Inflammatory disease of the alveolitis of the lungs

Alveolitis - a disease that involves the defeat of the alveoli or pulmonary vesicles. The inflammatory process often leads to fibrosis of the lung tissue. Alveolitis develops independently under the influence of a number of external stimuli or is a consequence of another disease.

There are the following types of the disease:

Idiopathic fibrosing alveolitis

It is called diffuse or interstitial pneumofibrosis, Hemman-Rich syndrome. This type of alveolitis is less common than others, and men suffer from it more often than women. Hamman-Rich syndrome is manifested in the form of lesions of the pulmonary interstitium, further leads to the development of respiratory failure and pneumosclerosis.

The main symptoms of idiopathic alveolitis are severe coughing and shortness of breath. The disease is rarely detected in the early stages, so the exact diagnosis in most cases is made with a history of at least 3 months, and often several years. The first symptoms of idiopathic alveolitis do not cause anxiety in patients. The body gradually adapts to shortness of breath and coughing. To avoid the manifestation of these symptoms, patients, as a rule, begin to lead a less mobile lifestyle. When conducting an X-ray examination, a picture shows a deformed pulmonary pattern, an increased amount of connective tissue that grows as the disease progresses.

The development of pulmonary fibrosis gradually reduces the chances of recovery. The treatment started in time allows almost completely to get rid of idiopathic alveolitis. However, patients have to be under the supervision of a doctor all their life and periodically undergo examination. If untreated, in most cases a few months or years later there is a lethal outcome.

Exogenous allergic alveolitis

The cause of the development of the disease are external stimuli: dust of plant origin, fungal spores, drugs. There are two ways of their entry into the body: inhalation and non-inhalation, which is very rare. A large number of subspecies of exogenous allergic alveolitis was isolated, depending on the specific type of stimulus. Lovers of birds and furriers suffer from this disease, which is caused by the constant work with fur and feather, farmers who deal with rotten hay.

Depending on the frequency of contact with the irritant that caused the alveolitis, an acute, subacute and chronic form is possible. The lungs of the patient have blackouts, their transparency is reduced. In the chronic form, the density of the respiratory tract tissues gradually increases. The basis of effective treatment of allergic alveolitis is the elimination of contact with an irritant. Without this, the use of drugs will be ineffective.

Toxic alveolitis

Appears under the influence of the direct action of toxic substances on the lungs. Drugs that cause the development of the disease are medicines, for example, sulfonamides, immunosuppressants, or chemical toxicants, such as zinc, talc, ammonia, chlorine. They can be ingested with blood or directly in the process of respiration.

If you do not stop the effects of irritants, the disease will become chronic. It is dangerous to form fibrous tissue, replacing damaged epithelial. Over time, this will lead to the loss of their main functions by the alveoli.

Symptoms of alveolitis of the lungs

The following symptoms of alveolitis can be distinguished:

Dyspnea. At first, patients may not attach much importance to it and do not seek help from specialists, since breathing difficulties occur only during the performance of active movements. But gradually, shortness of breath increases, occurs even when walking at a moderate pace. Most often, patients with alveolitis are treated by a doctor 3 months after it appears or even several years later.

Cough. Most common in idiopathic alveolitis. Cough may be accompanied by wheezing, especially in patients with bronchitis, but the blood is not expectorated.

Pains They are felt in the chest and under the shoulder blades. Discomfort in this area may prevent deep breaths.

Deterioration of the patient’s general condition. Many patients lose weight, they have constantly increased body temperature and weakness. Patients with alveolitis may have pains in their joints and muscles. Fibrosing alveolitis leads to deformity of the fingers.

enlarged veins of the neck and swelling,

This condition is characterized by an extreme form of exhaustion, in which the patient complains of a general weakness in the body and loses weight. All this is accompanied by a slowdown in physiological processes and adversely affects the psyche. Loss of appetite leads to a lack of vitamins, as a result of which the skin acquires an earthy pale tint. The patient becomes sluggish, his performance decreases, and the subcutaneous tissue decreases sharply.

Causes of lung alveolitis

The following causes of alveolitis are distinguished:

Viruses. Among them are the hepatitis C virus, herpevirus, cytomegalovirus, HIV. By acting on the immune system, they weaken it, as a result of which the body is more susceptible to external stimuli.

Heredity. The exact effect of this cause has not been established, however, there is an assumption that genes also influence the development of alveolitis.

They can be chemicals or natural substances, such as feathers and bird droppings, fur, bark, fungus spores, sawdust, hay, coffee, and even some types of cheese. However, they can cause alveolitis with constant contact. Typically, such external stimuli of natural origin lead to the development of an allergic type of disease, and chemicals - to toxic.

What diseases can be associated with?

Fibrosing alveolitis can be combined with various diseases. First of all, it is vasculitis, affecting the pulmonary walls. He is diagnosed during radiography. Alveolitis may also be accompanied by candidiasis. This secondary disease manifests itself in the form of the appearance of dark spots on the lungs and leads to their fibrosis.

Often, along with alveolitis diagnosed with lupus erythematosus, hepatitis C, HIV. A connection has been established even with rheumatoid arthritis. Viral infections, such as HIV and hepatitis C, in some cases cause alveolitis. The disease has similar symptoms with sarcodic and pneumonia. This requires additional research to make an accurate diagnosis.


If untreated, alveolitis leads to the development of serious complications, including progressive respiratory failure, pulmonary heart and even pulmonary edema. It is caused by the ingress of a liquid portion of blood into the lung tissue, as a result of which gas exchange is disturbed. In this case, the patient must provide urgent medical assistance in time, otherwise there is a lethal outcome.

Depending on the course, pulmonary edema can be of several types:

Lightning fast - characterized by rapid development and a sharp deterioration in the patient’s condition, as a result of which death occurs,

Acute - develops within a few hours and often also causes a fatal outcome,

Subacute - in this case, the manifestation of symptoms alternately intensifies and weakens,

Protracted - this type of pulmonary edema is more characteristic of the alveolitis, develops within 12-24 hours.

How to treat alveolitis?

Alveolitis treatment should be carried out under the constant supervision of a physician. Specific methods vary according to the type of disease. With toxic and allergic alveolitis, along with the use of drugs, it is necessary to eliminate the external irritant that caused its development.

For fibrosing alveolitis, glucocorticoids are used. In this case, it is important to start treatment in time, as the rapid replacement of epithelial fibrous tissue becomes the reason for the termination of the involvement of the alveoli in the respiratory process, which can lead to a detailed outcome. If glucocorticoids are ineffective, penicillamine and immunodepressants come to the rescue (read more about the treatment of exogenous allergic alveolitis).

Allergic and toxic alveolitis requires the use of glucocorticosteroids. But above all, the external irritant that caused the disease is eliminated. Allergic alveolitis is also dangerous in the development of fibrosis. To accelerate the recovery of patients with this disease allows an additional course of vitamins, breathing exercises and special physical exercises. (More on the treatment of idiopathic fibrosing alveolitis)

What kind of drugs to treat alveolitis?

As part of the drug treatment of alveolitis, various antidepressants are widely used, for example, Azathioprine. This drug blocks cell division and slows fibrosis. Aminophylline is used to improve lung function and stimulate the work of the respiratory center in alveolitis. Dexamethasone has anti-inflammatory and anti-allergic effects.

Prednisolone is also often used to treat alveolitis, which is a glucocortroid. They, together with means for improving immunity, are very effective in alveolitis. Antihistamines can block histamine receptors, which provoke the appearance of allergic reactions, including pulmonary edema. They require treatment for allergic and toxic alveolitis.

Alveolitis treatment at home

At home, treatment of alveolitis can be made only with the permission of a specialist. In most cases, therapy in the clinic is more effective, since the patient is constantly under the supervision of doctors. With fibrosing alveolitis full cure is impossible. After the patient undergoes a course of treatment in the hospital, he is discharged home and the further struggle with the disease continues, accompanied by regular specialist consultations.

Treatment of alveolitis should be carried out under the supervision of a physician with the help of various medications, but after consulting with a specialist, it can be supplemented with traditional methods, which will make it possible to achieve a positive effect more quickly. So, it is recommended to drink pumpkin juice, which allows you to cope with swelling in the lung area. In the day it should drink no more than 1.5 liters.

When alveolitis is also useful tincture made from the leaves of lingonberry. 10 g of dry leaves are brewed with boiling water (250 ml), then the mixture is boiled for 15 minutes. When the tincture is cool, it should be drunk in small sips. This portion is designed for a day.

Treatment of alveolitis during pregnancy

Pregnant women should pay special attention to their health, to prevent the development of alveolitis. This disease is dangerous to the health of the mother and child. In addition, it is extremely difficult to carry out his treatment. Many drugs that are used to combat various types of alveolitis are contraindicated for pregnant women, some of them cause vomiting, dizziness and other side effects.

If the disease could not be avoided, you should contact a highly qualified specialist. He will be able to prescribe treatment that is safe and effective for pregnant women, as well as assess the risk of fetal damage and a threat to the health of the mother.

Prevention of alveolitis

Prevention of alveolitis involves compliance with the rules of work with toxic substances, the elimination of irritants that cause an allergic reaction. It is necessary to undergo regular examination by a pulmonologist and a rheumatologist. Prevention of alveolitis with drugs is not provided.

About the doctor: From 2010 to 2016 practicing physician of the therapeutic hospital of the central medical and sanitary unit No. 21, the city of Elektrostal. Since 2016 he has been working in the diagnostic center №3.

Causes and risk factors

Exogenous allergic alveolitis develops on the background of allergic reactions (often allergens are plant and household dust, drugs, pet hair, components of microscopic fungi, industrial irritants, etc.). The entry of an allergen into the body causes the formation of IgG. Immune complexes (antigen-antibody) are deposited on the surface of the alveoli, which causes damage to the cell membrane, the release of significant amounts of biologically active substances with the development of the inflammatory process. In the development of this form of alveolitis an important role is played by the repeated ingress of an allergen into the body.

The causes of idiopathic fibrosing alveolitis are not completely understood. It is assumed that the disease may be of an autoimmune nature, occurring against the background of infection with some viruses (hepatitis C virus, herpes virus, cytomegalovirus, adenoviruses). Risk factors for the development of this form of the disease include work in the agricultural sector, the woodworking industry, metallurgy, and smoking. At the same time, the inflammatory process in the pulmonary alveoli leads to an irreversible thickening of their walls with a subsequent decrease in permeability to gas exchange.

The main reason for the development of toxic fibrosing alveolitis is the direct or indirect effect on lungs of toxic substances that enter the pulmonary alveoli by hematogenous or aerogenic (among other such drugs as Azathioprine, Mercaptopurin, Methotrexate, Furadonin, Cyclophosphamide).

Secondary alveolitis occurs against the background of other pathological processes. Most often it is sarcoidosis, tuberculosis, diffuse connective tissue diseases.

Risk factors include:

Forms of the disease

Depending on the etiological factor, as well as the characteristics of the course of the disease, there are:

  • idiopathic fibrosing alveolitis,
  • toxic fibrosing alveolitis,
  • exogenous allergic alveolitis.

Alveolitis can be primary and secondary, as well as acute, subacute and chronic.

Idiopathic fibrosing alveolitis is prone to gradual progression with the development of complications. Because of the increasing irreversible changes in the alveolar-capillary system of the lungs, the risk of death is high.

Stage of the disease

Depending on the histological picture, five stages of idiopathic fibrosing alveolitis are distinguished:

  1. Infiltration and thickening of the pulmonary alveolar septa.
  2. Filling of pulmonary alveoli with cellular composition and exudate.
  3. Destruction of pulmonary alveoli.
  4. Changing the structure of lung tissue.
  5. Formation of cystic-modified cavities.


The diagnosis is determined on the basis of data obtained during the collection of complaints and anamnesis, physical diagnostics, studies of respiratory function, and radiography of the lungs.

In the course of X-ray examination with exogenous allergic alveolitis, a decrease in the transparency of the lung tissue with the formation of a large number of small focal shadows is detected.In order to confirm the diagnosis, laboratory immunological diagnostics, provocative inhalation tests, computed tomography of the lungs are carried out. In diagnostically difficult cases, lung tissue biopsy is resorted to, followed by histological examination of the material obtained.

Exogenous allergic alveolitis differentiate with bronchial asthma, atypical pneumonia, tuberculosis, sarcoidosis, and other forms of alveolitis of the lungs.

In the case of idiopathic fibrosing alveolitis, small-focal diffuse changes are defined on the radiograph of the lungs on both sides, more pronounced in the lower sections. In the later stages of the disease, secondary cystic changes are detected in the lung tissue. Data computed tomography of the lungs allow you to determine the area of ​​the altered lung tissue for subsequent biopsy. The results of the electrocardiogram indicate the presence of hypertrophy and overload of the right heart.

Differential diagnosis of this form of alveolitis is carried out with pneumonia, granulomatosis, pneumoconiosis, diffuse forms of amyloidosis and lung neoplasms.

Radiographic changes in acute toxic fibrosing alveolitis may be absent. Further, the deformation and diffuse amplification of the pulmonary pattern, as well as diffuse fibrosis are determined.

Secondary alveolitis occurs against the background of other pathological processes. Most often it is sarcoidosis, tuberculosis, diffuse connective tissue diseases.

Alveolitis of the lungs - what is it

By its nature, alveolitis of the lungs is different from pneumonia and pneumonitis. In the case of the latter disease, interstitial tissue is involved in the pathological process, in the case of pneumonia, the parenchyma and interstitium.

With alveolitis, it is the alveoli that are the main component of the parenchyma.

Normally, lung tissue consists of a large part — the parenchyma and a smaller one — the interstitium. The parenchyma carries the main functional load, there is a gas exchange between the environment and blood.

Interstitium consists of a small amount of connective tissue and vessels located in it.

The pulmonary vessels abut close to the alveoli, which allows oxygen to pass from the lumen of the alveolar sacs through the wall of the alveoli into the capillary blood flow. Carbon dioxide moves in the opposite direction - from the bloodstream into the lumen of the alveoli.

In order for such circulation of gases to be possible, the wall of the alveoli must be very thin. Normally, the alveoli lining a row of cells arranged in a single layer.

During inflammation, the wall of the alveoli collapses.

The fluid from the vessels penetrates the alveolar tissue. This process leads to a deterioration in the diffusion of gases. At the same time, cells called fibroblasts are activated in the interstitium.

These cells synthesize collagen - the main component of connective tissue. Gradually, connective tissue replaces the destroyed alveoli.

Possible complications of alveolitis and consequences

Complications of the alveolitis can be chronic bronchitis, pulmonary hypertension, pulmonary heart, right ventricular heart failure, interstitial fibrosis, pulmonary emphysema, respiratory failure, pulmonary edema.

With timely adequate treatment of acute exogenous allergic, as well as toxic fibrosing alveolitis, the prognosis is usually favorable. When the disease becomes chronic, the prognosis worsens.

Idiopathic fibrosing alveolitis is prone to gradual progression with the development of complications. Because of the increasing irreversible changes in the alveolar-capillary system of the lungs, the risk of death is high. Five-year survival after surgical treatment reaches 50-60%.


Depending on the etiological factor, alveolitis happens:

  • fibrosing idiopathic - differs in that it occurs against a background of incomprehensible factors, but there is an assumption that its progression is influenced by a genetic predisposition and a person’s lifestyle,
  • exogenous allergic - occurs on the background of ingestion of antigens of various nature through the respiratory organs,
  • toxic - based on the name, is formed due to the influence of some chemical elements. This form is quite easy to treat, one has only to stop contact with the chemical.

Depending on the course of the disease, alveolitis is divided into:

  • chronic - characterized by a slow course, because of which the diagnosis of the disease is rather late, when it is difficult to cure the disease. The period of exacerbation of symptoms is replaced by a long time of their retreat,
  • acute - with this form, the first signs begin to appear in the interval from four to twelve hours.

Symptoms of fibrosing alveolitis are:

  • shortness of breath that occurs on the background of performing heavy physical exertion. In the later stages, such a sign is observed even with a slight activity,
  • cough without sputum or with a small amount of it,
  • a sharp decrease in body weight
  • swelling,
  • joint pain,
  • wheezing while breathing,
  • an increase in neck vein size,
  • human fatigue
  • the skin takes on a blue tint
  • severe pain in the chest, often passing under the shoulder blades,
  • muscle weakness
  • fever.

Signs of allergic alveolitis are:

  • inability to take a deep breath,
  • severe pain in the chest,
  • sputum cough
  • decreased performance on the background of rapid fatigue,
  • decrease or complete lack of appetite, which reduces body weight,
  • increased sweat
  • chills,
  • finger deformation
  • increase in body temperature
  • the blueness of the skin,
  • bouts of severe headache.

Upon termination of contact with the allergen, all the symptoms of alveolitis pass on their own.

General information

Alveolitis of the lungs refers to diffuse parenchymal lung diseases. This is a non-bacterial inflammation of interstitial tissue. A large group of parenchymal diseases (alveolitis) is united by a similar x-ray picture, in the clinic they are dominated progressive dyspnea (in this case, breathing is difficult) and there are functional impairments (mainly of a restrictive type).

The basis of respiratory disorders are changes in the elasticity of the lung tissue and limiting their smoothing during inhalation. About half of the alveolitis are diseases with an unknown etiology.

Interstitium this disease is the target of damage. This is the anatomical part of the lungs, actually their connective tissue skeleton and skeleton, in which there is a dense network of vessels, bronchi and bronchioles, alveoli. The interstitium is strong because it supports the shape of the respiratory tract, small vessels and air-containing spaces. On the other hand, it is thin and elastic, therefore it does not interfere with the processes. gas exchange. Especially thin and elastic interlobular interstitium, which supports the shape of the alveoli and thin capillaries involved in gas exchange.

The bronchi, as they branch in the lung tissue, decrease in diameter and the smallest alveolar bronchioles end with pulmonary alveoli (vesicles). The totality of them forms, in fact, the tissue of the lungs. These are spaces containing air separated by the thinnest partitions. Each partition is at the same time a wall of two alveoli, through which gas exchange occurs - oxygen enters and carbon dioxide is removed. It has collagen and elastic fibers that give elasticity, so the alveoli easily change the volume during inhalation and exhalation. The surface area of ​​the alveoli far exceeds the volume, which is important for high-quality gas exchange. The walls are lined with surfactant and liquid in which gases dissolve. Oxygen from the environment enters the alveoli, then capillaries and transferred to the cells of the body.

A special role in the process of breathing is given surfactant - fat-like substance that lines the alveoli. It reduces the tension force of the moisture in the alveoli and resists the collapse of the alveoli with a deep expiration. Without it, the surface tension would be 10 times higher than the norm, and the alveoli after exhalation stuck together and more effort would be required to expand them during inhalation. When inhaling, this substance is less densely distributed, so the lungs are well stretched. In addition to participating in the act of inhalation and exhalation, the surfactant dissolves oxygen and carbon dioxide (facilitates their diffusion), regulates the exchange of water and microcirculation in the lungs. Also helps to neutralize bacteria that have penetrated the alveoli. Surfactant is produced in utero and is constantly maintained throughout the life of a person.

Various lesions of the lung tissue somehow cause a thickening of the interstitium, changes in the alveoli and the quality of surfactant. Some changes pass after treatment, others take the form of chronic and incurable.

In general, these diseases are initially severe and progressive - in the interstitial tissue quickly develop cicatricial changes (fibrosis). If speak about idiopathic fibrosing alveolitis, it is very rare, with the highest prevalence among men (1.9: 1 in women) aged 40-70 years. Prevalence exogenous allergic alveolitis in recent years has increased. The frequency of occurrence is 42 per 100 thousand population.

To date, the causative factor that triggers the characteristics of idiopathic fibrosing alveolitis (ELISA) changes in lung tissue. Many authors consider fibrosing alveolitis autoimmune disease. In favor of this theory - the presence of circulating immune complexes, hypergammaglobulinemia and rheumatoid factor.

The role is discussed. adenoviruses, hepatitis C virus and Epstein-Barra. Indeed, viral proteins can increase chronic inflammation and activate collagen production.

Phased process in the lung tissue looks like this:

  • thickening and inflammatory infiltration of the alveolar wall,
  • filling the lumen of the alveoli with a secret and various cells
  • the loss of their usual structure,
  • violation of the architectonics of the lung tissue when bronchi and blood vessels are involved in the process,
  • development of cystic cavities.

In the later stages, the normal parenchyma is replaced by connective tissue, into which the expanded cystic alveoli are lined up, lined with hyperplastic epithelium, which does not fulfill its function. The lungs look compacted and shriveled.

The main place in the pathogenesis has alveolar macrophage - it is a cellular barrier in the way of penetration of components from the inhaled air. These cells are involved in the capture of alien respirable particles and the formation of an inflammatory response. The answer may be minimal or very active - up to damage to the lung tissue.

Under the action of immune complexes with an antigen (it is not known by ELISA) the macrophage is activated and secretes mediators. Some of them stimulate neutrophils and lymphocytes and cause their enhanced migration from the capillaries to the alveoli (edema inside the alveoli is formed).

Exudate with desiccated alveolar cells appears in the lumen of the air cavities. This stage corresponds to inflammation (alveolitis). The inflammatory process is first limited, then it can spread. Inside the alveoli is also found mucin, protein, crystals cholesterol, and neutrophils, macrophages and white blood cells. The walls of blood vessels, in the area captured by the inflammatory process, also thicken, and in the unaffected tissue may be normal.

In this disease, a characteristic is a change in the composition and amount of surfactant. With a decrease in its number or destruction, the ability of the lungs to stretch while inhaling is significantly reduced. Therefore, the depth of breaths in a patient decreases, and the frequency of breathing increases. Outwardly, it appears superficial and frequent breathing (tachypnea).

If alveolitis is not resolved independently or during treatment, inflammatory infiltration captures the interalveolar septum and fibrosis develops under the action of a different group of mediators that cause the growth of fibroblasts and smooth muscle cells. First, the structure of the small bronchioles and the interstitium surrounding them changes. Fibrotic processes extend to the vessels (they subside, causing deformation of the alveoli). When you break the walls of the alveoli and merge them with the bronchioles, smooth-walled cavities arise. As a result of such changes, the architectonics is completely disturbed - cystic cavities arise in the lungs, which are described by X-ray examination and CT scan as "cellular lung».

It should be noted that the process fibrosing very intense, so the primary role in the pathogenesis of the disease is assigned to fibrosing without a pronounced inflammatory process. In the processes of fibrosis, the significance is also assigned to mast cells, the number of which in areas of fibrosis is sharply increased. An increase is also found. histamine and tryptase (these are mast cell products). In patients with the progression of fibrosis and respiratory failure, chronic pulmonary heart arises.

Condition of development exogenous allergic alveolitis (EAA) is the inhalation of any antigenic material in a sufficient dose and a certain time. If the antigen has a size of up to 5 microns, it is deposited in the alveoli and bronchioles, giving rise to the development of the disease. Larger particles are fixed in the bronchi of a larger caliber, and if the allergen is soluble, then it dissolves and causes the same effect. Most people do not get sick, which is probably due to genetic factors and an immune response.

Surely allergic alveolitis - It is an immunopathological disease, since in its occurrence its main role is played by allergic reactions (type 3 and 4). Non-immune inflammation also matters. The third type is associated with the formation of immune complexes that play a role in the early stages of the disease. In the interaction of antigen and IgG in the interstitium, immune complexes are formed, which have a damaging effect on the interstitium and alveoli. As a result of increased capillary permeability, neutrophils rush into the zone.

Immune complexes activate alveolar macrophages. Active neutrophils and macrophages, in addition to the release of pro-inflammatory agents, produce toxic products (cytokines and oxygen radicals). They in turn cause further damage to the interstitium and increase the inflammatory response. In addition, lymphocytes and monocytes are attracted to the zone of inflammation, which already support delayed-type allergic reactions.

Type 4 immune responses are associated with T lymphocytes and determine the reaction of the delayed type. These reactions develop two days after inhalation of the antigen. Cytokines, which were released in the first stage of damage, significantly increases the influx of lymphocytes and monocytes into the focus. CD4 + lymphocytes secrete gamma interferon, which activates macrophages. Thus, the delayed type reactions are constantly maintained, and this causes the formation of granulomas, activates fibroblasts, an excessive synthesis of collagen, which ultimately leads to interstitial fibrosis. The presence of T-lymphocytes (in the blood of the patient and lungs) histological confirmation of granulomas and interstitial fibrosis are evidence of the presence of type 4 reactions in the patient's body.


All interstitial lung diseases can be divided into diseases of unknown nature, known and secondary (for example, in systemic diseases, hepatitis, biliary cirrhosis, Crohn's disease, CKD, chronic lymphocytic leukemia, thyroiditis Hashimoto).

The classification of interstitial lung diseases (1984) identifies the following types of alveolitis:

  • allergic alveolitis of the lungs,
  • idiopathic fibrosing alveolitis,
  • toxic fibrosing alveolitis.

From the title exogenous allergic alveolitis (EAA) it follows that the disease has a precisely established allergic nature and develops under the influence of allergeningested from the outside. Exogenous allergic alveolitis can cause more than 200 allergens, prolonged inhalation of which causes immune inflammation in the lungs and activates the development of fibrosis. So, there are known diseases that are caused by inhaling dust with animal and vegetable proteins (syndromes: "farmer's lung», «light cheese», «poultry farmer's lung»).

The list of these factors is constantly expanding, which is associated with the emergence of new medical products, industrial development and constant environmental pollution. Therefore, today emit toxic alveolitisassociated with the inhalation of vapors of heavy metals or taking certain medications (mainly chemotherapeutic bleomycin and busulfan, and Amiodarone).

In this regard, there is another classification of interstitial lung diseases, which is based on the etiological principle (for the causes of the disease). Selected diseases associated with hazards and exposure to drugs:

  • exogenous allergic alveolitis,
  • toxic fibrosing alveolitis,
  • pneumoconiosis,
  • interstitial fibrosisthat occurred during radiation injuries.

Generalized data tables will help to understand this in more detail.

Thus, exogenous allergic alveolitis (synonym - hypersensitive pneumonitis) Is a group of related diseases that combine diffuse changes of the parenchyma and bronchioles, which have arisen in response to repeated inhalations of various antigens. The description of the first cases of the disease among farmers who worked with moldy hay dates back to 1932, and in 1965 the disease was described among amateurs who bred pigeons. A common cause of the acute and recurrent form of the disease in adults are mold and yeast-like fungi, subacute - animal proteins, and chronic - dust (library or building).

In this regard, allergic alveolitis has a different course and prognosis. In some cases, the disease is completely reversible, in others, irreversible damage to the lung tissue occurs. It depends on many factors: the exposure of the antigen, the immune response of the person, the nature of the inhaled allergen.

Since the clinic and course are diverse, in most cases this group of diseases is not diagnosed in a timely manner, which ultimately leads to the progression of the disease. Most researchers come to the conclusion that 5-15% of those who have been exposed to a high concentration agent, develop EAA. The prevalence of the disease by inhalation of low concentrations of the allergen has not been established.

Fibrosing alveolitis has a different origin. Term idiopathic fibrosing alveolitis (ELISA) means, first of all, the unknown nature of the occurrence of this pathology and its characteristic rapid development of fibrosis - the progressive replacement of normal lung tissue with connective tissue. This process is accompanied by a violation of gas exchange, rapidly progressive respiratory failure and the rapid death of the patient. Since the existing theories of viral and autoimmune origin did not receive the necessary evidence, there are certain difficulties in treating this disease. Currently synonymous with ELISA is "common interstitial pneumonia».

As stated above, nature idiopathic fibrosing alveolitis until the end is unclear. A certain role is played by provoking factors, of which you can specify:

  • smoking,
  • environmental aggression (ozone, chlorine, sulfur oxide, industrial and automotive emissions),
  • genetic factors
  • occupational hazards.

According to one theory, professional factors are related to the causes: contact with metal (brass, lead, nickel, steel) and wood dust (in carpenters). The role of asbestos, silicate and silicon dust is not excluded. The presence of familial forms of the disease is in favor of genetic theory.

The etiology of exogenous alveolitis is associated with antigenswith which a person is constantly confronted by the nature of his professional activity. The most important in agriculture are bird antigens and actinomycetes (bacteria that possess the properties of fungi). The latter are found in soil, water, and compost. They actively reproduce during decay and in the water of heating systems (the optimum temperature for this is 50-60 0 С). Actinomycetes cause the development of "easy farmer", growing mushrooms, working with sugar cane and in persons using air conditioning.

Avian antigens are proteins gamma globulin and albumin, which contain the secretion of glands and excrement of pigeons, turkeys, parrots, canaries, and others. Fungal antigens more common Aspergillus spp.callingbrewer's lung», «cheese makers», «farmer», suberosis (when working with cork) and the disease in persons staying in damp and unventilated areas.

Ideopathic fibrosing alveolitis (ELISA)

Symptoms of alveolitis are non-specific and, at first, do not allow a correct diagnosis. The onset of the disease is invisible and the main symptom is dyspnea at first not very pronounced and does not bother the patient. There may be a rare cough without sputum. Such a clinical picture is characteristic of the subacute course. With exacerbations and progression of the disease, shortness of breath increases, there is a periodic increase in temperature.

ELISA in some cases begins with acute symptoms like a viral infection. Increasing shortness of breath, coughing and fever make the patient consult a doctor, but he is diagnosed pneumonia of bacterial genesis and treatment antibiotics does not bring results. The condition improves somewhat, but without proper treatment, the disease progresses.

When listening to the lungs is determined by a characteristic phenomenon - crepituslikecellophane crack". It is heard most often in the lower back areas, but in 1/5 of the patients, crepitus appears in the upper sections. Unlike crepitus with other pulmonary in this case, it is not loud and is heard at the height of inhalation.

When working with chemical compounds (plastics, polyurethane dyes, resins), this disease can also occur. In Moscow, avian and fungal antigens are the leading causes of allergic alveolitis.

In chronic course, the condition gradually worsens, and the patient adapts to shortness of breath, reducing activity and may not consult a doctor for a long time. Most at the time of treatment and examination have experience of the disease from 6 months to a year. With a sharp progression, which is associated, for example, with a viral infection or adherence pneumonia, the condition worsens considerably: due to shortness of breath, the patient cannot walk and even speak, let alone serve himself, a rise in temperature is possible. 50% of patients noted tachypia (rapid shallow breathing), which requires less energy.

For fibrosing alveolitis in the late stages is characterized by the development of emphysematous bullthat burst and spontaneous arises pneumothorax. This emergency condition also makes you consult a doctor.

Other symptoms are weakness, pain in the joints and muscles, weight loss, changes in the phalanges of the nails ("Drumsticks", This symptom prevails in men). The presence of the patient symptom "drum sticks"Combined with a heavier prognosis.

The terminal stage of fibrosing alveolitis is characterized by severe respiratory failure and the development of pulmonary heart. The patient is celebrated cyanosisswelling, swelling of the neck veins.

Cyanosis in pulmonary insufficiency is due to poor saturation of blood in the lungs. Its intensity increases, it is diffuse, but more pronounced at the tips of the ears, nose and fingers. The swelling of the cervical veins is the result of increased venous pressure in the systemic circulation and indicates a decompensated pulmonary heart.

Edema occurs in right ventricular failure in conditions of severe hypercapnia. When this occurs, enhanced reabsorption of sodium in the kidneys, which leads to fluid retention. Edema first appear on the feet and legs, and then spread to the upper parts of the body. In the morning hours, swelling is less, and in the evening they increase.

At this stage, there are constricting and pressing pains in the region of the heart, which are associated with:

  • metabolic disorders in the myocardium due to hypoxia,
  • undeveloped network of collaterals in hypertrophied heart tissue,
  • myocardial overload due to increased pressure in the pulmonary artery,
  • narrowing of the coronary vessels (pulmonary coronary reflex).

Laboratory research

In the diagnosis of allergic alveolitis, importance is attached to the identification of specific antigens. Of particular importance is the determination of precipitating antibodies to the antigen by methods immunoelectrophoresis and immunoassay. Precipitating antibodies are detected in the acute course, and are detected in the serum for another 1-3 years after the cessation of contact with the antigen. In chronic course, antibodies are not detected. There are also false-positive test results. When EAA level of antibodies is not associated with disease activity. Thus, the presence of antibodies does not in all cases confirm the diagnosis, their absence does not exclude its presence.

Laboratory tests for idiopathic form are not of great importance, since in all cases there is an increase ESR, detected CIC (immune complexes), increased levels of immunoglobulins. A promising marker is the level of surfactant proteins A and D. In view of the increased permeability of the membrane of the alveoli, surfactant proteins increase, which reflect the activity of the process. Blood test mucinantigenov also allows to evaluate the activity of alveolitis.

X-ray of the lungs

It is not specific, especially in the early stages, and does not make it possible to reliably distinguish ELISA from other diffuse lung diseases. On the radiograph there is a symmetrical amplification of the pulmonary pattern, and then its deformation, which are more pronounced in the lower sections. In the early stages, a decrease in the volume of the lung fields and a decrease in their transparency can be detected (the phenomenon offrosted glass"). Characteristic development bullous emphysema, which may appear earlier than other changes in the pulmonary pattern. Not characterized by the involvement of the pleura, the increase in lymph nodes, as well as local seals in the parenchyma. In this disease, the lung tissue is affected evenly.

It is important to study in dynamics, when the progression of the pulmonary pattern becomes coarse, and cysts 1-2 cm in size reflect the reticular type of the lung parenchyma structure. This indicates the development of "cell lung»(Light as a honeycomb): thickened partitions between the alveoli cover swollen lobules and acini. In the later stages, the trachea is shifted to the right and its increase. However, in some patients, already with a histologically proven diagnosis, there may be no radiographic changes.

Changes on radiographs with allergic alveolitis are the same, and vary from normal (with acute and subacute forms) to pronounced fibrosis and "cell lung". Also, it is possible that the changes on the radiograph are absent even with fibrous changes in the biopsy material and hypoxemia in the patient. In acute and subacute form, changes like “frosted glass". Changes in the X-ray of the lungs in acute alveolitis are resolved within 4-6 weeks, if repeated contact with the allergen is ruled out. The situation is much more complicated in the chronic form, which reaches the phase “cell lung».

CT scan

It helps to reliably diagnose and judge the degree of activity. The accuracy of diagnosis reaches 90%. Signs of "cell lung"Are found in 70% of cases, compared with 15-20% during radiography. Changes are localized mainly in the basal regions of the lungs.

Phenomenon "frosted glass"Appears with a slight thickening of the walls of the alveoli and interstitium and a small filling of the alveoli with liquid or cells. CT picturefrosted glassIs a more favorable prognostic sign. Such patients respond well to treatment. steroids, and the improvement of their condition is reflected in the improvement of the picture on CT. The inflammatory response (namely, alveolitis) is an indication for corticosteroid therapy, from which an effect can be expected. This survey allows us to estimate the prevalence of the lesion when compared with a biopsy specimen taken from one area.

In the presence of emphysema, a CT scan can assess its severity and distinguish it from cystic changes that reflect the final stage of the disease. Dynamic computed tomography provides insights into changes in hemodynamics in the lungs and pulmonary hypertension. Thus, this examination is comparable in significance to a biopsy, which is considered the “gold standard” for diagnosing this disease. The use of CT is important to monitor the effectiveness of treatment. In the case of the allergic nature of the disease, the changes have much in common. After the disappearance of contact with the agent, the changes may diminish and even disappear.

Investigation of respiratory function

The total capacity of the lungs is reduced, the bronchial patency is significantly reduced, the ability to expand the lung tissue is lost. A valuable indicator in this study is the diffusion capacity of the lungs. It is closely related to the symptom dyspneaand a pronounced decrease indicates the development pulmonary hypertension. Functional changes in EAA are non-specific and completely coincide with those in ELISA.

Bronchoalveolar lavage

This is a way to get flushes from the bronchioles and alveoli for subsequent different types of research. It is important that in this study material is obtained from the lower parts of the pulmonary tree. When compared to biopsy, then in this survey material is obtained from a larger number of alveoli. The method is not invasive (the fence is carried out through bronchoscope), it can be repeated many times, and it has diagnostic significance, since the course and prognosis of fibrosing alveolitis is assessed.

The total number of cells in the washout with this disease is significantly increased and mainly due to neutrophilic. But in addition, an increased amount of collagenase - a product of neutrophil secretion, namely, it plays a role in the pathogenesis of fibrosis. There is also an increase eosinophil.

Eosinophilia is often associated with a poor prognosis and such patients have an insufficient response to steroid therapy, and treatment cyclophosphamide and Prednisone in combination gives a good result.The number of neutrophils and eosinophils correlates with activity. Sometimes detected lymphocytosis (high content of lymphocytes), which indicates a pronounced alveolar inflammation and in the absence of a “cellular lung” steroid therapy gives a good result.

Diagnostic value and other components

For example, circulating immune complexes that are significantly elevated in this disease. Some studies have shown that with their high level, steroid therapy is effective. Immunoglobulin G is also elevated. The lipid composition reflects the state of surfactant, which changes significantly (the number of phospholipids decreases and the ratio of fractions changes). The more phospholipids in a wash, the more favorable the prognosis. Another component of surfactant (surfactant protein A) is a marker of activity, but its content in ELISA is significantly reduced.

Blood Gas Analysis

In the early stages, the gas analysis of blood at rest almost does not change, and during exercise it is noted desaturation (decrease in blood oxygen saturation). As it progresses hypoxemia (decrease in oxygen content) is recorded at rest and, in addition, is accompanied by hypocapnia (excess CO content2) at terminal stages.

In case of doubt, recommend lung biopsy. Indications for use is:

  • inability to establish a diagnosis
  • lack of "cell lung»,
  • choice of treatment method.

This method is necessary for reliable diagnosis and the appointment of the correct treatment, which has serious side effects, so it is unacceptable to subject the patient with an unspecified diagnosis. A biopsy can determine the specific factor that caused fibrosis (for example, asbestosis), and also allows you to confirm other diagnoses (sarcoidosis, alveolar carcinoma, lymphoma, eosinophilic pneumonia).

The diagnostic information content of this method is more than 94%, and the number of complications ranges from 6–19%.

There are several methods of biopsy:

  • open biopsy
  • transbronchial,
  • videothoracoscopic,
  • percutaneous puncture.

Open biopsy make in case of impossibility of carrying out less traumatic biopsy. It is performed under anesthesia through the cuts of the chest wall from the sites with the greatest changes, which are determined on radiography (CT), and from the site where the parenchyma is still preserved. 2 - 4 samples are taken from the lower and upper lobes. The material is used for morphological, bacteriological studies, as well as other studies (immunofluorescent, immunohistochemical). For patients who have pronounced functional disorders of the lungs, surgery is a serious intervention, and it is contraindicated.

Transbronchial It is performed during bronchoscopy by taking tissue through a puncture of the bronchus. The disadvantage of this type of biopsy is the small size of the sample and less informative. When ELISA does not matter much and informative, and when EAA applies. The advantage is safety compared to the previous option.

Videothorascopic It gains great popularity, in view of the smallest traumatization (two small punctures are made), but it allows to make samples in the same amount as with the open method. The study and the fence is carried out under visual control. thoracoscopewhich is inserted through punctures. This examination reduces the complications and the duration of the patient's stay in the hospital.

Percutaneous biopsy. It is performed under conduction anesthesia with a cutting needle, the device of which allows carving a piece of the parenchyma or aspirating the material. Place of entry is chosen under the control of CT. Informativeness is 70%.

The listed procedures are more often performed by the patient of younger age and with not expressed functional disturbances.

Causes of pathology

Alveolitis occurs when any aggressive factor damages the thin wall of the alveoli.

In the event that the cause of such damage is unknown, talk about idiopathic alveolitis. As an independent disease, alveolitis of the lungs can also occur with certain allergic reactions and chemical damage.

The disease resulting from allergies is called exogenous alveolitis. Most often it causes prolonged contact with hay, spores of fungi, plant particles and various dust. In the alveoli of the lungs penetrate only the smallest invisible particles that cause inflammation of an allergic nature.

In addition, there is a kind of alveolitis, which occurs due to the direct toxic effects of certain substances. Most often, such substances are aggressive chemical compounds, for example, mercury vapor.

All of these options are separate nosological forms of alveolitis. But the latter can occur not only as a separate disease, but also as a syndrome of other pathological processes.

These include systemic lupus erythematosus, sarcoidosis, systemic scleroderma, rheumatoid arthritis, vasculitis, and certain liver diseases.

In these cases, in addition to the underlying disease, there is a lesion of the alveolar sacs with a gradual degeneration of the lung parenchyma into the connective tissue.

Fibrosing idiopathic alveolitis

Presumably, the lung tissue is damaged due to a poorly studied autoimmune response. The disease has a progressive nature and is very difficult to treat.

The danger of fibrosing alveolitis is that it is impossible to exclude a factor that damages the lungs. The body itself begins to destroy the alveolar sacs.

At the same time, connective tissue appears quickly enough in different parts of the lungs. For a long time, the disease does not make itself felt, manifesting itself only when some parts of the lungs can no longer be saved.

According to the author, this pathology is called Hammen-Rich syndrome. The old name for pathology is diffuse interstitial pneumofibrosis. This is a diagnosis of exclusion, which is made after any probable etiological factor of alveolitis is excluded.

Exogenous alveolitis

This pathology most often develops in agricultural workers. The reason for this is the constant inhalation of dust containing particles of hay and grain crops, tree bark, spores of mushrooms, fur of various animals and even pieces of cheese. The mechanism of inflammation in this case is allergic. Aggression factors damage the alveoli indirectly through inhaled dust.

Exogenous alveolitis can be acute, subacute and chronic.

Acute occurs when a very large number of damaging particles enters the alveoli simultaneously. He can pass without a trace.

Subacute exogenous alveolitis is a consequence of a prolonged acute illness. Chronic pathology develops gradually, it is extended over time for several years.

The process can be stopped by eliminating the damaging factor. It is recommended that such patients change their occupation and sometimes their place of residence.

Alveolitis of the lungs - symptoms

Any type of alveolitis may be asymptomatic for a long time. The exception is those acute processes that lead to pulmonary edema. In chronic course, symptoms develop gradually.

Symptoms of alveolitis of the lungs include:

  • Reduced tolerance to physical exertion. At rest, the lungs do not function fully, but during physical exertion, they need the entire volume stock. Since part of the parenchyma is replaced by connective tissue, there is no increase in volume during loading. This leads to intolerance to playing sports. Even those that used to be familiar. This symptom is an early precursor of fibrosis in the alveolitis.
  • Cough. This symptom may occur as in acute alveolitis due to exudation of the alveoli, and in the chronic process. In the first case, cough is most often productive, but rare. In the second case, the patient suffers from a chronic dry cough, sometimes with a small amount of sputum. It appears when fibrous tissue affects the bronchi and irritates the cough receptors that are in them.
  • Dyspnea. Shortness of breath is a late symptom that occurs with the development of respiratory failure. At the beginning it appears during physical exertion, then with any movements, and after - and at rest. The severity of shortness of breath is directly related to the volume of the affected tissue.

The most variable is pain syndrome. In some patients it is expressed quite intensively, in others it is completely absent.

Pain syndrome with alveolitis

A large number of receptors contains the pleura, covering the lungs. If any irritating factor affects it, the patient experiences severe chest pain.

Alveolitis of the lungs may be accompanied by damage to the pleura. This occurs in those cases, if the connective tissue is too much, it grows on the periphery, forming small tubercles.

These bumps irritate the pleura and each breathing movement causes severe pain in the chest. Pain in patients with alveolitis appears in the later stages of the disease.

Principles of therapy

The treatment of this pathology depends on its type.

Fibrosing alveolitis is treated by suppressing immune responses. To do this, glucocorticosteroid drugs are first used, for example, dexamethasone.

For the treatment of exogenous toxic alveolitis, it is necessary, first of all, to exclude the effect of the damaging factor. In the initial stages of the disease this may be enough.

In case of severe inflammation, glucocorticosteroids are used as anti-inflammatory drugs. At the same time, their local use is possible in the form of inhalations, for example, beclomethasone.

Prognosis and prevention

The prognosis of alveolitis depends on its type and on how quickly it was diagnosed. The most unfavorable is idiopathic alveolitis of the lungs, since in this case it is impossible to remove the aggression factor. This pathology has a progressive course and is difficult to treat.

Early diagnosis and timely treatment can stop the progression of the disease and preserve most of the lung. Prevention of the development of alveolitis is the exclusion of the effect of damaging factors on lung tissue. For this, compliance with safety regulations and the wearing of personal protective equipment at work is important.


Of corticosteroids applied Prednisolone. The mechanism of anti-inflammatory action of the drug is versatile. It suppresses the release of inflammatory mediators and reduces vascular permeability. In addition, reduces the sensitivity of receptors to inflammatory mediators. Also important is its immunosuppressive effect - reduces the production of antibodies, prevents the migration of lymphocytes and blocks the synthesis of interferons. The clinical effect is manifested by a decrease in inflammation and swelling of the tissues, suppression of the development of connective tissue.

The drug is prescribed at 1.0-1.5 mg per kg of body weight per day (or equivalent in equivalent dose) during the first 4 weeks. If there is an improvement, the next 3 months the dose is reduced to 0.5 mg and gradually reduced to 0.25 mg per kg of body weight over 6 months - this is the minimum duration of treatment. Most often, the entire dose is prescribed in the morning after breakfast. GCS treatment is effective in only 15–20% of patients. The main mechanisms of action of corticosteroids: the suppression of migration in the lung tissue of neutrophils and monocytes, the suppression of the release of cytokines and the suppression of the immune response.


If, despite treatment with sufficiently high doses of corticosteroids, there has been a deterioration in clinical and functional parameters, the issue of prescribing cytotoxic drugs — second-line drugs — is decided.

From this group more often use Azathioprine. The main mechanism of its action is the blockade of DNA synthesis, the suppression of the number of lymphocytes (T and B lymphocytes, the proliferation of which is one of the components of the immune response) and the synthesis of antibodies. Assign it at a dose of 2-3 mg per kg of body weight (maximum daily dose of 150-200 mg). Treatment begins with 25 mg, increasing by 25 mg every two weeks to the maximum dose.

From the group of cytostatics can be assigned cyclophosphamide. Its action is expressed in reducing the number of lymphocytes. The drug inhibits the proliferation of predominantly B-lymphocytes, which are involved in the immune response. Assign 2 mg per kg of body weight (maximum dose is also 150 mg per day). The appointment is the same as the previous drug: from the minimum dose to the maximum.

With rapid progression, intravenous courses are effective. Prednisolone 250 mg (pulse therapy) every 6 hours or administration cyclophosphamide 2 mg / day for 3-4 days in a row.

Azathioprine, compared with the last drug, has a lower immunosuppressive effect, but has a stronger anti-inflammatory effect. The effectiveness of treatment with cytostatics is estimated after 3 months.


CyclosporineBUT - A selective immunosuppressant acting on T lymphocytes is specific and reversible and prevents their activation. The latter play a role in the process of inflammation in this disease. The drug suppresses humoral and cellular immunity. Combination it with Prednisone showed sufficient effect. Unlike cytostatics, it does not suppress hematopoiesis, but the severity of other adverse reactions (arterial hypertension and renal failure) requires discontinuation of the drug.

Preparations inhibiting collagen synthesis

The effectiveness of drugs that inhibit the synthesis of collagen (Kuprenil, Colchicine) not fully proven. It should be noted that these drugs cause side effects, so they are used according to the decision of the doctor if necessary.

D-penicillamine,Kuprenil inhibits further fibrosis and is more effective with the rapid progression of the disease. The initial dose of 300 - 450 mg / day with an increase of 300 mg weekly. The maximum daily dose of 1800 mg.

ColchicineIt may be a promising drug, because it reduces the conversion of procollagen to collagen and inhibits the proliferation of fibroblasts. Assign 0.6–1.2 mg / day along with prednisone. This combination caused an improvement in 22% of patients and stabilization of indicators. Nevertheless, progression of the disease was observed in 39% of patients. Adverse reactions include diarrhea and muscle weakness.

In combination with GCS and cytostatics prescribed drugs Omega-3 PUFAs that have an anti-inflammatory effect affecting the exchange of arachidonic acid. Daily dose Omega-3 PUFA 0.8-1.0 g. For the purpose of blood thinning, which is observed in the later stages, intravenous administration of the solution is indicated. sorbitol.

Mucolytic Acetylcysteine also known as an antioxidant. Publications of some authors indicate its effective use for fibrosing alveolitis when included in the treatment regimen with prednisone. When applied during the year in patients with decreased progression of respiratory failure.

Possible adverse reactions

Treatment of corticosteroids and cytostatics causes the development of adverse reactions. However, remission in cases of fibrosing alveolitis does not occur without treatment, and there is no alternative to the above groups of drugs.

Taking glucocorticosteroids may provoke stomach ulcer, cataract, obesityan increase in intraocular pressure and general blood pressure menstrual disordersa rise in blood sugar and hypokalemia. Serious complications are spinal fractures, myopathy, bone necrosis, osteoporosis. Even a short course of SCS can cause osteoporosis. Elderly cases are frequent depressions and psychosis.

Treatment with cytostatics requires mandatory monitoring of leukocytes and blood platelets. With a decrease in their level of treatment, they either suspend or reduce the dose by 50%. Weekly monitor the degree of recovery of leukocytes and platelets. If their number is not restored, cytostatics cancel until the normalization of the blood.

In addition to the negative effects on the blood, Azathioprine has a pronounced hepatotoxic effect. Therefore, patients are determined monthly transaminase. If their level exceeds the norm by 3 times, the treatment is stopped or the dose of the drug is reduced. At reception Cyclophosphamide hemorrhagic cystitis may develop, so patients are advised to drink plenty of liquids, and check urinalysis twice a month. The entire period of treatment, except for monitoring the clinical and biochemical analysis of blood, the patient is carried out spirometry 1 time per month.

Treatment of exogenous allergic alveolitis

The principles of treatment of EAA of any form are the same, but the main point is the elimination of the allergen. While maintaining contact, there is a risk of developing an irreversible chronic disease. That is why early diagnosis is important because progression can be prevented.

The use of systemic corticosteroids remains the only method of treatment. In acute cases, a dose of prednisone 0.5 mg per 1 kg of body weight is recommended, which is recommended for 3-4 weeks. According to the treatment regimen, with subacute and chronic allergic alveolitis, the dose Prednisolone increase to 1 mg per kg of body weight and prescribe up to 2 months. Then gradually reduced to 5-10 mg per day. Cancel the drug when achieving improvement, as well as in the absence of effect. The possibilities of inhalation use of corticosteroids are not well understood.

If no effect is assigned D-penicillamine and Colchicine. Results of successful treatment were obtained on animal models. Cyclosporin.

A drug Ambroxol It stimulates the production of surfactant, which stimulates the activity of macrophages, therefore its inclusion in the treatment is reasonable. Ambroxol appointed in the form of nebulizing inhalations (15 mg / day) 2 times a day while taking GCS, but in a reduced dose - 10 mg / day. This treatment regimen is most often used for subacute course. In the chronic variant, the combination of GCS and cyclophosphamide.

As the progression of the alveolitis of any genesis, the pulmonary heart failure increases, which requires additional therapy. The main treatment areas include the following groups of drugs.

  • Diuretics: Veroshpiron, Furosemide, Torasemide and others.
  • Nitrates. Reduce the pressure in the pulmonary artery, providing a vasodilating effect mainly on peripheral vessels (veins). This reduces the venous return of blood, and the filling of the left ventricle. Moderate dilatation of arterioles reduces peripheral resistance. Thus reduce pre-and afterload. In addition, they eliminate coronary spasm and dilate the arteries of the heart, reducing pain. Apply on doctor's prescription: Nitroglycerine, Nitrocore, Nitrosorbide, Olikard, Monosan, Pectrol.
  • ACE inhibitors. The result of their action is a decrease in peripheral resistance and an increase in cardiac output. They have a uniform arterial and venous vasodilation, their important effect is to reduce the retention of salt and water. Use: Lipril, Perindopril, Ramipril, Ranite, Akkupro, Tritatse.
  • Calcium Antagonists. This group of drugs is preferable in the presence of hypertension in the elderly, pain in the heart area and associated broncho-obstructive diseases. The drugs slow down the progression of myocardial hypertrophy. Verapamil, Nifedipine, Kordafen, Nimodipine, Felodipine, Amlodipine, lercanidipine.
  • Potassium and Magnesium Preparations shown in the appointment of diuretic drugs that cause electrolyte disturbances. From this group apply Aspark, Doppelgerts Active Magnesium + Potassium other.

Procedures and operations

The most important treatment at the stage "cell lung" is an oxygen therapy not less than 15 hours a day. Breaks between sessions no more than 2 hours. Its task is correction hypoxemia. For oxygen therapy, autonomous or portable sources of oxygen (gas cylinders or tanks with liquid oxygen) are necessary.

As oxygen delivery systems are used nasal cannula. Oxygen delivery occurs in the initial phase of inhalation, and the rest, unfortunately, is spent idly. For more efficient delivery, oxygen-saving devices are used: pulsating devices, reservoir cannulas and transtracheal catheters.

A prerequisite for the application of this method is constant monitoring of the state oxygenation. Held pulse oximetry - measurement of oxyhemoglobin in the blood. You can determine the gas composition of blood. Long-term oxygen therapy is an expensive way, but in the stage of the “cellular lung” it is an opportunity to prolong life. However, the survival rate of patients on long-term oxygen therapy is low.

With the ineffectiveness of conservative treatment is recommended. lung transplantation. Indications for it: dyspnea - class III, hypoxemia during exercise, a decrease in DLCO below 30%. However, being on the waiting list, you can wait several months or years, and this is very much for patients with ELISA, because they have the lowest survival rate compared with patients with other bronchopulmonary pathology and in need of transplantation.

Fibrosing alveolitis in children occurs very rarely, and the problem of allergic diseases at this age is relevant. Not well-known pediatricians is a form of allergic lung disease - exogenous allergic alveolitis. Nevertheless, this is the most severe pathology of the lungs of an allergic nature at this age, which, taking a chronic course, leads to disability. However, early diagnosis and adequate treatment can prevent progression and improve the prognosis.

This disease occurs in the range from 1 year to 16 years. Caused by the same factors as adults. But children who have a predisposition to allergic reactions usually get sick. Most manage to trace the causal relationship: living in damp areas, close contact with animals and birds (parrots). Often the disease occurs after a stay in the village, where the child has been in constant contact with poultry and animals. For the most part, children are ill - the villagers who have contact with hay and birds, or living in the area of ​​the elevator.

Clinical manifestations

In young children, the disease begins acutely, with severe shortness of breath, intoxication, cough and the presence wheezing in the lungs, fever. In children with an allergic predisposition, the onset of alveolitis occurs in dyspnea as in bronchial asthma. The severity of the manifestations is always expressed and requires hospitalization.

When contact with an allergen is terminated, recovery is possible, and with continued contact with allergens, relapses occur which are longer and harder. With constant contact, while remaining unrecognized, the disease becomes chronic.

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