Eosinophilic pneumonia is an allergic inflammatory lesion of the lung tissue, accompanied by the formation of unstable migrating infiltrates of eosinophilic nature and the development of hypereosinophilia. The disease usually proceeds with malaise, subfebrility, a small dry cough, sometimes with scanty sputum; in acute form – with chest pain, myalgia, the development of acute respiratory failure. To establish eosinophilic pneumonia, data from radiography and CT of the lungs, general blood analysis, bronchoalveolar lavage, allergy tests, serodiagnostics allow. The basis of treatment is specific hyposensitization and hormone therapy.
J82 Pulmonary eosinophilia, not classified elsewhere
Eosinophilic pneumonia is a respiratory disease associated with the pathological accumulation of eosinophils in the alveoli and an increase in their levels in the blood and sputum. Eosinophilic pneumonia is more often diagnosed in the population and tourists in countries with a tropical climate (Indonesia, India, Malaysia, tropical Africa, South America).
Eosinophilic pneumonia proceeds by the type of lobar pneumonia or bronchopneumonia, usually affects the upper parts of the lungs. There is focal or diffuse inflammation of the alveoli, interstitial tissue, vessels, bronchioles with their abundant infiltration by eosinophils. The transient nature of infiltrates with complete regression without secondary scarring and sclerotic tissue changes is typical.
There are 3 forms of pulmonary eosinophilia – simple (Leffler’s pneumonia), acute and chronic (Lehr-Kindberg syndrome). The chronization of the process is indicated by a long (>4 weeks) persistence and recurrence of eosinophilic infiltrates. Eosinophilic pneumonia is equally common for people of both sexes, mainly at the age of 16-40; the chronic form develops more often in women suffering from bronchial asthma.
Causes of eosinophilic pneumonia
Eosinophilic lesion of the lung tissue is initiated by pathogens of an infectious-allergic and allergic nature that cause sensitization of the patient’s body. They can be:
- Parasitic (helminthic) invasion. In 1932, Leffler first identified the role of helminths in the etiology of eosinophilic pneumonia, which occurs with transient damage to lung tissue during the migration of parasite larvae through the lungs. Almost any helminthiasis can lead to the appearance of Leffler’s pneumonia – ascariasis, strongyloidosis, schistosomiasis, hookworm, paragonimosis, toxocarosis, trichinosis, etc. Quite often, with pulmonary eosinophilia, the nematodes Toxocara cati and T. canis, ascarids of dogs and cats are detected. Larvae and eggs of worms can enter the lung tissue with blood flow, adult parasites (Paragonimus westermani) – through the intestinal wall, diaphragm and pleura, causing eosinophilic inflammation with the formation of infiltrates.
- Inhalation and medicinal allergens. Eosinophilic pneumonia can be the result of an allergic reaction to taking medications (penicillin, acetylsalicylic acid, sulfonamides, nitrofurans, isoniazid, hormonal and X-ray contrast preparations, gold compounds), to contact with chemical agents in production (nickel salts), flower pollen (lily of the valley, lilies, linden). Leffler’s pneumonia may be a manifestation of serum sickness, have a connection with an allergy to tuberculin.
- Fungal infection. Atopic sensitization of the respiratory tract to fungal spores (especially of the genus Aspergillus) also contributes to the development of eosinophilic pulmonary infiltrates.
The development of eosinophilic pneumonia is mediated by immediate hypersensitivity reactions. In addition to hypereosinophilia, elevated levels of IgE (hyperimmunoglobulinemia) are often detected in the blood of patients. Mast cells activated by immune (IgE) and non-immune (histamine, complement system) mechanisms and producing allergy mediators (mainly eosinophilic chemotactic anaphylaxis factor) are responsible for the formation of allergic inflammatory foci in the lung tissue. In some cases, eosinophilic pneumonia develops due to the production of precipitating antibodies to antigens (reactions like the Arthus phenomenon).
Symptoms of eosinophilic pneumonia
The clinical picture can be very variable. Allergic pneumonia can have an asymptomatic course with no or very poor severity of complaints and can be determined only by X-ray and clinical laboratory method. Often, Leffler’s pneumonia proceeds with minimal manifestations, manifesting symptoms of catarrhal rhinopharyngitis. Patients feel a slight malaise, weakness, fever to subfebrile, a slight cough, more often dry, sometimes with slight viscous or bloody sputum, soreness in the trachea.
With a massive hematogenic spread of eggs and larvae of worms in the body, a rash on the skin, itching, shortness of breath with an asthmatic component joins. Eosinophilic infiltration of other organs is accompanied by mild, rapidly disappearing signs of their lesion – hepatomegaly, symptoms of gastritis, pancreatitis, encephalitis, mono- and polyneuropathy.
Acute eosinophilic pneumonia is severe, with intoxication, febrility, chest pain, myalgia, rapid (within 1-5 days) development of acute respiratory failure, respiratory distress syndrome. For the chronic form, a subacute course is typical with sweating, loss of body weight, an increase in shortness of breath, and the development of pleural effusion.
Eosinophilic pneumonia usually lasts from a few days to 2-4 weeks. Recovery can occur spontaneously. In the chronic form, the prolonged existence of infiltrates and relapses contribute to the gradual progression of the disease, the development of pulmonary fibrosis and respiratory failure.
Diagnosis of eosinophilic pneumonia includes radiography and CT of the lungs, general blood analysis, stool analysis for worm eggs, bronchoalveolar lavage, allergy tests, serological (RP, RSC, ELISA) and cellular tests (reactions of basophil and mast cell degranulation). Patients with eosinophilic pneumonia, as a rule, have a previous allergic history. Auscultation determines a small amount of moist, fine-bubbled wheezing or crepitation. With extensive infiltrates, the shortening of the pulmonary sound during percussion is noticeable. Instrumental and laboratory complex:
- X-ray of the lungs. The images show subpleurally located single (rarely multiple, bilateral) fuzzy darkening of medium intensity of irregular shape up to 3-4 cm in size. Surrounded by the infiltrate, the pulmonary pattern is enhanced, the shadow of the lung root is slightly expanded. There is a rapid dynamics of infiltrates with migration through the pulmonary fields and disappearance no later than 1-2 weeks after detection (more often after 1-3 days) without residual scarring. With long-term infiltrative inflammation, fibrous foci and cystic cavities may form in the lung tissue.
- Laboratory data. In the peripheral blood at the initial stage of the disease, leukocytosis, hypereosinophilia (10-25%) is registered, with the chronization of the process, the level of eosinophils is close to normal. A high IgE content in the blood (up to 1000 IU /ml) is often detected. In the analysis of lavage fluid, eosinophils also appear (in acute form – up to 40% or more) and Charcot-Leiden crystals. Analysis of feces, carried out taking into account the development cycle of parasites, with some helminthiasis, allows you to detect worm eggs. According to the biopsy data, eosinophils, lymphocytes and macrophages, granulomas, and lesions of small vessels are detected in the alveoli and interstitium.
- Allergy tests. Etiological diagnosis of eosinophilic pneumonia includes provocative nasal and inhalation tests, skin tests with allergens of pollen, helminths, fungal spores, serological analyses. “Nickel” eosinophilic pneumonia is usually combined with allergic contact dermatitis and is confirmed by a positive compression (application) test with nickel.
- FER. Bronchial patency is assessed during spirometry, bronchomotor tests.
It is necessary to differentiate eosinophilic pneumonia with pneumonia of bacterial and viral genesis, tuberculosis, Weingarten syndrome, alveolitis, desquamative interstitial fibrosis. With atopic burden, an allergist’s consultation is indicated, with respiratory rhinitis – an otolaryngologist.
Eosinophilic pneumonia treatment
The main thing in the treatment is the elimination of the action of an etiologically significant factor: contact with allergens (aeroallergens, medicines), deworming. Antihistamines and antiparasitic agents are prescribed. There are cases of spontaneous recovery without pharmacotherapy. In the case of severe helminthic invasion with dehydration of the body or the inability to completely remove the allergen from the environment, treatment is carried out inpatient, in the department of pulmonology.
In the acute form of eosinophilic pneumonia, glucocorticoids are used, against which a rapid (within 48 hours) regression of inflammation occurs. The dose of GC is selected individually and reduced gradually in order to avoid exacerbation. In severe cases, ventilators and long-term hormone therapy are required. With bronchial obstruction, inhaled HA, beta-adrenomimetics are indicated. Expectorants and breathing exercises are used for better sputum discharge. Concomitant bronchial asthma is being treated.
Prognosis and prevention
The prognosis of eosinophilic pneumonia is generally favorable, spontaneous resolution of infiltrates is possible. Proper treatment and monitoring by a pulmonologist allows you to avoid chronicling the process and relapses. Prevention of eosinophilic pneumonia is reduced to hygiene measures that prevent infection of the body with helminths, control over medication intake, restriction of contact with aeroallergens, and specific hyposensitization. If necessary, it is recommended to change the place of work.
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