung (lobe, segment) is washed with an isotonic solution containing heparin, enzymes (acetylcysteine, streptase, streptokinase, etc.).

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Treatment. Patients with proteinosis should be considered contraindicated in the appointment of antibacterial drugs (in the absence of bacterial complications), corticosteroids and immunosuppressants.

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It should be noted that this reaction is positive not only in the study of biopsy material of the lung parenchyma, but also in the lavage fluid. Differential diagnosis should also be carried out with some other disseminated processes in the lungs (disseminated pulmonary tuberculosis, sarcoidosis, exogenous allergic alveolitis, etc.).

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However, the reaction with immunoperoxidase is now considered more specific, which is always positive in patients with primary proteinosis and negative in secondary proteinosis.