Pulmonary eosinophilia: causes, symptoms, diagnosis, treatment

Pulmonary eosinophilia is a group of diseases and syndromes characterized by transient pulmonary infiltrates and blood eosinophilia exceeding 1.5 x 10 ⁹ /l.

The following groups of pulmonary eosinophilia are distinguished:

1. Local pulmonary eosinophilia
   • Simple pulmonary eosinophilia (Loeffler syndrome).
   • Chronic eosinophilic pneumonia (long-standing pulmonary eosinophilia, Lehr-Kindberg syndrome).
   • Pulmonary eosinophilia with asthmatic syndrome (atopic bronchial asthma; non-atopic bronchial asthma; allergic bronchopulmonary aspergillosis; tropical eosinophilia).
2. Pulmonary eosinophilia with systemic manifestations
   • Allergic eosinophilic granulomatous angiitis (Churg-Strauss syndrome).
   • Hypereosinophilic myeloproliferative syndrome.

Localized pulmonary eochinophilia

Simple pulmonary eosinophilia

Simple pulmonary eosinophilia (Leffler's syndrome) is a combination of transient "flying" pulmonary infiltrates with high blood eosinophilia of 1.5 x10 ⁹ /l.

Causes of pulmonary eosinophilia

The main etiological factors of Löffler syndrome are:

• sensitization to pollen allergens;
• sensitization to fungal allergens, primarily aspergillus;
• helminth infestations (ascariasis, strongyloidiasis, schistosomiasis, ancylostomiasis, paragonimiasis, toxacariasis, etc.) - the causative agents of helminthiasis go through the larval migration phase and enter the lung tissue;
• work in industries involving the use of nickel (inhalation of nickel carbonate vapors);
• drug allergy (to antibiotics, sulfonamides, nitrofuran compounds, salicylates, anti-tuberculosis drugs, other drugs);
• allergies to various food products;

If it is impossible to establish the cause, one should speak of cryptogenic (idiopathic) Leffler syndrome.

Pathogenesis of pulmonary eosinophilia

In pulmonary eosinophilia, there is an accumulation of eosinophils in the lung tissue in response to the above-mentioned etiologic factors - antigens. On the membrane surface of eosinophils there are receptors for chemotactic factors that cause the accumulation of eosinophils in the lungs. The main chemotactic factors for eosinophils are:

• eosinophil chemotactic factor of anaphylaxis (secreted by mast cells and basophils);
• eosinophil migration stimulating factor (secreted by T-lymphocytes);
• neutrophil eosinophil chemotactic factor.

Eosinophil chemotaxis is also stimulated by activated components of the complement system; histamine and other mediators released during mast cell degranulation (tannins, leukotrienes); helminth antigens; and tumor tissue antigens.

Eosinophils rushing into the lung tissue have both a protective and immunopathological effect.

The protective action of eosinophils consists of secreting enzymes that inactivate kinins (kininase), histamine (histaminease), leukotrienes (arylsulfatase), platelet-activating factor (phospholipase A) - i.e. mediators that participate in the development of inflammatory and allergic reactions. In addition, eosinophils produce eosinophilic peroxidase, which destroys schistosomes, toxoplasms, trypanosomes, and causes the destruction of tumor cells. These effects are mediated by the production of large amounts of hydrogen peroxide under the influence of the peroxidase enzyme.

In addition to their protective effects, eosinophils also have a pathological effect by secreting large basic protein and eosinophil cationic protein.

Large basic protein of eosinophilic granules damages the cells of the ciliated epithelium of the bronchial mucosa, which naturally disrupts mucociliary transport. In addition, under the influence of large basic protein of eosinophilic granules, the release of histamine from mast cell granules is activated, which aggravates the inflammatory reaction.

Eosinophilic cationic protein activates the kallikrein-kinin system, fibrin formation, and simultaneously neutralizes the anticoagulant effect of heparin. These effects can contribute to increased platelet aggregation and impaired microcirculation in the lungs.

Eosinophils also secrete large amounts of prostaglandins E2 and R, which have a regulatory effect on inflammatory and immune processes.

Thus, the main pathogenetic mechanisms of development of pulmonary eosinophilia in general and simple pulmonary eosinophilia (Leffler syndrome) in particular are associated with the functional activity of eosinophils accumulated in the bronchopulmonary system. The trigger for the development of eosinophilic alveolitis under the influence of an antigen is the activation of the complement system in the lungs due to the fact that local production of complement components C3 and C5 is possible in the lungs. Subsequently, an immune complex reaction (most often) or an immediate-type allergic reaction (IgE-dependent) develops.

The main pathomorphological features of Löffler syndrome are:

• filling of the alveoli with eosinophils and large mononuclear cells;
• infiltration of the interalveolar septa by eosinophils, plasma cells, mononuclear cells;
• vascular infiltration with eosinophils;
• formation of platelet aggregates in the microcirculatory bed, but without signs of necrotizing vasculitis and development of granulomas.

Symptoms of pulmonary eosinophilia

Patients suffering from Löffler syndrome present fairly typical complaints of dry cough (less often with the separation of "canary" colored sputum), weakness, decreased performance, significant sweating, and increased body temperature (usually not higher than 38°C). Some patients complain of chest pain that intensifies with coughing and breathing (usually when Löffler syndrome is combined with dry pleurisy). Hemoptysis may occur with helminth infections (the phase of larval migration and their entry into the lungs). Skin itching, sudden and recurrent Quincke's edema, and urticaria may occur. However, the disease is often asymptomatic and is discovered only during a random examination of the patient for some other reason.

The general condition of patients is satisfactory in most cases. Physical examination of the lungs reveals dullness of percussion sound over the area of the infiltrate. In the same area, moist fine-bubble rales are heard against the background of weakened vesicular breathing. With a combination of "flying" eosinophilic infiltrate and dry (fibrinous) pleurisy, pleural friction noise is heard. Rapid dynamics (rapid reduction and disappearance) of physical symptoms are characteristic.

Laboratory data

1. General blood test - characteristic features - eosinophilia, moderate leukocytosis, possible increase in ESR.
2. Biochemical blood test - increased content of seromucoid, sialic acids, fibrin (as a manifestation of non-specific biochemical "inflammatory syndrome"), less often the level of a2- and y-globulins increases.
3. Immunological studies - a decrease in the number of suppressor T-lymphocytes, an increase in the level of immunoglobulins, the appearance of circulating immune complexes are possible, however, these changes are not consistent.
4. General urine analysis - no significant changes.
5. General clinical examination of sputum - cytological examination reveals a large number of eosinophils.

Instrumental research

1. X-ray examination of the lungs. Non-homogeneous, fuzzy-edged foci of infiltration of varying sizes are detected in the lungs. They are localized in several segments of one or both lungs; in some patients, the infiltration focus is small and may occupy only one segment. The most characteristic feature of these infiltrates is their "volatility" - in 7-8 days the infiltrates are absorbed, in rare cases they persist for 3-4 weeks, but then disappear without a trace. In some patients, an increase in the pulmonary pattern may persist at the site of the disappeared infiltrate for 3-4 days. The "volatility" of the infiltrate is the main differential diagnostic feature that distinguishes this disease from pneumonia and pulmonary tuberculosis. If Leffler's syndrome is caused by helminthic infections, the formation of foci of destruction in the lung tissue, their slow disappearance, and in some patients, the formation of cysts with calcium salt deposits is possible.
2. Study of the ventilation function of the lungs. As a rule, there are no significant violations of the external respiratory function. With extensive infiltrates in the lungs, moderate respiratory failure of a mixed restrictive-obstructive type (decreased VC, FEV1) may be observed.

The course of simple pulmonary eosinophilia is favorable, no complications are observed, and complete recovery occurs. If the allergen cannot be eliminated, relapses of the disease are possible.

Survey program

1. General tests of blood, urine, feces (for helminths), sputum (cytological analysis).
2. Biochemical blood test - determination of the content of seromucoid, sialic acids, fibrin, total protein, protein fractions.
3. Immunological studies - determination of the content of B- and T-lymphocytes, subpopulations of T-lymphocytes, immunoglobulins, circulating immune complexes.
4. ECG.
5. X-ray of the lungs in three projections.
6. Spirometry.
7. Allergological examination to identify sensitization to pollen, food, fungal, helminth, medicinal and other allergens.

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