|Exogenous allergic alveolitis|
|ICD-10||J 67 67.|
|ICD-9-KM||495 and 495.9|
|eMedicine||med / 1103 ped / 2577 ped / 2577|
Exogenous allergic alveolitis, hypersensitive interstitial pneumonitis, allergic pneumonitis caused by reactions of the immune system to external (exogenous) antigens (hypersensitivity types III and IV). The prevalence of this type of alveolitis is growing rapidly.
Allergens that cause this type of disease can be spores of fungi, which are found in hay, maple bark, less often - plant dust, protein antigens, house dust, medicines. They enter the body with inhaled air or (rarely) non-inhalation. As with ELISA, in exogenous alveolitis, the main role in the pathogenesis is played by the immune complex mechanism of tissue damage. The antigen-antibody complexes are deposited in the walls of the alveoli, the smallest bronchioles and blood capillaries, causing their inflammation with the outcome in fibrosis, the formation of granulomas is possible.
Depending on the etiological factor, there are several variants of allergic alveolitis, which have quite exotic names.
|Alveolitis type||Allergen source||Allergens, to which there are precipitates|
|Barn disease||Sprinkled wheat||Barn Weevil (Sitophilus granarius)|
|Bagassoz||Moldy Sugar Cane||Thermoactinomyces vulgaris|
|Disease inhaling pituitary powder||Powder dried pituitary pigs and cattle||Pituitary antigens|
|Coffee thresher disease||Coffee beans||Coffee Beans Dust|
|Disease washable in the sauna||Wet wood||Pullularia|
|Disease working with wood pulp||Pulp||Alternaria|
|Disease workers cheese dairy||Some varieties of cheese||Penicillium casei|
|Weavers Cough||Moldy cotton|
|Lung piper||Dirty wind instruments||Fusarium oxysporum|
|Light tanners||Moldy maple bark||Cryptostroma corticale|
|Easy bird lovers||Dung and feathers of pigeons, chickens, budgerigars||Whey proteins|
|Lung of furriers||Astrakhan, fox fur|
|Lung threshers||Ground pepper|
|The lungs of the inhabitants of New Guinea||Moldy Cane Dust|
|Lung working with mushrooms||Fungal spores||Thermoactinomyces vulgaris|
|Lung working with malt||Prey barley |
|Farmer's lung||Preyloe hay||Micropolyspora faeni|
|Summer hypersensitive Japanese pneumonitis||Wet warm indoor air containing mushroom spores||Thermoactinomyces vulgaris|
|Lycoperdiasis||Mushroom Spore Disputes|
|Sequoia||Mahogany sawdust||Aureobasidium pullulans|
|Suberosis||Cork dust||Mold dust balsa wood|
Exogenous allergic alveolitis is characterized by the presence of granulomas in the walls of the alveoli and bronchioles, inflammatory infiltration by lymphocytes and plasma cells, and exudate concentration. Granulomas are formed by epithelioid cells that are surrounded in the center by lymphocytes and plasma cells. In more pronounced stages of the pathological process, pulmonary fibrosis appears.
An acute form of exogenous allergic alveolitis occurs 4-12 hours after the ingestion of the antigen in the patient’s airway, orally or parenterally. Patients complain of fever, chills, dry cough or with the release of a small amount of mucous sputum, general weakness, pain in the chest, muscles, joints, shortness of breath at rest and, especially, during exercise. Asthma attacks are also possible. During an objective examination observed cyanosis, shortness of breath (expiratory). When auscultation of the lungs determine the crepitus, small and medium bubble rales, sometimes dry wheezing. After the termination of the influence of an exogenous allergen, the above symptoms quickly disappear.
A subacute form of exogenous allergic alveolitis occurs when the body is exposed to relatively small doses of antigen. The disease develops gradually and is characterized by shortness of breath, severe general weakness, sweating, subfebrile body temperature, cough with the release of a small amount of mucous sputum, decreased appetite. Auscultation of the lungs determines the crepitus, fine bubbling rales. After the cessation of contact with the allergen, the clinical manifestations decrease, after repeated contact the disease becomes more acute.
Chronic form occurs when many years of exposure to small doses of the allergen. This form of the disease is characterized by a steady decrease in body weight, sweating, cough with the release of mucous sputum. Auscultation of the lungs determines crepitus, fine bubbling rales, squealing symptom (in the presence of pleuro-and pneumofibrosis). Over time, a chronic pulmonary heart is formed.
A clinical study of peripheral blood reveals leukocytosis, leukocyte shift to the left, eosinophilia, increased ESR, with biochemical - hypergammaglobulinemia, increased seromcoid, haptoglobin, sialic acids. An immunological study of blood allows the reduction of a subpopulation of T-lymphocyte suppressors, positive rbTL, inhibition of leukocyte migration with a specific antigen, an increase in the number of circulating immune complexes. It is possible to detect specific IgG antibodies using the Ouchterloni precipitation reaction, passive haemagglutination, and counter immunoelectrophoresis.
Differential diagnosis of exogenous allergic alveolitis should be carried out with idiopathic fibrosing alveolitis, occupational bronchial asthma, COPD, tuberculosis, sarcoidosis, Wegener's granulomatosis.
Treatment of exogenous allergic alveolitis involves the termination of the patient’s contact with the source of antigens. In the acute phase, GCS is prescribed (1 mg / kg of prednisone for 1-3 days with a further dose reduction for 3-4 weeks.). In the presence of contraindications to the appointment of GCS or their inefficiency, it is advisable to use azathioprine 150 mg per day for 1-1.5 months, another 4-6 months. - 100 mg, in the future - 50 mg per day.
D-penicillamine (cuprenyl), 150-200 mg per day for 4-6 months, is used to inhibit fibrosis formation. with the transition to 100 mg for 2 years, glutamic acid, multienzyme preparations (systemic enzyme therapy).
Certain prospects have the use of in vitro detoxification methods: plasmapheresis, plasma, immuno-, lympho-sorption.
Primary prevention of exogenous allergic alveolitis is carried out when considering technological projects for the construction of industrial and agricultural enterprises, as well as during the professional selection of workers. Work associated with the influence of allergens is not recommended for patients with chronic nonspecific lung diseases, frequent acute respiratory viral infections, allergic reactions.
When conducting clinical examination of the relevant contingents of workers they are divided into three groups:
persons in contact with allergens, having specific antibodies to them in the blood serum, but without cellular and radiological manifestations of exogenous allergic alveolitis and with normal indicators of respiratory function,
sensitized persons with minimal clinical symptoms of dysfunction of the respiratory system (vasomotor rhinitis, chronic bronchitis),
patients with exogenous allergic alveolitis with a developed clinical picture, fibrous changes of the lung tissue.
Prevention in the 1st group (risk) provides for recreational activities (hardening, exercise therapy, breathing exercises), and after having had ARVI, nonspecific desensitization courses are prescribed (antihistamines, calcium preparations).
In the 2nd group, prophylactic treatment of the underlying disease is carried out with a temporary cessation of the patient’s contact with the allergen (sanatorium, dispensary).
In the 3rd group, rational employment of patients after the completion of treatment was recommended in order to exclude further contact with antigens.
When working with the influence of allergens, it is necessary to use personal protective equipment (respirators, masks).
A common sign of exogenous allergic alveolitis is the presence of granulomas without signs of caseous, which can be found in 67-90% of cases. These granulomas differ from those in sarcoidosis: they are smaller in size, less clearly delineated, contain a greater number of lymphocytes, are accompanied by widespread thickening of the alveolar walls and diffuse lymphocytic infiltrates. The presence of giant cells and Taurus Taurus is an important feature, but it is not specific for EAA. Granulomas are usually resolved within 6 months in the absence of repeated contact with the antigen.
Another characteristic symptom of the disease is alveolitis, the main inflammatory elements of which are lymphocytes, plasma cells, monocytes and macrophages. Foamy alveolar macrophages predominate in the luminal regions, i.e. inside the alveoli, while the lymphocytes are in the interstitium. In the early stages of EAA, intraalveolar fibrinous and protein effusion can be detected. Morphological changes can also occur in the small airways. They include obliterating bronchiolitis, peribronchial inflammatory infiltrates, lymphatic follicles.
Granulomatosis, alveolitis and bronchiolitis make up the so-called triad of morphological signs in exogenous allergic alveolitis, although all elements of the triad are not always found. Vasculitis with EAA is extremely rare and has been described with a fatal outcome of the disease. With the development of pulmonary hypertension, hypertrophy of the arteries and arterioles is noted.
In the chronic course of EAA, fibrous changes are detected, expressed in varying degrees. Sometimes fibrosis is associated with moderate lymphocytic infiltration, poorly defined granulomas, in this case, the diagnosis of exogenous allergic alveolitis can also be assumed according to morphological studies.
However, histological changes in chronic EAA often do not differ from those in other chronic interstitial lung diseases. The so-called non-specific pulmonary fibrosis may be the ultimate manifestation of universal reactions to the damaging factor in various interstitial diseases. In advanced stages, changes in the architectonics of the pulmonary parenchyma of the type of “cellular” lung are noted.
The differential diagnosis should be carried out with other disseminated lung lesions (alveolar and metastatic cancer, miliary tuberculosis, sarcoidosis and other fibrosing alveolitis, etc.).
Cancer lesion of the lungs differs from exogenous allergic alveolitis by the lack of association of the disease with exposure to an exogenous allergen, steady progression and greater severity of the disease, features of radiological signs of lung lesions, lack of precipitating antibodies to any allergen in the blood serum.
Miliary tuberculosis of the lungs differs from exogenous allergic alveolitis by the lack of communication with allergen exposure, a more pronounced severity and duration of the disease, a feature of radiological manifestations, positive serological reactions with the tuberculosis antigen, the lack of elevated titers of precipitating antibodies to any exoallergen that can not be in any serum that cannot be given to any exoallergen that can not be in the serum, which does not allow any exoallergen that cannot be tested. to allergic alveolitis.
Distinctive features of fibrosing alveolitis with systemic lesions of the connective tissue are the presence of vasculitis and multiple lesions. In cases where the differential diagnosis is particularly difficult, for example, in the chronic course of allergic alveolitis, a lung tissue biopsy is performed with a histological examination of the biopsy.
In sarcoidosis, there is no connection with the profession, it affects not only the lungs, but other organs as well, hypercalciuria develops, radiological in the chest often reveals a bilateral increase in the root lymph nodes, there is a weak or negative reaction to tuberculin, a positive Kveyma, there is a histological confirmation of the sarcoid process.
It is necessary to differentiate alveolitis from ordinary pneumonia, which is associated with a cold, radiologically - subsegmental, segmental or lobar darkening due to infiltration.
According to ICD-10, exogenous allergic alveolitisclassified in class X "Diseases of the respiratory system":
• J 66 Respiratory tract disease caused by specific organic dust.
• J 66.0 Byssinosis.
• J 66.1 Flax scabs disease.
• J 66.2 Cannabiosis.
• J66.8 Respiratory disease caused by other specified organic dust.
• J 67 Hypersensitive pneumonitis.
• J 67.0 Farmer's Lung (Agricultural Worker).
• J 67.1 Bagassoz (from sugarcane dust)
• J 67.2 Poultry breeder lung.
• J 67.3 Suberose.
• J 67.4 Malt working easy.
• J 67.5 Mushrooming Lung.
• J 67.6 Easy maple bark collector.
• J 67.8 Hypersensitive pneumonitis caused by other organic dust.
• J 67.9 Hypersensitive pneumonitis caused by other unspecified organic dust.
Examples of the formulation of the diagnosis
1. Exogenous allergic alveolitis ("farmer's lung"), acute form.
2. Drug allergic alveolitis caused by furasolidone, subacute form, respiratory failure (DN) I.
3. Exogenous allergic alveolitis ("poultry farmer's lung"), chronic form. Chronic bronchitis, bronchospastic syndrome. NAM III. Pulmonary hypertension III degree. Chronic pulmonary heart decompensated.
The basis of EAA treatment is the elimination of contact with the “guilty” agent. To achieve adequate control, an occupational health system is needed, including the use of masks, filters, ventilation systems, environmental changes and habits. Recognition and early diagnosis of EAA is very important because the progression of the disease can be prevented. While maintaining contact with the antigen, the development of a serious and irreversible chronic disease is possible.
In acute, severe and progressive forms of the disease, glucocorticosteroids are recommended. In the acute course of exogenous allergic alveolitis, a dose of prednisone 0.5 mg per 1 kg of patient's body weight for 2-4 weeks with a further decrease in dosage may be sufficient.
The empirical scheme for the subacute and chronic course of EAA involves the appointment of prednisone at a dose of 1 mg / kg for 1-2 months, followed by a gradual reduction of the dose to maintenance (5-10 mg / day). Prednisolone is canceled when a clinical improvement is achieved or in the absence of a clinical and functional response to it. If during the period of prednisolone dose reduction, the course of the disease worsens, then one should return to the previous stage of therapy.
In recent years, Ingacort, a metered-dose inhaled corticosteroid, has proven itself well. The optimal daily dose - 2 breaths 2 times (1000 mcg / day).
When the disease is resistant to corticosteroids, D-penicillamine or colchicine is sometimes prescribed, but the effectiveness of this therapy has not been proven. In patients with airway hyperreactivity, the use of inhaled bronchodilators has been shown. When complications occur, symptomatic therapy is carried out: oxygen for respiratory failure, antibiotics for bacterial bronchitis, diuretics for congestive heart failure, etc.