Pulmonary eosinophilia: causes, symptoms, diagnosis, treatment

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

Distinguish the following groups of pulmonary eosinophilia:

1. Local pulmonary eosinophilia
   • Simple pulmonary eosinophilia (Leffler's syndrome).
   • Chronic eosinophilic pneumonia (prolonged pulmonary eosinophilia, Lera-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 (Charge-Strauss syndrome).
   • Hypereosinophilic myeloproliferative syndrome.

Local pulmonary eohinophilia

Simple pulmonary eosinophilia

Simple pulmonary eosinophilia (Leffler's syndrome) is a combination of transient "volatile" lung infiltrates with high blood eosinophilia 1.5 x ^{10 9} / L.

Causes of pulmonary eosinophilia

The main etiological factors of the Leffler syndrome are:

• sensitization to pollen allergens;
• sensitization to allergens of fungi, primarily aspergillus;
• invasions of helminths (ascariasis, strongyloidosis, schistosomiasis, ankylostomiasis, paragonimosis, toxakaroz, etc.) - causative agents of helminthoses pass through the stage of larval migration and enter the pulmonary tissue;
• work in industries associated with the use of nickel (inhalation of nickel carbonate vapor);
• drug allergy (to antibiotics, sulfonamides, nitrofuran compounds, salicylates, anti-tuberculosis drugs, other drugs);
• allergy to various foods;

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

Pathogenesis of pulmonary eosinophilia

With pulmonary eosinophilia, there is an accumulation of eosinophils in the lung tissue in response to the effects of the aforementioned etiological 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:

• eosinophilic chemotactic factor of anaphylaxis (excreted by mast cells and basophils);
• a factor that stimulates the migration of eosinophils (secreted by T-lymphocytes);
• eosinophilic chemotactic factor of neutrophils.

Chemotaxis of eosinophils is also stimulated by activated components of the complement system; histamine and other mediators released during degranulation of mast cells (tannins, leukotrienes); antigens of helminths; antigens of tumor tissues.

Rushing into the pulmonary tissue, eosinophils exert both protective and immunopathological effects.

The protective effect of eosinophils is the isolation of enzymes inactivating kinins (kininase), histamine (histaminase), leukotrienes (arylsulfatase), a factor activating platelets (phospholipase A) - i.e. Mediators involved in the development of inflammatory and allergic reactions. In addition, eosinophils produce eosinophilic peroxidase, which destroys schistosomes, toxoplasma, trypanosomes, causes the destruction of tumor cells. These effects are mediated by the production of a large amount of hydrogen peroxide under the influence of a peroxidase enzyme.

Along with protective effects, eosinophils also have a pathological effect, releasing a large base protein and an eosinophilic cationic protein.

A large basic protein of eosinophil granules damages cells of the ciliated epithelium of the bronchial mucosa, which, naturally, disrupts mucociliary transport. In addition, under the influence of a large basic protein of eosinophil granules, the release of histamine from the granule of mast cells is activated, which aggravates the inflammatory response.

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

Eosinophils in large amounts are also allocated prostaglandins E2 and R, which have a regulatory effect on inflammatory and immune processes.

Thus, the main pathogenetic mechanisms of the 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 starting point for the development of eosinophilic alveolitis under the influence of the antigen is activation of the complement system in the lungs due to the fact that the local production of complement components C3 and C5 is possible in the lungs. In the future, an immunocomplex reaction (most often) or an allergic reaction of the immediate type (IgE-dependent) develops.

The main pathomorphological features of the Leffler syndrome are:

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

Symptoms of pulmonary eosinophilia

Patients suffering from Leffler's syndrome present fairly characteristic complaints of dry cough (less often with sputum separation of "canary" color), weakness, decreased efficiency, sweating, increased body temperature (usually not higher than 38 ° C). Some patients complain of pain in the chest, worse with coughing and breathing (usually with a combination of Leffler's syndrome and dry pleurisy). The appearance of hemoptysis is possible with helminth infections (the phase of migration of larvae and their entry into the lungs). Perhaps the appearance of skin itch, sudden and recurrent edema of Quinck, urticaria. However, often the disease is asymptomatic and is only detected when the patient is randomly examined for any other reason.

The general condition of the patients is in most cases satisfactory. In the physical examination of the lungs, blunting of percussion sound over the area of the infiltration is determined. In the same zone, moist, finely bubbling rales are heard against the background of weakened vesicular breathing. When combined with a "volatile" eosinophilic infiltrate and dry (fibrinous) pleurisy, pleural friction is heard. Typical rapid dynamics (rapid decrease and disappearance) of physical symptoms.

Laboratory data

1. A general blood test - a characteristic feature - eosinophilia, mild leukocytosis, possibly an increase in ESR.
2. Biochemical analysis of blood - an increase in the content of seromucoid, sialic acids, fibrin (as a manifestation of the nonspecific biochemical "inflammation syndrome"), the level of a2 and y-globulins increases less often.
3. Immunological studies - it is possible to reduce the number of T-lymphocytes-suppressors, increase the level of immunoglobulins, the appearance of circulating immune complexes, but these changes are not regular.
4. General analysis of urine - without significant changes.
5. General clinical study of sputum - in the cytological study, a large number of eosinophils are found.

Instrumental research

1. X-ray examination of the lungs. In the lungs, non-homogeneous, fuzzy outbreaks of infiltration of different sizes are detected. They are localized in several segments of one or both lungs, in some patients the infiltration site is small and can occupy only one segment. The most characteristic feature of these infiltrates is their "volatility" - after 7-8 days infiltrates dissolve, in rare cases they persist for 3-4 weeks, but then completely disappear. In some patients, the strengthening of the pulmonary pattern may persist for 3-4 days at the site of the disappeared infiltrate. 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 helminth infections, it is possible to form foci of destruction in lung tissue, their slow disappearance, and in some patients the formation of cysts with the deposition of calcium salts.
2. Research of ventilating function of the lungs. As a rule, there are no significant violations of the function of external respiration. With extensive infiltrates in the lungs, moderate respiratory failure of the mixed restrictive-obstructive type can be observed (decreased GEL, FEV1).

The course of simple pulmonary eosinophilia is favorable, complications are not observed, there is a complete recovery. If the allergen can not be eliminated, recurrence of the disease is possible.

Survey program

1. General tests of blood, urine, feces (for helminths), sputum (cytological analysis).
2. Biochemical analysis of blood - 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. Radiography of the lungs in three projections.
6. Spirography.
7. Allergological examination for the detection of sensitization to pollen, food, fungal, helminthic, medicinal and other allergens.

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