Allergic alveolitis is inflammation of the bronchioles and alveoli caused by inhaled allergens. Symptoms are mainly such components as a feeling of lack of air, cough, pain in the bronchial area. When the disease is acute, it resembles the flu. To diagnose the disease, you need to undergo computed tomography of the chest area, x-rays, do spirometry, as well as detect antibodies in the blood and conduct a biopsy of lung tissue. Treatment consists primarily of eliminating the allergen that caused the disease and, in some cases, the use of glucocorticosteroid drugs.

The causes of the occurrence is the penetration of the allergen with the air. Also important is the number of particles in the air, as well as human immunity and the property of the antigen. Most allergens are fungal spores, which are very numerous in dry grass, humus, tree bark. It is not uncommon for the provocateur of the disease to be ordinary household dust and medicines.

Allergic alveolitis is divided into the following types:

• "farmer's lung" - occurs due to frequent contact with old hay
• "light birder" - occurs in people involved in the breeding and maintenance of birds
• bagassosis occurs due to frequent contact with sugar cane
• "malt lung" occurs due to frequent contact with fine particles of barley
• "lung of a person, frequently used air conditioner"
• "Cheese maker's lung" occurs in cheese makers
• "mushroom picker's lung" occurs in people who grow mushrooms
• many other species caused by contact with harmful allergens

The disease can occur in:

1. acute form
2. subacute form
3. become chronic.

Acute leakage occurs within 12 hours after contact with microparticles of foreign bodies, the chronic form occurs as a result of prolonged inhalation of a small dosage of foreign body microparticles, the subacute form manifests itself as a result of not a large number microparticles in the air.

Symptoms of this type of disease can be:

• fever
• headaches
• joint pain
• heat
• pain in the bronchi
• cough with phlegm
• shortness of breath and blueness of the extremities, as well as pain in them.

When the allergen is removed, all symptoms disappear within three days. Weakness of the whole body and difficult breathing may persist for two weeks. The subacute form is most often found on house allergens. At first, there is fever, cough, fatigue. The chronic form of the disease is often a relapse of the other two forms or an independent form. The chronic form is characterized by severe shortness of breath and cough, weight loss and poor health. Fingers on the hands thicken due to lack of air. The result of this form of the disease may be the development of destructive fibrosis, heart failure. In people suffering from the chronic form, chronic bronchitis occurs ten years later.

With the timely elimination of the allergen that caused the development of allergic alveolitis, the outcome is without complications. With repeated disease, the development of cardiac and lung failure. Preventive measures are to exclude the factors that provoked the development of the disease, systematic examinations by a doctor. Allergic alveolitis of the lungs can still cause complications. The entire respiratory system is affected by the disease and gradually weakens. This leads to the rapid impact of others infectious diseases on the body. The result of this is a weakened body and weight loss. If the treatment was not provided on time, then the acute and subacute form flow into a more complex - chronic form. The chronic course of the disease is much more difficult to cure and block all kinds of attacks that provoked toxic-allergic alveolitis. Early treatment makes it possible to restore the functionality of the lungs slowly but completely. When a person does not want to take treatment for allergic alveolitis, then the person's body will be able to resist the allergens that cause the disease. This leads to the growth of the connective tissues of the lung and is able to completely affect the alveolus. Such changes cannot be corrected.

Exogenous allergic alveolitis

This is an allergic disseminated lesion of the acinus and lung tissue, which develops due to intense and prolonged inhalation of dust. More than three hundred foreign microparticles can serve as the causes of occurrence, only about ten are the main ones. This disease is a hypersensitivity reaction of contact with an allergen. People with a genetic predisposition are more prone to complications such as: acute neutrophilic alveolitis or acute mononeclear alveolitis, fibrosis can also develop.

Symptoms of the disease

Atypical inflammation of the lungs over sensitivity is a syndrome that is caused by sensitivity to a substance and is expressed by cough, shortness of breath and general weakness. Symptoms directly depend on the form of the disease. Usually, the first manifestations begin a few weeks after contact with the irritant. The acute form is manifested by high temperature, sensations of pressure in the sternum, lack of air. Such symptoms appear within six hours from the moment the person comes into contact with the irritant.

A chronic course of the disease is also observed, usually people who are in daily contact with an irritant, for example, rearing birds, are susceptible to this. The disease progresses for several years and manifests itself as banal shortness of breath during exercise. The patient can also observe weight loss, weakness, and so on.

The subacute form is just a transitional phase from the acute form to the chronic form. Symptoms of this form are also weight loss, cough, weakness of the body. This form continues for several weeks.

Diagnostics

It is possible to diagnose exogenous allergic alveolitis by studying the data of the course of the disease, radiation studies, microscopy and biopsy. Therapy is carried out with the help of glucocortisone and prednisolone, this makes it possible to block the first symptoms of the disease. The main thing in treatment is to avoid contact with the allergen, but, unfortunately, this is not always possible, since the allergen is often associated with the work of a person. In such cases, it is necessary to reduce the concentration of the allergen with a protective mask.

If this type of disease is found in early stage, then all changes in the body return to normal. The chronic form is more complex and can cause complications in the form of fibrosis.

Allergic alveolitis in children

Allergic alveolitis in children can begin at any age. Almost half of the patients are children of school age. A third of children suffering from allergic alveolitis have not reached the age of three. The rest are preschoolers. Symptoms directly depend on the allergen that caused the disease, how long it affected the body, and also on the immunity of the child. Symptoms occur a couple of hours after strong contact with the allergen. Most of the children suffering from allergic alveolitis lived in villages and were constantly connected with hay, household chores related to cleaning up after animals and their droppings. Only 20% of the disease was caused by the presence of a parrot in a child. Also, the disease can occur in connection with a change in the area of ​​\u200b\u200bresidence, as well as mold that occurs in damp houses.

The first signs can be confused with symptoms commonly seen in children with the flu. Heat body, muscle pain, migraine and so on. Affected lungs give out the disease with a cough, lack of air for the child, and the presence of wheezing. A child with atopy may experience asthma-like attacks. During an exacerbation, leukocytes with neutrophilia increase.

When interaction with the allergen that caused the disease is completely excluded, all symptoms disappear within a week. If the interaction with the allergen is restored, then relapse cannot be avoided. The recurrence of the disease takes longer and is much more severe. If the interaction with the allergen has not stopped, then over time the disease will take on a chronic form.

Chronic form of the disease

The chronic form of the disease is characterized by severe shortness of breath, as well as a strong cough with mucus. The doctor can listen to wheezing in the lungs. The chronic form gives a complication in the form of compaction of the chest, an increase in the width of the fingers, during exercise, the limbs turn blue, lethargy, low activity, loss of appetite and, as a result, severe loss of body weight. The index of circulation of immune complexes increases during the period of exacerbation. The lining of the bronchi does not change. Almost all patients with an electrocardiogram show changes in the myocardium and tachycardia. Approximately fifteen percent of patients have an overload of the right side of the heart.

X-ray shows small changes in the form of small foci that are located in the middle of the lung. Low transparency of the lung tissue is also often observed. Also, in about ten percent of children, there is a change in the pattern on the lungs. Fifteen percent of children have an increase in part of the trachea and an increase in the pulmonary artery.

In the acute form of the disease, after recovery, all changes in the body return to normal, but with chronic form changes in the body can continue even after contact with the allergen is stopped. But in children, the outcome of the chronic form is easier.

Exogenous allergic alveolitis (EAA) (synonyms: hypersensitivity pneumonitis, inhalation pneumopathy) is a pathological process in the lungs that occurs in response to a known causal factor: organic or inorganic dust, fungi, bacteria, etc. Hyperergic reaction in the lung parenchyma depends on both antigenic features of the factors listed above, and on the characteristics of the response of the macroorganism.

Etiology. The following factors contribute to the development of EAA:

1) bacterial (thermophilic actinomycetes, Bacillus subtilis, Micropolispora faeni, etc.);

2) fungal (Aspergillus fumigatus, Alternaria, Penicillium casei, Penicillium casei, Penicillium glaucum, Cravinum aureobasidium pullans, Cryptostroma corticale, various molds);

3) protein antigens of animal origin (whey proteins and excrement of chickens, pigeons, parrots and other birds, cattle, pigs, wheat weevil antigens, fish fly dust, wheat fly dust, bovine pituitary gland dust (adiurecrine), mites : Sitophilus granarius, Dermatophagoides pteronissimus, Euroglyphys maynei, Europhagus putrescentiae);

4) antigens of plant origin (sawdust of oak, cedar, maple bark, mahogany, moldy straw, extracts of coffee beans, dust containing particles of cotton, flax, hemp, etc.);

5) drug antigens (antimicrobial, enzymes and other medicines protein origin, contrast agents, etc.).

There are a number of industries where work can lead to the development of EAA:

Agriculture: employees of poultry farms, livestock complexes, grain farms, people working in silos, etc.;

Food industry: production of dairy products, cheeses, beer, yeast, etc.;

Textile and clothing industry: processing of fur, cotton, hemp, flax;

Chemical and pharmaceutical industry: production of detergents, plastics, dyes; production of medicines;

Wood processing industry (wood processing, paper production, contact with pentachlorophenols in wood processing).

EAA can occur in response to the allergenic effect of certain groups of drugs, not only during their production, but also when administered to patients sensitized to a particular drug.

The most common types of EAA are considered to be "farmer's lung", "poultry breeder's lung" (including "pigeon breeder's lung"), "drug allergic alveolitis". "Farmer's Lung" is found in geographic latitudes characterized by damp and cold climates, mountainous areas after the rainy season. The thermophilic actinomycetes Thermoatinomyces vulgaris and Micropolyspora faeni, as well as fungi of the genus Aspergillus fumigatus, play the main role in the emergence of the "light farmer". The most pathogenic are Thermoactinomyces vulgaris and Micropolyspora faeni.

Clinical symptoms, the course of the disease, immunological disorders and pathomorphological changes that occur in the lungs under the influence of the above etiological factors do not have fundamental differences, which makes it possible to combine them with the concept of "exogenous allergic alveolitis".

In etiological terms, EAA and exogenous (atopic) bronchial asthma have much in common. The same antigens in one case can cause an asthma attack (type I hypersensitivity reaction, according to Gell and Coombs), in the other - the occurrence of EAA (type III hypersensitivity reaction). Often there is a combination of these reactions with the predominance of one of them. The predominant type of reactions, which is realized in a specific clinical symptomatology, in each case depends on many reasons: dispersion and duration of exposure, as well as on the characteristics of the patient's immune response.

Pathogenesis. Particles larger than 2-3 microns usually lead to an asthma attack, since their penetration into the alveoli is difficult. Finely dispersed particles (less than 2-3 microns), which have antigenic properties, penetrate deep into the distal airways and are the cause of the development of EAA. With repeated and prolonged exposures, rather large particles (up to 10 microns) can also penetrate into the pulmonary alveoli. Thus, some patients have clinical manifestations of type I and type III hypersensitivity reactions.

The participation of class E immunoglobulins in the pathogenesis of EAA can not always be proved. Often, patients with EAA have normal lgE levels, there is no peripheral blood eosinophilia, and there is no tendency to allergic reactions.

The most important role in the pathogenesis of EAA is given to alveolar macrophages. Performing protective functions, they capture foreign particles that enter the respiratory tract. Hydrolytic enzymes secreted by alveolar macrophages cause complement cleavage.

Activation of the production of immunoglobulins by B-lymphocytes due to their antigenic irritation leads to the formation of immune complexes (ICs) consisting of the antigen and precipitating antibodies of classes G and M. The resulting ICs can activate the complement system, as well as stimulate alveolar macrophages and their secretion of enzymes. The affinity of IR for certain tissues is determined by the antibody that is part of it. With an excess of antigen, IC circulate in the blood in a soluble state. An increase in the permeability of the vascular wall due to the release of vasoactive amines (platelet lysis in the presence of CI, immune adhesion of platelets in the presence of neutrophils, etc.) creates conditions for the deposition of CIC on the basement membrane of the pulmonary vessels. Complement fixation on the surface of the EC makes the latter available for absorption by phagocytes. The lysosomal enzymes released during this (as already noted) can have a damaging effect on the lung parenchyma in the manner of the Arthus phenomenon.

Despite intensive study of various aspects of circulating CIs, their role in the pathogenesis of EAA is not completely clear. In particular, it is not known whether there is a division into protective and damaging ICs or whether the function of the same ICs can change depending on specific conditions.

In the process of neutralization and elimination of the antigen from the body, EAA includes reactions cellular immunity. The result of the interaction of sensitized lymphocytes with a specific antigen is the production of lymphokines (a group of mediators of cellular immunity), which have an effect that not only neutralizes the antigen, but also damages tissues. The significance of cell-related immunity in the pathogenesis of EAA is confirmed by pathomorphological examination of lung biopsies of patients and experimental animals, the identification of granulomas and infiltrates consisting of multinucleated cells.

The mechanism of occurrence of drug-induced EAA is also based on a semi-delayed hypersensitivity reaction. Medicines (or their decay products) can bind to body proteins and acquire the properties of haptens, in response to which the immune system produces antibodies (class G and M immunoglobulins). Antigens in their excess form soluble circulating ICs with antibodies. Fixation of the formed CIs on the walls of small vessels of the lungs and complement activation lead to changes in the lung parenchyma similar to the Arthus phenomenon.

With drug-induced EAA, type I hypersensitivity reactions can also occur, accompanied by peripheral blood eosinophilia, bronchospasm, or proceeding according to the type of Loeffler's syndrome. Immunological studies (inhalation and skin tests) in these cases reveal a combination of immediate and semi-delayed hypersensitivity.

Factors contributing to the emergence of drug-induced EAAs are polypharmacy, simultaneous administration of drugs that enhance each other's side effects, disorders of the functional state of the liver, kidneys, reticuloendothelial system, endocrine glands, vitamin deficiency, etc.

To date, the question of the cause (causes) of the formation of granulomas in EAA (reaction to a foreign body, imbalance between the T- and B-systems of immunity, other reasons) has not been finally resolved. An important role is assigned to mediators of cellular immunity - lymphokines. In cases of a continuing antigenic stimulus, the disease can move into a qualitatively new phase - the phase of fibrosis. This is facilitated by a factor secreted by alveolar macrophages, which induces the growth of fibroblasts and their production of collagen. The secretion of fibroblasts (changed qualitatively and increased in number) of collagen leads to the development of interstitial pulmonary fibrosis.

The humoral form of the response associated with the B-system of immunity is activated already at the first stage of the disease (semi-delayed type of hypersensitivity). With the continuation of the antigenic stimulus, the reactions of cellular immunity associated with the T-system and determining the further course of the disease are switched on.

Pathoanatomy. Histological changes in the lung tissue in patients with EAA largely depend on the form of the disease (acute, subacute, chronic). In the acute form of EAA, edema of the interstitial lung tissue, infiltration of the alveoli and interalveolar septa by lymphocytes, plasma cells, and histiocytes are histologically determined.

An important diagnostic value in EAA is the identification of epithelioid cell granulomas. The formation of noncaseating granulomas of the sarcoid type is characteristic of the subacute stage of EAA and reflects a pathomorphological type IV hypersensitivity reaction.

The duration of the granulomatous stage is not long. Over time, proliferative processes begin to predominate. An increase in the cellular and non-cellular components of the connective tissue contributes to the formation of interstitial and intra-alveolar fibrosis. The replacement of elastic fibers with procollagenous and collagenous fibers leads to collagenization of the interstitial lung stroma. Granulomas are transformed into connective tissue structures. The number of lymphocytes, plasma cells, histiocytes and eosinophils in the interstitium of the lungs decreases. The pathomorphological picture of EAA at this stage completely loses its specific features, therefore, the absence of granulomas in the biopsy material does not exclude the diagnosis of EAA.

Granulomas, determined by EAA, have many similarities with sarcoid, turbeculosis, mycotic granulomas. The greatest diagnostic difficulties arise when differentiating from sarcoid granulomas, since tuberculous ones are characterized by caseous necrosis in the center, and mycosis can be differentiated using serological and microbiological methods.

Granulomas with EAA are less regular in shape, with indistinct boundaries, smaller in size, are detected in a small amount, usually disappear after a few months after cessation of contact with the antigen. Infiltration by lymphocytes and plasma cells in sarcoidosis is determined only around the granulomas, with EAA there is no such pattern. There are certain differences in the location of the granulomas. In sarcoidosis, they are found not only in the interstitial tissue of the lungs and in the submucosal layer of the large bronchi, but also peri- and intravascularly. For EAA, granulomas in the interstitium of the lungs are more characteristic. It has already been mentioned that with EAA there is always no necrosis in the center of the granulomas, while with sarcoidosis hyaline necrosis is sometimes detected, and with tuberculosis often caseous necrosis.

The cause of obliteration of the alveoli is the organization of endobronchial exudate, which appears in the bronchioles in the acute stage of the disease. The progression of the process towards fibrosis leads to deformation of the bronchioles, which also contributes to their obliteration.

In patients with chronic EAA, interstitial fibrosis with deformation of the bronchioles was verified. There were areas of emphysema and dystelectasis. At this stage, granulomas were practically not determined.

Elastic fibers fragmented, disappeared; fibroblasts surrounded by collagen fibers were visible.

Immunofluorescent examination of lung tissue biopsy material revealed deposits of immune complexes on the walls of the alveoli.

Clinical symptoms of EAA depends on many factors: the degree of antigenicity of the causative allergen, the massiveness and duration of the antigenic effect, the characteristics of the macroorganism. The same factors determine the course of the disease (acute, subacute, chronic).

The manifestation of acute EAA, as a rule, develops 4-8 hours after the antigen enters the body (by inhalation, orally, parenterally). Characteristic signs of the disease are fever, chills, shortness of breath, dry cough or with scanty mucous sputum, weakness, pain in the chest, muscles, joints, headaches. Along with this, some patients experience attacks of shortness of breath, the phenomena of vasomotor rhinitis.

Auscultation during the acute phase of the disease revealed small and medium bubbling rales, often over the entire surface of the lungs. In the presence of symptoms of bronchospasm, dry whistling rales were heard. In cases of termination of contact with the antigen, the listed symptoms may disappear without treatment within a short time (12-48 hours).

When exposed to small doses of the antigen, there is no clear temporal relationship between the intake of the antigen into the body and clinical symptoms. In such cases, the onset of the disease is not so demonstrative and patients do not always go to the doctor in a timely manner. The gradual development of the symptoms of the disease makes it difficult (for both the doctor and the patient) to identify the relationship between the symptoms of the disease and the impact of any particular professional or domestic factor. In these cases, we are talking about the subacute form of EAA, which is characterized by the following clinical symptoms: cough with a small amount of mucous sputum, shortness of breath with moderate physical exertion, subfebrile body temperature, increased fatigue, loss of appetite, weight loss. Repeated contacts with the causative factor cause an exacerbation of the listed symptoms of the disease.

It is even more difficult to trace the time dependence of the symptoms of the disease on the intake of the corresponding antigen in the chronic course of EAA. Prolonged and repeated exposure to small doses of the antigen leads to the development of a fibrosing process in the lungs, accompanied by progressive dyspnea, cyanosis, weight loss and other subjective and objective signs that do not differ from those in ELISA. The chronic course of EAA was characterized by slowly progressive dyspnea, subfebrile body temperature, and increased fatigue. Crepitus was heard on auscultation.

Diagnostics. Hemogram changes in EAA are determined by the severity of the process and the stage of the disease. Leukocytosis, a shift to the left of the leukocyte formula, increased ESR are characteristic of acute and less characteristic of the subacute course of EAA. The hemogram of the examined patients with the acute form of EAA was characterized by severe leukocytosis (10-20x10 9 /l), a shift to the left of the leukocyte formula (6-15% of stab neutrophils), an increase in ESR to 20-50% mm/h. Some patients had moderate eosinophilia (4.9±1.0%). Hypereosinophilia occurs, as a rule, with EAA caused by aspergillus. The hemogram of patients with chronic EAA practically does not differ from that in ELISA. In the study of protein fractions in patients with chronic EAA, dysproteinemia (hypergammaglobulinemia) is determined.

It should be noted that changes in the listed laboratory parameters are nonspecific and should be taken into account, first of all, to assess the activity and severity of the pathological process.

An important place in the diagnosis of EAA is given to the identification of specific precipitating antibodies belonging to the IgG class. Depending on the presence or absence of specific precipitins, 3 groups of people can be distinguished:

patients with EAA with specific precipitins;

patients with EAA without specific precipitins;

persons with precipitins, but without clinical signs of the disease.

In recent years, provocative inhalation tests have become more widely used in the diagnosis of EAA. The inhalation test is assessed as positive if, after inhalation of aerosols containing putative antigens, the subjective state worsens, which the patient assesses as influenza-like, body temperature and respiratory rate increase; decreases VC. Provocative inhalation tests are most informative in the acute stage, less informative in the subacute stage, and practically uninformative in the chronic stage of the disease.

The technique of carrying out provocative inhalation tests in production conditions (at the workplace) is becoming widespread. In this case, the patient is examined before starting work and, depending on the state of health, at a certain interval or at the end of the working day. First of all, the following indicators are evaluated: respiratory rate, body temperature, VC value. This list may be supplemented by other features.

Thus, despite the availability of numerous laboratory tests, the diagnosis of EAA remains clinical, since only a thorough clarification of the conditions in which the disease arose, an adequate assessment of the clinical symptoms, allows a correct diagnosis to be made.

In this regard, a detailed analysis of production factors, living conditions, geographical and climatic features is extremely important for the diagnosis of EAA.

X-ray changes in the lungs with EAA have their own characteristics depending on the form of the disease (acute, subacute, chronic). At the stage of alveolitis, inhomogeneous shading is characteristic, mainly in the lower lobes. In cases of swelling of the interalveolar septa, the shading may become homogeneous. Edema and cellular infiltration of the interstitial stroma of the lungs lead to an increase in the pulmonary pattern due to the interstitial component. The mesh structure during the summation of changes can create a picture of miliary foci. Termination of exposure to the antigen leads to the reverse dynamics of these changes within a few weeks. In the subacute stage of EAA, small focal shadows are found, which can be combined with both signs of edema and signs of fibrosis of the interstitial tissue. The transition of the disease to a chronic form is accompanied by the progression of the fibrosing process, which at the final stages of the disease can lead to the formation of a "cellular" lung.

Thus, radiological changes in the lungs in patients with acute EAA are characterized by a predominantly alveolar type of lesion with the appearance of infiltrates of varying intensity and length in the lung tissue without a clear segmental localization and rapid reverse dynamics.

The X-ray picture in EAA should be differentiated, first of all, from acute pneumonia, for which most patients received antibiotic therapy for a long time.

Radiological manifestations of the subacute form of EAA are difficult to distinguish from changes in lung sarcoidosis. In favor of sarcoidosis in these cases, the identification of enlarged bronchopulmonary lymph nodes may speak. For EAA in acute and subacute course, infiltrative changes in the lungs were characteristic, while for ELISA - interstitial changes.

The study of the function of external respiration in EAA allows us to detect in most cases a typical picture of obstructive disorders of the ventilation capacity of the lungs in the acute phase of the disease and the addition of a restrictive syndrome in the later stages of the disease.

VC in the acute phase of the disease is usually little changed (at the lower limit of normal or moderately reduced), TRL is moderately increased, TRL is within the normal range. Bronchial patency disorders are more pronounced in this phase, however, with a standard spirographic study, these disorders cannot always be detected, since they mainly affect small airways. In the acute form of EAA, the bronchospastic component dominates with a characteristic obstructive syndrome of ventilation disorders.

Pulmonary gas exchange at the acute stage of EAA usually remains without significant changes until the stage of fibrosis of the pulmonary interstitium, a decrease in exercise tolerance, and, in advanced cases, a decrease in arterial blood Po2.

An increase in the content of total protein by 10-40 times, an increase in the level of immunoglobulins A, G and M are revealed. At the same time, the degree of change in these indicators correlates with the severity of the clinical picture. Normally, 73% of lymphocytes in the lavage fluid are T-cells, in peripheral blood they make up 70%. In patients with EAA, the percentage of T-lymphocytes in the lavage fluid (according to the data of the cited authors) turned out to be higher, and in the blood - lower (80±4% and 57±2%, respectively). A decrease in the number of lymphocytes in the lavage fluid is regarded as a favorable prognostic sign.

EAA treatment. The effectiveness of therapeutic measures in the acute course of EAA depends on the timeliness of stopping contact with the etiological factor and measures aimed at eliminating the allergen from the body. Usually these measures are enough for the complete recovery of the patient.

In cases of prolonged and massive exposure to the allergen, the patient's condition may be moderate or severe. In these cases, it becomes necessary to prescribe corticosteroid drugs based on their anti-allergic and anti-inflammatory effect.

The question of the initial dose of corticosteroids and the duration of treatment in each case should be decided individually. In this case, it is necessary to take into account the severity of the process (the severity of clinical manifestations), age, body weight, the presence of concomitant diseases (hypertension, diabetes peptic ulcer of the stomach or duodenum). The duration of taking corticosteroids depends on the speed of the reverse dynamics of the clinical manifestations of the disease, radiological changes and immunological parameters (primarily precipitins). It should be emphasized that when deciding on the duration of treatment, the identification of precipitins does not have independent significance. As a rule, in the acute course of EAA, the duration of treatment with corticosteroids does not exceed 1 month, in the subacute course - up to 3 months. In the section "Clinical symptoms and course of EAA" there is an observation of patient M. With a subacute course of the disease and favorable dynamics against the background of corticosteroid therapy for 1 1/2 months.

In cases where the disease is accompanied by bouts of shortness of breath, bronchodilators are prescribed in generally accepted dosages.

The appointment of antibiotics for EAA is contraindicated, given the immunoallergic nature of the pathological process.

Characteristically, at the stage of fibrosis, EAA loses its clinical, radiological, and functional features that distinguish it from ELISA. Accordingly, there are no fundamental differences in treatment tactics for these two diseases.

It should be noted that the search for a causative factor is mandatory at any stage of the disease, since only when it is eliminated can one count on a certain therapeutic effect of the prescribed drugs.

Dispensary observation of patients with EAA. The volume of therapeutic measures in the process of dispensary observation of patients with EAA depends on the characteristics of the course of the disease. The presence of shortness of breath, restrictive syndrome, corresponding radiographic changes is considered as an indication for the appointment of corticosteroid drugs, the maintenance dose of which usually does not exceed 5-10 mg / day. Against the background of a decrease in corticosteroids in the presence of moderate peripheral blood eosinophilia, bronchospasm phenomena, desensitizing (tavegil, suprastin, etc.) and bronchodilator drugs can be added to the treatment.

The first examination of patients with acute or subacute course of EAA after discharge from the hospital should be carried out in a month, a second examination - after 3 months. In the future, depending on the characteristics of the course of the disease (or compensation of the patient's condition), this period can be extended to six months or more.

The criterion for reducing the dose of corticosteroids or their cancellation is the dynamics of clinical signs of the disease (respiratory failure, bronchospastic syndrome), radiological, functional and immunological parameters (concentration of specific precipitins, titer of circulating immune complexes).

Dispensary observation of patients with EAA in the presence of progressive pneumofibrosis does not differ from that in ELISA.

Prevention of EAA. As is known, environmental factors play an important role in the occurrence of EAA of the "light farmer" type: the disease occurs more often in climatic zones with cold and rainy summers, in areas with a mountainous climate. Technological processes of procurement and storage of agricultural products (hay, straw, grain, flour, silage, animal feed, etc.) are often violated under adverse weather conditions. Hay with a moisture content of about 16% has a poor microflora and does not heat up during long-term storage. Hay with a high moisture content (20-40%) is heated during storage to 50-60 0 C, which creates favorable conditions for intensive reproduction of thermophilic actinomycetes, which are the most common cause of EAA. Those working on farms with worse working conditions are more likely to develop EAA of the "farmer's lung" type. Mechanization and automation of the most labor-intensive processes associated with the formation of dust when working with grain, flour and other agricultural products can significantly reduce the risk of EAA. This fully applies to the EAA of the "poultry breeder's lung", "cheese maker's lung" and other forms, the occurrence of which is largely related to working conditions in the respective industries and does not depend on the characteristics of the geographical area.

Considering that thermophilic actinomycetes are most often the cause of EAA, it is recommended to remove flower pots with a peat-and-earth mixture, often containing pathogenic fungi, from pulmonology departments. The source of fungal allergization can be, according to the cited author, the patients themselves - carriers of pathogenic fungi (the frequency of which reaches 3%). This predetermines the need for a thorough mycological examination of all patients entering the pulmonology department.

Along with the improvement of working conditions in industries associated with an increased formation of organic or inorganic dust (agriculture, food, textile, woodworking, pharmaceutical and other industries), importance is attached to the use of dust respirators, appropriate overalls, which also reduces the risk of EAA .

It is necessary to emphasize that EAA prevention measures are part of the measures aimed at reducing air pollution with industrial waste.

Prevention of drug-induced EAAs is reduced to the issues of rational prescribing of drugs (primarily antibiotics), taking into account the allergic history, with the exception of polypharmacy, self-treatment.

Of great importance is the rational employment of persons who have undergone an acute or subacute form of EAA, as well as persons at risk of developing EAA.

It is important to carry out appropriate clinical and epidemiological studies in industries that are potentially dangerous in terms of the development of EAA.

Clinical and epidemiological research should be two-stage (preliminary and in-depth). Preliminary allows you to identify individuals who need in-depth examination in a hospital (risk group for developing EAA and a group of patients with EAA).

The group of increased risk of developing EAA included persons who had specific precipitins in the absence of respiratory symptoms (i.e., practically healthy people, but sensitized by the corresponding antigens) or bronchopulmonary symptoms were detected in the absence of specific precipitins.

At the stage of a mass examination of people employed in industries that are potentially dangerous in terms of the development of EAA, it is advisable to use special questionnaires to optimize the processing of the data obtained and standardize the results. This approach allows not only to improve the diagnosis of EAA, but also to form a group of people with an increased risk of developing the disease and those in need in carrying out appropriate preventive measures.

Respiratory damage with acute intoxication

irritant substances

One of the most common adverse factors in the production environment is the gas contamination of working premises. In production conditions, contact with chemicals irritant to the respiratory organs. The main groups of irritating substances that cause predominant damage to the respiratory system are shown in Table 7. Chlorine and its compounds (hydrochloric acid, hydrochloric acid, chloropicrin, phosgene, etc.) are most often encountered in production conditions; sulfur-containing substances (sulfur dioxide, sulfuric acid, hydrogen sulfide); nitrogen compounds (nitrogen oxides, nitric acid, ammonia); fluorine compounds (hydrofluoric acid, hydrofluoric acid, fluorides); chromium-containing substances (chromic anhydride, chromium oxide, potassium and sodium dichromates, chromic alum).

Table 7

Irritant toxic substances

The irritating effect of these substances can be manifested not only when exposed to the respiratory system, but also when in contact with the skin, as well as when it comes into contact with the eyes. Combined forms of intoxication with simultaneous damage to the respiratory system, eyes and skin are known.

The listed chemicals can cause acute and chronic forms of lesions.

Acute intoxication can occur in emergency situations, when it is possible to inhale significant concentrations of toxic irritating substances. The degree of damage in acute intoxication is determined by several factors:

the concentration of poison in the air,

the duration of its action,

general reactivity of the organism,

as well as the features of the action of the most toxic substance.

Depth of defeat respiratory tract largely depends on the degree of solubility of the poison in water. Toxic irritating substances, easily soluble in water (chlorine, sulfur dioxide, ammonia), act mainly on the mucous membrane of the upper respiratory tract, trachea and large bronchi. The action of these substances occurs immediately after contact, without any latent period. Substances of irritating action, sparingly soluble in water (nitrogen oxides, phosgene), affect mainly the deep sections of the respiratory tract. The first clinical signs of intoxication when exposed to these substances, as a rule, develop after a latent period of varying duration.

A significant place in the course of acute intoxication, in addition to the irritating effect on the mucous membrane, belongs to reflex influences, which are caused by strong irritation of the bronchial tree by the interoreceptor and may be accompanied by a disorder of the bronchial tree and may be accompanied by a disorder of its motility.

In acute intoxication with irritating substances, the following can be observed:

acute damage to the upper respiratory tract - acute toxic nasopharyngolaryngotracheitis;

acute toxic bronchitis, characterized by diffuse lesions of the bronchi of large and medium caliber;

acute toxic bronchiolitis;

acute toxic pulmonary edema;

acute toxic pneumonia.

Pathogenesis . Assessing the essence of clinical syndromes in acute lesions with irritating substances, it should be emphasized that they have a close relationship due to a similar pathogenesis.

The main formation of pathology is the development of reactive toxic-chemical inflammation in the respiratory organs. It can be localized at the level of the upper respiratory tract, capture the bronchi, bronchioles and reach the alveolar spaces.

At present, it is considered proven that the development of hyperemia, extravasation and hypersecretion of mucus in the bronchial tree can be caused not only by an infectious onset, but also by exposure to toxic substances. Such an idea of ​​the pathogenesis of developing pathology brings together all forms of damage observed in case of poisoning with irritating substances. Aseptic toxic inflammation is observed both in lesions of the upper respiratory tract and bronchi, and in toxic bronchiolitis and toxic pneumonia. Very closely adjacent to this group is toxic pulmonary edema - “acute serous toxic pneumonia”. The abacterial period in these clinical forms may have favorable course with the reverse development of all pathological manifestations and complete recovery. The most dangerous and frequent complication is the addition of an infection, the unfavorable course of which causes a significant violation of the morphological integrity of the mucous membranes of the respiratory tract, a change in the local lymph and blood circulation, as well as a decrease in the overall reactivity of the body under the influence of toxic effects.

The pathogenesis of toxic pulmonary edema cannot be considered definitively elucidated. The leading role in its development belongs to the increase in the permeability of the alveolar-capillary membrane, which is facilitated by damage to the alveolar epithelium and capillary endothelium. Permeability increases with the participation of histamine, active globulins and other substances released or formed in the tissue when exposed to stimuli.

Of great importance in the regulation of capillary permeability are neuro-reflex influences.

Based on the clinical picture of toxic edema with the presence of leukocytosis and temperature reaction, as well as histological data indicating the presence of confluent catarrh in the absence of microbial flora, there is reason to consider toxic pulmonary edema as one of the variants of toxic pneumonia. The localization of the main pathological processes at the level of the alveoli allows us to attribute this form to the number of acute toxic alveolitis.

The development of acute toxic damage to the lungs causes significant violations of the respiratory function: arterial hypoxemia and hypercapnia. There is a thickening of the blood, an increase in its viscosity, microcirculation processes are disturbed. All this leads to insufficient supply of tissues with oxygen, hypoxia with a simultaneous increase in metabolic acidosis.

The presence of such disorders in the gas exchange function of the lungs served as the basis for calling a group of irritating substances asphyxiating poisons.

pathological anatomy. When exposed to compounds that are highly soluble in water, a lesion is noted with predominant localization in the upper respiratory tract, trachea and large bronchi. Hyperemia, swelling, burns of the mucous membranes, thickening of the submucosal layer, ulcerations and hemorrhages are noted. Microscopic examination reveals areas of necrosis of the mucous membrane, impregnation of the submucosal layer with serous fluid, and places of hemorrhage.

When exposed to compounds that are sparingly soluble in water, changes in the trachea and large bronchi are small. The most pronounced lesions of medium and small bronchi, bronchioles.

With toxic edema, the lungs are enlarged in volume, do not collapse when opening the chest. In the trachea, in all parts of the bronchial tree, as well as in the lungs, there is a significant amount of yellowish liquid, slightly cloudy.

Microscopic examination of the lung parenchyma shows the accumulation of fluid that fills and stretches the alveoli. The fluid, almost free of fibrin and cellular elements, fills not only the lumen of the alveoli, but also accumulates in the perivascular spaces. The interalveolar septa are thickened and torn in places.

Those who died at a later date after poisoning show signs of bronchobronchio- litis and pneumonia, sometimes with necrosis.

Clinic. Depending on the severity, three degrees of severity of acute intoxication are distinguished: mild, moderate and severe.

Mild cases of intoxication, as a rule, are characterized by damage to the upper respiratory tract, trachea and large bronchi. Intoxication of moderate severity corresponds to the clinical picture of acute toxic bronchitis, when bronchi of large, medium and partially small caliber are involved in the process. Severe forms of intoxication occur with a picture of diffuse bronchiolitis or toxic pulmonary edema. Asphyxic forms of acute intoxication, caused by reflex spasm of the muscles of the larynx and vocal cords, which can be fatal, can also be classified as severe.

Despite the general direction of the toxic effect, characteristic of all irritating substances, the clinical manifestations in acute poisoning have some differences due to the peculiarities of their toxicochemical properties.

So, chlorine, hydrogen chloride, hydrogen sulfide, sulfur dioxide, ammonia, hydrogen fluoride often cause changes in the upper respiratory tract and bronchi. However, when high concentrations of these substances are inhaled, the deeper sections of the respiratory tract can be affected, up to pulmonary edema.

Inhalation of significant amounts of vapors of metal carbonyl compounds (nickel carbonyl, iron pentacarbonyl), soluble beryllium compounds, as a rule, is characterized by damage to the deep sections of the respiratory tract by the type of toxic bronchiolitis, toxic pneumonia or toxic pulmonary edema with a pronounced general toxic effect. For exposure to nitrogen oxides, phosgene, perfluoroisobutylene, the development of toxic pulmonary edema is characteristic.

Many toxic substances of irritating action are characterized by combined damage to the respiratory organs with damage to the eyes. Chloropicrin, dimethyl sulfate and ammonia have the most pronounced toxic effect on vision. In mild cases, the process is limited to conjunctivitis (hyperemia, swelling, photophobia). Often at the same time there is swelling of the eyelids, blepharospasm. When droplets of irritating substances get into the eyes, burn phenomena are observed with a sharp chemosis of the conjunctiva, turbidity and melting of the cornea. In this case, an infection often joins, purulent exudate is determined in the anterior chamber, fibrinous adhesions, clouding of the lens. In these cases, a significant decrease in vision or complete blindness is possible.

Some irritants, when in contact with the skin, can lead to the formation of chemical burns, being obligate skin irritants. The most common skin burns in contact with concentrated acids: hydrochloric, sulfuric, hydrofluoric.

Acute lesions by some irritant substances are combined with a general toxic effect, which causes damage to other organs and systems. In this case, changes in the nervous system are often observed.

The most powerful nerve poison is hydrogen sulfide, which inhibits the enzymes of tissue respiration, which leads to the development of histotoxic hypoxia. Therefore, in severe forms of hydrogen sulfide poisoning, the clinical picture is dominated by signs of damage to the central nervous system. The most unfavorable is the fulminant form of acute poisoning, in which, under the influence of a high concentration of hydrogen sulfide, as a result of respiratory paralysis and the vascular center, death occurs instantly. In severe cases of hydrogen sulfide poisoning, a coma often develops. When leaving the coma, pronounced motor excitation is noted, followed by sleep. In some cases, with a protracted course of coma, changes in the central nervous system can become persistent, and in the future various organic symptoms appear. Changes nervous system in these cases, they are combined with damage to the respiratory organs of varying severity - from mild forms to toxic pulmonary edema.

Nitric oxides in acute intoxication also cause damage to the central nervous system, in mild cases manifested by transient cerebral disorders: headaches, dizziness, nausea, vomiting; in severe cases, coma and seizures may develop. Nitric oxides have a nitrite effect, which is manifested by methemoglobinemia and a drop in blood pressure.

Changes in the nervous system (excitation, followed by depression) are also observed in acute hydrazine poisoning.

Alveolitis is one of the most common inflammatory diseases affecting the respiratory parts of the respiratory tract. Despite the fact that they can act as separate pathologies, as well as symptomatic manifestations of other diseases, alveolitis is characterized by some unique features. Thus, inflammation in this case does not have a clear localization and over time leads to the formation of connective tissue in place of the lung - fibrosis. To independent species include toxic, fibrosing and exogenous allergic alveolitis. The latter is being discovered more and more often, so it deserves more detailed consideration.

There are a lot of pathogens that can provoke exogenous allergic alveolitis. Mostly they enter the body with the inhaled air. It can be:

• fungal spores, most of which are found in damp hay or maple bark;
• particles of plants, animals and birds (often pigeons and parrots);
• house dust;
• medical preparations;
• microparticles of household chemicals;
• dust particles exfoliated from some food products(flour, coffee, malt and others).

After the allergen enters the respiratory system, the body starts active production of antibodies. The so-called immune complex is formed, which accumulates in the alveolar walls, the smallest branches of the bronchial tree and capillaries. When a certain concentration is reached, an inflammatory process begins, accompanied by the release of a large amount of serotonin and histamine from the blood cells. In addition, eosinophils and neutrophils are activated, increasing inflammation.

If the causative agents are fungal spores, granulomas begin to form in the alveoli, eventually leading to the growth of connective tissue and replacing it with lung tissue. Sometimes due to inflammation blood vessels fluid is released in the tissue and cavity of the lungs, causing the destruction of their individual sections, which in the future is fraught with the development of emphysema.

Symptoms

Depending on the type of pathogen, exogenous allergic alveolitis can occur in three forms with different symptoms:

• Acute. It mainly manifests itself 5-6 hours after the allergen enters the body. Patients complain of shortness of breath, cough, headache, general malaise. This form is often accompanied by fever and chills. People suffering from others allergic diseases, the condition may worsen after 10 minutes. In this case, spasmodic contraction of the muscles of the bronchial wall occurs, making breathing difficult.
• Subacute. Here, the symptoms are a little blurry, and it is more difficult to establish the specific pathogen that caused allergic alveolitis. Patients have shortness of breath, cough, lethargy, weight loss, often there are signs of bronchitis.
• Chronic. Occurs with constant penetration into the lungs of an allergen over a long period. It is characterized by a wet cough, severe shortness of breath (sometimes even at rest), muscle pain, lethargy, lack of appetite, weight loss. If there is no timely treatment, this form of exogenous alveolitis causes emphysema.

The acute form of alveolitis usually resolves after elimination of the pathogen. But sometimes, due to stagnation of sputum, an infection can occur that has symptoms of bronchitis or pneumonia. Then recovery will not come until the secondary inflammation is cured.

Diagnostics

When diagnosing exogenous alveolitis, it is primarily assumed that it develops in people who do not suffer from allergic diseases. The following studies are carried out:

• X-ray. The acute form is characterized by small darkened foci, with subacute focal fibrosis. If the alveolitis is chronic, areas of overgrown connective tissue become clearly visible.
• Blood test . At the same time, moderate leukocytosis is detected with an increase in neutrophilic granulocytes. Since the symptoms of subacute and chronic forms do not give a clear idea of ​​the nature of the pathogen, a blood test for serology helps here.
• Allergic tests. Most often, intradermal is done, although this method sometimes gives a false positive result, and a slight excess of the dose of the allergen can adversely affect the patient's health.
• Differential Studies. To do this, it is necessary to exclude fibrosing and toxic alveolitis, sarcoidosis of the lungs, infectious pneumonia, tuberculosis, which has multiple foci.

Treatment

First of all, the treatment of exogenous alveolitis should begin with the elimination of the very cause that caused it. That is, the patient must in every possible way avoid contact with the pathogen. To restore the normal functioning of the body in acute and subacute forms, corticosteroid therapy (Prednisolone) is prescribed. If the alveolitis is chronic, antihistamines and restorative drugs are additionally prescribed. Also, Kuprenil has proven itself well, contributing to the rapid destruction of immune complexes.

Features in children

Allergic alveolitis often occurs in children, and is observed in a fairly wide age range (1.5 - 16 years). Almost half of the patients are schoolchildren. Since, unlike adults, the cause of the disease here is not related to professional activity, most patients are residents of rural areas.

It should be noted that there have been repeated cases of people falling ill after moving to another apartment located in an area rich in pathogens (for example, not far from the elevator). Also, allergic alveolitis can provoke an abundance of woolen carpets or dampness in a living room - a favorable environment for the formation of mold.

Treatment this disease in children has the same specifics as in adults, differing only in the dosage of drugs. In addition to medicines, courses of physiotherapy exercises and massage are recommended for a speedy recovery.

In acute and subacute forms, the disease has a favorable prognosis, but when it becomes chronic, it can lead to serious complications. For example, in older people there have been cases of enlargement and expansion of the right heart, sometimes leading to death. Therefore, if allergic alveolitis is suspected, all necessary measures must be taken immediately to eliminate it.

Exogenous allergic alveolitis is a group of diseases that occur as a result of prolonged and intense inhalation exposure to antigens of organic and inorganic origin and are characterized by diffuse allergic damage to the alveoli and interstitial lung tissue.

Etiology

Etiological factors that can cause the development of exogenous allergic alveolitis are divided into three groups:

microorganisms (bacteria, fungi, protozoa) and their metabolic products (proteins, glyco- and lipoproteins, polysaccharides, enzymes, endotoxins);

biologically active substances of animal and vegetable origin (protein antigens of bird feathers, animal hair, fish proteins, milk, saliva, placenta, urine, serum, dust of coffee beans, rice, hemp);

low molecular weight compounds (diisocyanate, salts of heavy metals (gold) and drugs (antibacterials, nitrofurans, intal, antimetabolites).

Damage to the alveoli occurs under the condition of prolonged inhalation of high concentrations of dust with a particle size of up to 5 microns (2-3 microns). Soluble antigens do not cause the development of alveolitis.

Pathogenesis

Features of the pathogenesis of exogenous allergic alveolitis:

The location of the inflammatory process in the alveoli and interstitium of the lungs.

The pathological substrate of the lesion is a sarcoid-like granuloma, which includes T-lymphocytes and activated macrophages. The process ends with the development of interstitial fibrosis.

The occurrence of exogenous allergic alveolitis is associated with the development of immunocomplex (type III) and cell-mediated (type IV) allergic reactions. Atopic IgE-dependent mechanisms (type I) are not typical for exogenous allergic alveolitis.

With prolonged contact with the antigen, allergic reactions occur with the formation of specific antibodies and immune complexes that activate the complement system and alveolar macrophages. The latter secrete IL-2 and chemotactic factors that contribute to the infiltration of lung tissue by neutrophils, eosinophils, mast cells, and lymphocytes. Lymphocytes, in turn, secrete a number of biologically active substances with a pro-inflammatory and damaging effect on the alveoli. Sensitized T-lymphocytes-helpers produce IL-2, under the influence of which the activation of cytotoxic T-lymphocytes occurs, contributing to the development of an inflammatory cell-mediated reaction (delayed-type hypersensitivity reaction). Simultaneously with alveolitis, granulomas are formed, fibroblasts are activated and fibrosis of the interstitium of the lungs is stimulated (active collagen synthesis).

Pathological picture

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 concentration of exudate. Granulomas are formed by epithelioid cells, which are surrounded in the center by lymphocytes and plasma cells. In more pronounced stages of the pathological process, pulmonary fibrosis appears.

Clinical picture

The acute form of exogenous allergic alveolitis occurs 4-12 hours after the antigen enters the patient's respiratory tract, 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. Breathlessness is also possible. During an objective examination, cyanosis, shortness of breath (expiratory) are observed. Auscultation of the lungs determines crepitus, fine and medium bubbling rales, sometimes dry wheezing. After the cessation of the influence of the exogenous allergen, the above symptoms quickly disappear.

The subacute form of exogenous allergic alveolitis occurs when the body is exposed to relatively small doses of the antigen. The disease develops gradually and is characterized by shortness of breath, severe general weakness, sweating, subfebrile body temperature, cough with a small amount of mucous sputum, loss of appetite. On auscultation of the lungs, crepitus, fine bubbling rales are determined. After cessation of contact with the allergen, clinical manifestations decrease, after repeated contact, the disease worsens again.

The chronic form occurs with long-term exposure to small doses of the allergen. This form of the disease is characterized by a steady decrease in body weight, sweating, coughing with the release of mucous sputum. On auscultation of the lungs, crepitus, fine bubbling rales, a squeaking symptom (in the presence of pleuro- and pneumofibrosis) are determined. Over time, a chronic cor pulmonale is formed.

Diagnostics

In a clinical study of peripheral blood, leukocytosis, a shift of the leukocyte formula to the left, eosinophilia, an increase in ESR are detected, in a biochemical study - hypergammaglobulinemia, an increase in the level of seromucoid, haptoglobin, sialic acids. An immunological blood test makes it possible to establish a decrease in the subpopulation of suppressor T-lymphocytes, positive RBTL, inhibition of the migration of leukocytes with a specific antigen, and an increase in the number of circulating immune complexes. It is possible to detect specific antibodies class IgG using the Ouchterlony precipitation reaction, passive hemagglutination, counter immunoelectrophoresis.

Differential diagnosis of exogenous allergic alveolitis should be carried out with idiopathic fibrous alveolitis, occupational bronchial asthma, COPD, tuberculosis, sarcoidosis, Wegener's granulomatosis.

Treatment

Treatment of exogenous allergic alveolitis involves stopping the patient's contact with the source of antigens. In the acute phase, corticosteroids are prescribed (1 mg / kg of prednisolone for 1-3 days with a further dose reduction over 3-4 weeks.). If there are 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, later - 50 mg per day.

To inhibit fibrosis, D-penicillamine (cuprenil) is used at 150-200 mg per day for 4-6 months. with the transition to 100 mg for 2 years, glutamic acid, polyenzymatic preparations (systemic enzyme therapy).

The use of extracorporeal methods of detoxification has certain prospects: plasmapheresis, plasma-, immuno-, lymphosorption.

Working capacity examination

Issues of working capacity of persons with lung diseases caused by exposure to dust contaminated with antigens of microorganisms are solved in the same way as with the corresponding forms of dust lung diseases caused by other types of dust.

Prevention

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 related to the influence of allergens is not recommended for patients with chronic non-specific lung diseases, frequent acute respiratory viral infections, allergic reactions.

During the medical examination of the relevant contingents of workers, they are divided into three groups:

persons in contact with allergens, who have 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 dysfunction respiratory system(vasomotor rhinitis, chronic bronchitis);

patients with exogenous allergic alveolitis with a detailed clinical picture, fibrous changes in the lung tissue.

Prevention in the 1st group (risk) provides for recreational activities (hardening, exercise therapy, breathing exercises), and after acute respiratory viral infections, courses of nonspecific desensitization (antihistamines, calcium preparations) are prescribed.

In the 2nd group, preventive treatment of the underlying disease is carried out with a temporary cessation of the patient's contact with the allergen (sanatorium, dispensary).

When working with exposure to allergens, personal protective equipment (respirators, masks) must be used.

Also called hypersensitivity pneumonitis. The abbreviation for the disease is EAA. This term reflects a whole group of diseases that affect the interstitium of the lungs, that is connective tissue organs. Inflammation is concentrated in the lung parenchyma and small airways. It occurs when a variety of antigens (fungi, bacteria, animal proteins, chemicals) enter them from the outside.

For the first time, exogenous allergic alveolitis was described by J. Campbell in 1932. He identified it in 5 farmers who suffered from SARS symptoms after working with hay. Moreover, this hay was wet and contained mold spores. Therefore, this form of the disease began to be called "farmer's lung."

In the future, it was possible to establish that allergic alveolitis of the exogenous type can be triggered by other causes. In particular, in 1965, C. Reed and her colleagues found similar symptoms in three patients who were breeding pigeons. They began to call such an alveolitis "the lung of bird lovers."

The statistics of recent years indicate that the disease is quite widespread among people who, due to their professional activities, interact with feathers and down of birds, as well as with compound feed. Out of 100,000 population, exogenous allergic alveolitis will be diagnosed in 42 people. At the same time, it is impossible to accurately predict which particular person who is allergic to down or feathers will develop alveolitis.

As practice shows, from 5 to 15% of people who interacted with high concentrations of allergens will develop pneumonitis. The prevalence of alveolitis among individuals who work with low concentrations of sensitizing substances is not known to date. However, this problem is quite acute, as the industry develops more and more intensively every year, which means that more and more people are involved in such activities.

Allergic alveolitis develops due to the inhalation of an allergen, which enters the lungs along with the air. Various substances can act as an allergen. The most aggressive allergens in this regard are fungal spores from rotten hay, maple bark, sugar cane, etc.

Also, one should not write off plant pollen, protein compounds, house dust. Some medicines, such as antibiotics or nitrofuran derivatives, can cause allergic alveolitis even without previous inhalation, and after entering the body in other ways.

Not only the fact that allergens enter the respiratory tract is important, but also their concentration and size. If the particles do not exceed 5 microns, then it will not be difficult for them to reach the alveoli and provoke a hypersensitivity reaction in them.

Since allergens that cause EAA are most often associated with a person’s professional activities, varieties of alveolitis were named for various professions:

Farmer's Lung. Antigens are found in moldy hay, among them: Thermophilic Actinomycetes, Aspergillus spp, Mycropolyspora faeni, Thermoactinomycas vulgaris.

Lung of bird lovers. Allergens are found in the excrement and dander of birds. They become whey proteins of birds.

Bagassoz. The allergen is sugar cane, namely Mycropolysporal faeni and Thermoactinomycas sacchari.

Lung of persons growing mushrooms. Compost becomes the source of allergens, and Mycropolysporal faeni and Thermoactinomycas vulgaris act as antigens.

Lung of persons using conditioners. Humidifiers, heaters, and air conditioners are sources of antigens. Sensitization is provoked by such pathogens as: Thermoactinomycas vulgaris, Thermoactinomycas viridis, Ameba, Fungi.

Suberose. The bark of the cork tree becomes the source of allergens, and Penicillum frequentans acts as the allergen itself.

Lung malt brewers. The source of antigens is moldy barley, and the allergen itself is Aspergillus clavatus.

Cheesemaker's disease. The source of antigens is cheese and mold particles, and the antigen itself is Penicillum cseii.

Sequoyz. Allergens are found in redwood wood dust. They are represented by Graphium spp., upullaria spp., Alternaria spp.

Lung detergent manufacturers. The allergen is found in enzymes and detergents. It is represented by Bacillus subtitus.

Lung laboratory workers. The sources of allergens are dandruff and rodent urine, and the allergens themselves are represented by the proteins of their urine.

Lung sniffing pituitary powder. The antigen is represented by porcine and bovine proteins, which are found in the powder of the pituitary gland.

Lung employed in the production of plastics. The source leading to sensitization is diisocyanates. The allergens are: Toluene diiosocianate, diphenylmethane diiosocianate.

Summer pneumonitis. The disease develops due to the inhalation of dust from damp living quarters. The pathology is widespread in Japan. Trichosporon cutaneum becomes a source of allergens.

Of the listed allergens in terms of the development of exogenous allergic alveolitis, thermophilic actinomycetes and bird antigens are of particular importance. In areas with a high development of agriculture, it is actinomycetes that occupy a leading position in terms of the incidence of EAA. They are represented by bacteria that do not exceed a size of 1 micron. Distinctive feature of such microorganisms is reduced to the fact that they have the properties of not only microbes, but also fungi. Many thermophilic actinomycetes are located in the soil, in compost, in water. They also live in air conditioners.

Such varieties of thermophilic actinomycetes lead to the development of exogenous allergic alveolitis, such as: Mycropolyspora faeni, Thermoactinomycas vulgaris, Thermoactinomycas viridis, Thermoactinomycas sacchari, Thermoactinomycas scandidum.

All of the listed representatives of flora pathogenic for humans begin to multiply actively at a temperature of 50-60 °C. It is under such conditions that the processes of decay of organic matter are launched. A similar temperature is maintained in heating systems. Actinomycetes can cause bagassosis (lung disease in people who work with sugar cane), cause a disease called "farmer's lung", "lung of mushroom pickers (mushroom growers)", etc. All of them are listed above.

The antigens that affect humans interacting with birds are serum proteins. These are albumin and gamma globulins. They are present in bird droppings, in secretions from the skin glands of pigeons, parrots, canaries, etc.

People who care for birds experience alveolitis with prolonged and regular interaction with animals. Proteins of cattle, as well as pigs, are capable of provoking the disease.

The most active fungal antigen is Aspergillus spp. Different kinds This microorganism can cause suberosis, malt brewer's lung or cheese maker's lung.

It is in vain to believe that, living in the city and not doing agriculture, a person cannot get sick with exogenous allergic alveolitis. In fact, Aspergillus fumigatus thrives in damp areas that are rarely ventilated. If the temperature in them is high, then microorganisms begin to multiply rapidly.

Also at risk for the development of allergic alveolitis are people whose professional activities are associated with reactogenic chemical compounds, for example, plastic, resins, paints, polyurethane. Phthalic anhydride and diisocyanate are considered especially dangerous.

Depending on the country, the following prevalence of different types of allergic alveolitis can be traced:

The lung of budgerigar lovers is most often diagnosed in residents of the UK.

The lung of people who use air conditioners and humidifiers is in America.

The summer type of alveolitis, caused by the seasonal reproduction of fungi of the Trichosporon cutaneun species, is diagnosed in 75% of cases in the Japanese.

In Moscow and in cities with large industrial enterprises, patients with a reaction to bird and fungal antigens are most often detected.

The human respiratory system regularly encounters dust particles. This applies to both organic and inorganic contaminants. It has been established that antigens of the same type can cause the development various pathologies. Some people develop bronchial asthma, while others develop chronic asthma. There are also people who manifest allergic dermatosis, that is, skin lesions. We must not forget about conjunctivitis of an allergic nature. Naturally, exogenous alveolitis is not the last in the list of listed pathologies. What kind of disease will develop in a particular person depends on the strength of the exposure, on the type of allergen, the condition immune system body and other factors.

In order for a patient to manifest exogenous allergic alveolitis, a combination of several factors is necessary:

A sufficient dose of allergens that have entered the respiratory tract.

Prolonged exposure to the respiratory system.

A certain size of pathological particles, which is 5 microns. Less commonly, the disease develops when large antigens enter the respiratory system. In this case, they should settle in the proximal bronchi.

The vast majority of people who encounter such allergens do not suffer from EAA. Therefore, scientists believe that the human body should be affected simultaneously by several factors. They have not been studied enough, but there is an assumption that genetics and the state of immunity matter.

Exogenous allergic alveolitis is rightfully classified as an immunopathological disease, the undoubted cause of which are allergic reactions of types 3 and 4. Also, non-immune inflammation should not be ignored.

The third type of immunological reaction is of particular importance in the initial stages of the development of pathology. The formation of immune complexes occurs directly in the interstitium of the lungs when a pathological antigen interacts with antibodies of the lgG class. The formation of immune complexes leads to the fact that the alveoli and interstitium is damaged, the permeability of the vessels that feed them increases.

The resulting immune complexes cause the complement system and alveolar macrophages to become activated. As a result, toxic and anti-inflammatory products, hydrolytic enzymes, cytokines (tumor necrosis factor - TNF-a and interleukin-1) are released. All this causes an inflammatory reaction at the local level.

Subsequently, the cells and matrix components of the interstitium begin to die, inflammation becomes more intense. Significant amounts of monocytes and lymphocytes are supplied to the site of the lesion. They ensure the preservation of the delayed-type hypersensitivity reaction.

Facts that confirm that immunocomplex reactions are important in exogenous allergic alveolitis:

After interaction with the antigen, inflammation develops rapidly, within 4-8 hours.

In washings of exudate from the bronchi and alveoli, as well as in the serum part of the blood, high concentrations of antibodies of the lgG class are found.

In the lung tissue taken for histology, in patients with an acute form of the disease, immunoglobulin, complement components, and the antigens themselves are found. All these substances are immune complexes.

When performing skin tests using highly purified antigens that are pathological for a particular patient, a classic Arthus-type reaction develops.

After performing provocative tests with the inhalation of pathogens, the number of neutrophils in patients in the bronchoalveolar lavage fluid increases.

Type 4 immune responses include CD+ T-cell delayed-type hypersensitivity and CD8+ T-cell cytotoxicity. After antigens enter the respiratory system, delayed-type reactions develop in 1-2 days. Damage to immune complexes leads to the release of cytokines. They, in turn, cause leukocytes and the endothelium of the lung tissue to express adhesive molecules on the surface. Monocytes and other lymphocytes react to them, which actively arrive at the site of the inflammatory reaction.

At the same time, interferon gamma activates macrophages that produce CD4 + lymphocytes. This is the hallmark of a delayed-type reaction, which lasts for a long time thanks to macrophages. As a result, granulomas form in the patient, collagen begins to be released in excess quantities (fibroblasts are activated by growth cells), and interstitial fibrosis develops.

Facts that confirm that in exogenous allergic alveolitis, delayed type 4 immunological reactions are important:

T-lymphocytes are found in the blood memory. They are present in the lung tissue of patients.

In patients with acute and subacute exogenous allergic alveolitis, granulomas, infiltrates with accumulation of lymphocytes and monocytes, as well as interstitial fibrosis are detected.

Experiments on laboratory animals with EAA have shown that CD4+ T-lymphocytes are required for disease induction.

Histological picture of EAA

In most cases, patients with exogenous allergic alveolitis have granulomas, without curdled plaque. They are detected in 79-90% of patients.

In order not to confuse granulomas that develop with EAA and with sarcoidosis, you need to pay attention to the following differences:

With EAA, the granulomas are smaller.

Granulomas do not have clear boundaries.

Granulomas contain more lymphocytes.

Alveolar walls in EAA are thickened, they have lymphocytic infiltrates.

After contact with the antigen is excluded, the granulomas disappear on their own within six months.

In exogenous allergic alveolitis, the inflammatory process is caused by lymphocytes, monocytes, macrophages and plasma cells. Foamy alveolar macrophages accumulate inside the alveoli themselves, and lymphocytes in the interstitium. When the disease has just begun to develop, patients have a protein and fibrinous effusion, which is located inside the alveoli. Also, patients are diagnosed with bronchiolitis, lymphatic follicles, peribronchial inflammatory infiltrates, which are concentrated in the small airways.

So, the disease is characterized by a triad morphological changes:

Alveolitis.

Granulomatosis.

bronchiolitis.

Although sometimes one of the signs may fall out. Rarely, patients with exogenous allergic alveolitis develop vasculitis. He was diagnosed in a patient posthumously, as indicated in the relevant documents. In patients with pulmonary hypertension, hypertrophy of the arteries and arterioles occurs.

The chronic course of EAA leads to fibrinous changes, which can have different intensity. However, they are characteristic not only for exogenous allergic alveolitis, but also for other chronic lung diseases. Therefore, it cannot be called a pathognomic sign. With long-term alveolitis in patients, the lung parenchyma undergoes pathological changes in the type of honeycomb lung.

The disease develops most often in people who are not prone to allergic reactions. Pathology manifests itself after prolonged interaction with sources, the spread of antigens.

Exogenous allergic alveolitis can occur in 3 types:

Acute symptoms

The acute form of the disease occurs after a large amount of antigen enters the respiratory tract. This can happen both at home and at work or even on the street.

After 4-12 hours, a person's body temperature rises to high levels, chills develop, and weakness increases. There is heaviness in the chest, the patient begins to cough, he is haunted by shortness of breath. Aches appear in the joints and muscles. Sputum during the time appears infrequently. If it departs, then it is small and it consists mainly of mucus.

Another symptom characteristic of acute EAA is a headache that focuses on the forehead.

During the examination, the doctor notes cyanosis of the skin. When listening to the lungs, crepitations and wheezing are heard.

After 1-3 days, the symptoms of the disease disappear, but after another interaction with the allergen, they increase again. General weakness and lethargy, combined with shortness of breath, can disturb a person for several weeks after the resolution of the acute stage of the disease.

The acute form of the disease is not often diagnosed. Therefore, doctors confuse it with SARS, provoked by viruses or mycoplasmas. Experts should be alert to farmers, and also distinguish between the symptoms of EAA and the symptoms of pulmonary mycotoxicosis, which develop when fungal spores enter the lung tissue. In patients with myotoxicosis, lung radiography does not show any pathological changes, and there are no precipitating antibodies in the serum part of the blood.

subacute symptoms

Symptoms of the subacute form of the disease are not as pronounced as in the acute form of alveolitis. Such an alveolitis develops due to prolonged inhalation of antigens. Most often this happens at home. So, subacute inflammation in most cases is provoked by the care of poultry.

The main manifestations of subacute exogenous allergic alveolitis include:

Crepitus when listening to the lungs will be gentle.

It is important to distinguish subacute EAA from other interstitium diseases.

Symptoms of the chronic type

The chronic form of the disease develops in people who interact with small doses of antigens for a long time. In addition, subacute alveolitis can become chronic if it is not treated.

The chronic course of the disease is indicated by symptoms such as:

Increasing with time shortness of breath, which becomes apparent with physical activity.

Pronounced weight loss, which can reach up to.

The disease threatens to develop cor pulmonale, interstitial fibrosis, cardiac and respiratory failure. Since chronic exogenous allergic alveolitis begins to develop latently and does not give severe symptoms, its diagnosis is difficult.

To identify the disease, it is necessary to rely on an X-ray examination of the lungs. Depending on the stage of development of alveolitis and its form, radiological signs will differ.

The acute and subacute form of the disease leads to a decrease in the transparency of fields like ground glass and to the spread of nodular-mesh opacities. The size of the nodules does not exceed 3 mm. They can be found all over the surface of the lungs.

The upper part of the lungs and their basal sections are not covered with nodules. If a person stops interacting with antigens, then after 1-1.5 months, the radiological signs of the disease disappear.

If the disease has a chronic course, then linear shadows with a clear outline, dark areas represented by nodules, changes in the interstitium, and a decrease in the size of the lung fields are visible on the x-ray picture. When the pathology has a running course, then a honeycomb lung is visualized.

CT is a method that has a much higher accuracy compared to radiography. The study reveals signs of EAA, which are invisible with standard radiography.

A blood test in patients with EAA is characterized by the following changes:

Leukocytosis up to 12-15x10 3 /ml. Less commonly, the level of leukocytes reaches the level of 20-30x10 3 /ml.

The leukocyte formula shifts to the left.

An increase in the level of eosinophils does not occur, or it may increase slightly.

ESR in 31% of patients rises to 20 mm/h, and in 8% of patients up to 40 mm/h. In other patients, ESR remains within the normal range.

The level of lgM and lgG increases. Sometimes there is a jump in class A immunoglobulins.

In some patients, rheumatoid factor is activated.

Increases the level of total LDH. If this occurs, then acute inflammation in the lung parenchyma can be suspected.

To confirm the diagnosis, Ouchterlony double diffusion, micro-Ouchterlony, counter immunoelectrophoresis and ELISA (ELISA, ELIEDA) methods are used. They allow you to identify specific precipitating antibodies to the antigens that caused the allergy.

In the acute phase of the disease, precipitating antibodies will circulate in the blood of virtually every patient. When the allergen ceases to interact with the lung tissue of patients, the level of antibodies drops. However, they may be present in the serum part of the blood for a long time (up to 3 years).

When the disease is chronic, antibodies are not detected. There is also the possibility of false positive results. In farmers without symptoms of alveolitis, they are detected in 9-22% of cases, and in bird lovers in 51% of cases.

In patients with EAA, the value of precipitating antibodies does not correlate with the activity of the pathological process. Their level can be affected by a variety of factors. So, in smokers, it will be underestimated. Therefore, the detection of specific antibodies cannot be considered evidence of EAA. At the same time, their absence in the blood does not indicate that there is no disease. However, antibodies should not be written off, since in the presence of appropriate clinical signs they can strengthen the current assumption.

The test for a decrease in the diffuse capacity of the lungs is indicative, since other functional changes in EAA are characteristic of other types of pathologies accompanied by damage to the interstitium of the lungs. Hypoxemia in patients with allergic alveolitis is observed in a calm state, and increases during physical exertion. Violation of lung ventilation occurs according to the restrictive type. Signs of airway hyperreactivity are diagnosed in 10-25% of patients.

Inhalation tests were first used to detect allergic alveolitis as early as 1963. Aerosols were made from dust taken from moldy hay. They led to an exacerbation of the symptoms of the disease in patients. At the same time, extracts taken from "pure hay" did not cause such a reaction in patients. In healthy individuals, even aerosols with mold did not provoke pathological signs.

Provocative tests in patients with bronchial asthma do not cause the appearance of rapid immunological reactions, do not provoke disturbances in the functioning of the lungs. While in people with a positive immune response, they lead to changes in the functioning of the respiratory system, to an increase in body temperature, chills, weakness and dyspnea. After 10-12 hours, these manifestations disappear on their own.

It is possible to confirm the diagnosis of EAA without performing provocative tests, so they are not used in modern medical practice. They are used only by experts who need to confirm the cause of the disease. Alternatively, it is enough to observe the patient in his usual conditions, for example, at work or at home, where there is contact with the allergen.

Bronchoalveolar lavage (BAL) allows you to assess the composition of the contents of the alveoli and distant parts of the lungs. The diagnosis can be confirmed by the detection of a five-fold increase in cellular elements in it, and 80% of them will be represented by lymphocytes (mainly T-cells, namely CD8 + lymphocytes).

The immunoregulatory index in patients is reduced to less than one. With sarcoidosis, this figure is 4-5 units. However, if lavage was performed in the first 3 days after the acute development of alveolitis, then the number of neutrophils will be increased, and lymphocytosis is not observed.

In addition, lavage makes it possible to detect an increase in the number of mast cells tenfold. This concentration of mast cells can persist for up to 3 months or more after contact with the allergen. This indicator characterizes the activity of the fibrin production process. If the disease has a subacute course, then plasma cells will be found in the lavage.

Diseases from which exogenous allergic alveolitis must be distinguished: