Allergic alveolitis is an immunologically mediated inflammatory reaction of respiratory bronchioles and alveoli that develops in response to the ingestion of inhaled allergens. Symptoms are characterized mainly by inspiratory shortness of breath, cough, chest pain, and in acute cases – a flu-like condition. The diagnosis of allergic alveolitis is based on the results of spirometry, chest radiography and CT, bronchoalveolar lavage, lung tissue biopsy, and serum antibody levels. Therapy of allergic alveolitis begins with the elimination of the allergen, the appointment of glucocorticosteroids is possible.
J67 Hypersensitive pneumonitis caused by organic dust
Exogenous allergic alveolitis (hypersensitivity pneumonitis) is an interstitial lung disease with localization of the inflammatory process in the terminal parts of the respiratory tract (alveoli, bronchioles) that occurs as a result of exposure to external environmental factors. In practical pulmonology, various forms of allergic alveolitis related to occupational pathology, as well as those that have no connection with professional activity, are considered. The first cases of the disease were described in 1932 . among farmers (“farmer’s lung”), the second most frequent and important form is the “bird lover’s lung” found in pigeon breeders. The total incidence rate among the population is 42:100,000. Timely therapy of hypersensitivity pneumonitis can prevent the development of pulmonary fibrosis.
In all cases, the cause of allergic alveolitis is inhalation allergens that enter the body together with the inhaled air. At the same time, factors such as the size and concentration of inhaled particles, features of antigens and the patient’s immune response are of the greatest importance for the occurrence of the disease. It is known that in the presence of a high concentration of organic or chemical substances in the air, exogenous allergic alveolitis develops in about 5-15% of individuals. It was also found that dust particles with a diameter of up to 5 microns are able to freely penetrate into the alveoli and cause sensitization. Repeated inhalation of antigens plays an important role in the pathogenesis of allergic alveolitis.
Most often allergens are fungal spores contained in hay, compost, tree bark, etc. The etiological role of plant and household dust antigens, protein antigens, bacterial spores, medications (nitrofurans, penicillin, gold salts) has also been proven. Among the fungal antigens, the most common are radiant fungi – thermophilic actinomycetes and aspergillus. The first of them are associated with such forms of allergic alveolitis as “farmer’s lung”, bagassosis, “lung of people using air conditioners”, “lung of people growing mushrooms”. Various subspecies of Aspergillus are capable of causing “malt lung”, “cheese maker’s lung”, suberosis, etc.
Protein antigens are usually found in the excrement of birds (parrots, pigeons, canaries, etc.) and are associated with a form of pneumonitis “lung of bird lovers”. Occupational forms of allergic alveolitis may occur in persons who, by the nature of their activities, are associated with the production of polyurethane, dyes and resins in contact with metal vapors (cobalt), employed in the woodworking and wool processing industries.
Allergic alveolitis is an immunopathological disease. Hypersensitivity reactions of type III and IV play a fundamental role in the development of allergic alveolitis. In this case, in response to repeated contact with an inhaled allergen, specific precipitating antibodies and CEC appear in the blood, infiltration of the alveoli by lymphocytes, neutrophils, monocytes occurs with the development of granulomatous inflammation. The result of prolonged contact with a causally significant allergen is intensive collagen synthesis with an outcome in pulmonary fibrosis or obliterating bronchiolitis.
Taking into account the causal factors of allergic alveolitis and the source containing antigens, the following syndromes are distinguished:
- “farmer’s lung” – develops upon contact with moldy hay containing thermophilic actinimycetes
- “the lung of bird lovers” is found in poultry farmers and people caring for poultry; the source of antigens is bird droppings, fluff, secrets of the skin glands, etc.
- bagassosis – develops upon contact with sugar cane microfibers
- suberosis – the source of the antigen (mold fungus) is the bark of a cork tree
- “malt lung” – develops in persons in contact with barley dust
- “lung of persons using air conditioners” – occurs with frequent use of air conditioners, heaters and humidifiers
- “cheese maker’s lung” – the source of the antigen is cheese mold
- “lung of mushroom pickers” – develops in persons growing mushrooms; pathogens – fungal spores contained in compost
- other occupational allergic alveolitis: “lung producing detergents”, “lung of laboratory workers”, “lung engaged in the production of plastics”, etc.
The course of allergic alveolitis can be acute, subacute or chronic, which is appropriately reflected in the clinical picture. The acute form develops within 4-12 hours after contact with a massive dose of antigens; chronic – with prolonged inhalation of a low dose of antigens; subacute – with less exposure to antigens.
Symptoms of allergic alveolitis
The clinic of the acute form of the disease is accompanied by flu-like symptoms: fever, myalgia and arthralgia, headache. A few hours after the temperature rises, heaviness and pain in the chest, cough with scanty mucous sputum, shortness of breath join. If contact with a causally significant allergen is excluded, all symptoms disappear within 1-3 days, but may return again after repeated ingestion of the antigen. General weakness and shortness of breath associated with physical exertion persist for several more weeks.
The subacute form of allergic alveolitis is usually caused not by occupational hazards, but by exposure to antigens at home. At the onset of the disease, fever may occur, but more often the symptoms are limited to shortness of breath with physical exertion, productive cough, increased fatigue. Chronic allergic alveolitis can develop, both in the outcome of repeated episodes of acute or subacute process, and immediately independently. The course of this form is characterized by progressive inspiratory dyspnea, persistent cough, malaise, and weight loss.
The appearance of a symptom of “drumsticks” – thickening of the phalanges of the fingers indicates respiratory failure and serves as an unfavorable prognostic sign. The natural outcome of the chronic form of allergic alveolitis is the development of interstitial fibrosis, pulmonary hypertension, pulmonary heart, right ventricular heart failure. Most of the patients develop chronic bronchitis after 10 years or more, and a quarter are diagnosed with emphysema of the lungs.
At the initial consultation of a pulmonologist, anamnesis, including professional, the relationship of the manifestations of the disease with environmental conditions is studied. Objectively, allergic alveolitis reveals tachypnea, cyanosis, auscultation – crepitation, especially in the basal parts of the lungs, sometimes wheezing. A patient with allergic alveolitis should also be consulted by an allergist-immunologist.
In acute pneumonitis, lung radiography can detect small-nodular or diffuse infiltration; according to spirometry, a decrease in blood pressure and a violation of gas exchange are detected. In the chronic form, the X-ray picture indicates the development of pneumosclerosis or “cellular lung”, and the study of the function of external respiration indicates the presence of obstructive and restrictive disorders. CT of the lungs is a more sensitive method in terms of early detection of changes in lung tissue.
Laboratory data for allergic alveolitis are characterized by increased levels of IgG and IgM, sometimes IgA, rheumatoid factor. The greatest diagnostic value is the detection of precipitating antibodies to the suspected antigen. In bronchoalveolar flushes obtained by bronchoscopy, lymphocytes (T cells) predominate, the content of mast cells is increased. Provocative inhalation tests can be used, in response to which patients with allergic alveolitis develop a specific response after a few hours (weakness, dyspnea, fever, bronchospastic reaction, etc.).
Due to the rapid resolution of symptoms, acute allergic alveolitis is rarely diagnosed or regarded as ARVI. With a longer or recurrent course, bronchial asthma, atypical pneumonia (viral, mycoplasma), pneumoconiosis, miliary tuberculosis, aspergillosis, sarcoidosis, idiopathic fibrosing alveolitis, and other interstitial lung diseases can often be mistakenly diagnosed. For the purpose of differential diagnosis, a lung tissue biopsy with histological examination is possible.
Treatment of allergic alveolitis
The key point of pathology therapy is the elimination of contact with a causally significant antigen. In mild forms of the disease, this is enough for all signs of alveolitis to subside, so there is no need for medical treatment. In severe acute pneumonitis or progression of the chronic form, the appointment of glucocorticosteroids (prednisone) is indicated. Patients with corticosteroid-resistant forms of the disease received positive responses to the administration of D-penicillamine and colchicine. Symptomatic therapy of allergic alveolitis is carried out with the help of inhalation bronchodilators, bronchodilators, oxygen therapy.
Prognosis and prevention
A favorable outcome can be achieved only if the allergen is eliminated in a timely manner, and if necessary, active treatment of allergic alveolitis. In case of recurrence of hypersensitivity pneumonitis, development of cardiopulmonary insufficiency, the prognosis is relatively unfavorable. Primary prevention consists in eliminating harmful occupational and household factors (occupational hygiene, the use of protective clothing, ventilation of industrial premises, care for air conditioners, etc.), conducting periodic medical examinations of persons with an increased risk of developing allergic alveolitis. Secondary prevention measures include termination of contact with the allergen, and, if necessary, a change of professional activity.