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TREATMENT

1. General measures aimed at disconnecting the patient from the source of antigen: compliance with sanitary and hygienic requirements at the workplace, technological improvement of industrial and agricultural production, rational employment of patients.



2. Drug treatment. In the acute stage, prednisone 1 mg / kg per day for 1-3 days, followed by a dose reduction for 3-4 weeks; azathioprine - 150 mg per day for 1-1.5 months, then 4-6 months, first 100 mg, then 50 mg per day. Cyclophosphamide is contraindicated. With the development of fibrosis - d-penicillamine -150-200 mg per day for 4-6 months, followed by 100 mg per day for 2 years. In experimental studies, fibrosis was also delayed by ACE inhibitors (captopril).



3. Extracorporeal methods - plasmapheresis, hemosorption, immunosorption. The combination of extracorporeal methods with pulse therapy with prednisone.



The term "pulmonary eosinophilia" refers to a group of diseases and syndromes characterized by transient pulmonary infiltrates and blood eosinophilia in excess of l, cl * 109 / l.



The causes of pulmonary eosinophilia are divided into primary, or cryptogenic, when the etiological factor remains unclear, and secondary. Among the latter distinguish:



1. Parasitic infestations (ascariasis, toxocariasis, schistosomiasis, para-gonimiasis, microfilariasis, opisthorchiasis, etc.) - about 25% of all pulmonary eosinophilia.



2. Fungal sensitization (candidomycosis, allergic broncho-pulmonary aspergillosis) - (25% of patients).



3. Medicinal lung damage caused by PASK, isoniazid, penicillin, sulfonamides, gold salts, etc. - about 45% of patients.



4. Tumor diseases (gsmoblastoses, lymphomas, carcinomas, etc.) - less than 1% of pulmonary eosinophilia. The pathological mechanisms of hypereosinophilia with the development of pulmonary infiltrates are associated with the functions of eosinophils in the body. The role of eosinophils in the development of immune hypersensitivity reactions of an immediate type is known. Other important functions of eosinophils are their anthelmintic and antitumor activity, which is based on their cytotoxic (killer) effect. Helminth antigens are the strongest stimulators of IgE synthesis. The resulting immune complexes and antigens themselves are powerful chemotoxic factors for eosinophils. The interaction of IgE with cell receptors is accompanied by degranulation of eosinophils and the release of biologically active substances on the surface of parasite larvae, as a result of which they die. Such substances include large basic protein (BOB), eosinophilic cationic protein (ECB), eosinophilic neurotoxin (EN) and a large group of enzymes.



BOB - is involved in the destruction of parasite larvae, as well as tumor cells. However, in places of eosinophilic infiltration, it can also damage normal tissues - the intestines, spleen, endocardium, skin, mucous membrane of the respiratory tract, blood mononuclear cells.



ECB - does not have bacterial activity, but has a damaging effect on schistosomes. In addition, it binds heparin, activates the XII coagulation factor and kallikrein-kinin system. Clinically, this is manifested by thromboembolic complications, often associated with eosinophilic infiltrates.



EN - has the ability to cause the Gordon phenomenon, manifested by paralysis, imbalance.



Thus, hypereosinophilia in helminthiases is the basis of antiparasitic protection and is accompanied by an increase in IgE level. Hypeereosinophilia in tumors does not lead to an increase in the IgE titer, which is of differential diagnostic value.



Pathomorphologically pulmonary eosinophilia is characterized by infiltration of the alveoli and mucosa of the bronchial tree with eosinophils and neutrophils with the formation of focal necrosis. Further activation of anti-inflammatory systems (complement, neutrophils, macrophages) leads to vasculitis, subsequent mononuclear infiltration (lymphocytes, macrophages) and the formation of sacroid-like granulomas. With a long course of the disease, fibrosis forms. Simple pulmonary eosinophilia (Leffler's syndrome) is characterized only by eosinophilic alveolitis without signs of vasculitis and granulomatosis, while the latter are most characteristic for generalized forms.



Simple pulmonary eosinophilia (Leffler's syndrome I) The disease is a combination of transient lung infiltrates, determined by x-ray, with high blood eosinophilia (I ^ IO9 / ^ or more) with moderate leukocytosis.



The syndrome can be asymptomatic, sometimes there are signs of intoxication (weakness, sweating, subfebrile condition).
Patients may complain of a dry cough, less often sputum of "canary" color due to the decay of eosinophils. With extensive infiltrates, the nature of the percussion sound can change, fine bubbling rales are heard. X-ray in the lungs revealed foci of infiltration of various sizes with localization in one or more segments of one or both lungs. Infiltrates are not homogeneous, with fuzzy contours. Their distinctive feature is fast dynamics, in connection with which they are called “volatile”. At the site of the disappeared infiltrate, an increase in pulmonary pattern due to local hyperemia persists for several days. The “volatility” of dynamics allows us to differentiate infiltrates from pneumonia, tuberculosis foci, etc. The course of the disease is benign, complete resorption occurs after a few days, a maximum of a month.



In addition to the above general symptoms, there are some features of the clinical picture depending on the cause of the disease, which is important to consider for the etiological diagnosis of Leffler's syndrome.



1. Atopic sensitization to allergens of pollen (lily of the valley, lily, linden, etc.). The disease occurs during the flowering period, other clinical symptoms of hay fever accompany it. A high IgE titer is detected in the blood serum, the results of skin tests or the test of basophil degranulation are positive.



2. Sensitization to fungal allergens, especially the genus Aspergillus. As in the first case, there is a high titer of IgE, positive skin tests for the corresponding allergens (immediate erythematous and late erythematous proliferative reactions).



3. Helminths (ascariasis, strongyloidosis, schistosomiasis, hookworm, paragonimiasis, toxocariasis, etc.), the causative agents of which go through the stage of larval migration and thus enter the lung tissue and other organs. The clinical picture will be determined by both mechanical damage to the tissue (hemorrhage, necrosis) and an allergic reaction (eosinophilic infiltrates). Patients may experience hemoptysis, radiological signs of lung destruction with an outcome in cystic calcified changes. With concomitant damage to other organs along the migration of helminth larvae, there may be abdominal pain, gastrointestinal bleeding, cholecystitis, hepatitis, neurological symptoms (Jackson's epilepsy, paralysis). Diagnosis is facilitated by a thorough collection of epidemiological history, but a final answer is possible only if a pathogen or its larvae are found in feces, sputum, duodenal contents, lung and liver biopsy specimens.



4. The professional "nickel" nature of the eosinophilic infiltrate can be suggested on the basis of an anamnesis, a combination of Leffler's syndrome and contact dermatitis. Confirm the diagnosis using an application test with nickel.



5. Drug allergy to penicillins, sulfanilamides, nitroflurans, salicylates, PASK, radiopaque and other substances. In such cases, it is necessary to establish a connection between taking the drug and the appearance of pulmonary eosinophilia. The diagnosis is confirmed by the positive results of the basophil degranulation test and the reaction of blasttransformation of lymphocytes with approved drugs.



6. Food allergy as the cause of eosinophilic infiltrates is confirmed by the results of an allergological examination, including elimination diets, provocative leuko- and thrombopenic tests, and an allergy-absorbing test. In some cases, despite the implementation of the entire program of diagnostic studies, the etiology of pulmonary eosinophilia cannot be established (cryptogenic Leffler's syndrome).



TREATMENT. In most cases, it’s enough to eliminate the cause (stop taking the drug, deworming,



antifungal therapy, etc.).



If this is not enough, then small doses of gluco-corticoids (15-20 mg of prednisolone per day) are prescribed, which are canceled when the infiltrate is resorbed
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