Exogenous allergic alveolitis


Introduction to exogenous allergic alveolitis

Exogenous allergic alveolitis (extrinsicallergicalveolitis) is an allergic alveolitis caused by repeated inhalation of certain antigenic organic dust, often involving the terminal bronchioles. The US literature uses the name hypersensitivity pneumonitis. The domestic reports mainly include farmers' lungs, bagasse workers' lungs, mushroom workers' lungs, parrots' lungs and humidifiers' lungs. Although their causes are numerous, pathological, clinical symptoms, signs and X-ray findings are very similar.

basic knowledge

The proportion of illness: 0.002%

Susceptible people: no special people

Mode of infection: non-infectious

Complications: respiratory failure, pulmonary heart disease


Etiology of exogenous allergic alveolitis

Exogenous allergic alveolitis has many causes, such as actinomycetes and fungal spores, animal and plant proteins, bacteria and their products, insect antigens and certain chemical substances, and some of the dust's antigenic properties are still unclear. It is generally believed that the cause of peasant lungs is mainly common high-temperature actinomycetes. In recent years, domestic scholars have reported another high-temperature actinomycetes associated with peasant lungs, a thermostable Streptomyces, in many antigens, thermophilic Actinomycetes are the most common and important, especially microspores, followed by common high-temperature actinomycetes, which have the form of fungi, but belong to bacteria, which are produced in moist, warm, mildewed organisms, compost, soil, Food and contaminated water contain a large amount of this bacteria. Farmers inhale moldy hay, cereals and sugarcane are often prone to disease. There are many thermophilic actinomycetes in the air for planting mushroom fertilizer and production environment, and they are placed at ordinary high temperature. The main bacteria, the inhaler of the grower can cause the mushroom to work, the lungs of the poultry breeder (such as the pigeons, the parrots, etc.) are due to bird serum and bird droppings. It is caused by feather powder and bird eggs. Some people think that the powder cream on the pigeon feather is a keratin particle antigen of about 1 m in size, and its pathogenic effect is more important than pigeon serum and excrement. Textile workers inhaled the silk dust in the air of the workshop (probably sericin) and caused allergic alveolitis. The cause of the humidifier and air conditioner lung is white thermophilic actinomycetes, which is widely used in the chemical industry. After inhalation of isocyanide, phthalic anhydride, etc., its hapten effect may also cause allergic alveolitis. The antigenic properties of tobacco growers, tea growers, etc., are not fully understood.

In recent years, exogenous allergic alveolitis is considered to be an immune complex disease. Type III allergy is an important mechanism, and it also involves type IV allergy. Activation of the complement system has important significance, and activated alveolar macrophages may be the onset. The central link of the mechanism.

(1) Complement-mediated type III allergic reaction occurs 4 to 8 hours after the sensitized individual is exposed to the antigen again. Arthus reaction can occur 4 to 6 hours after intradermal injection of the antigen, and IgG is found in the skin specimen at the reaction site. And the precipitate of complement, the precipitated antibody (genus IgG) of the corresponding antigen can be found in the serum of most patients. The application of antigen for bronchial provocation test can show the same lung function change as clinical exogenous allergic alveolitis, so the disease and complement It is related to the type III allergy, and the immune complex is of great significance.

(II) T lymphocyte-mediated type IV allergic reaction In recent years, it is noted that type IV allergic reaction plays an important role in the pathogenesis of this disease. The pathology of patients has a formation of caseous granuloma, and lymphocytes encounter corresponding antigens in vitro. It can produce macrophage migration inhibitory factor (MIF). Animal experiments have found that sensitized T lymphocytes are implanted into experimental animals, and then inhaled antigen to stimulate, causing lung injury similar to human exogenous allergic alveolitis. In the bronchoalveolar lavage fluid of patients with exogenous allergic alveolitis, the increase of lymphokines was also found. All of the above findings support the role of type IV allergy in the pathogenesis of this disease.

(C) the role of local macrophages with mildew and subtilis can directly stimulate alveolar macrophages to cause proteolytic enzyme release, cleavage of C3 and release C3b, the latter binds to the complement receptor on the surface of macrophages Further activation of macrophages, followed by lung tissue lesions including granuloma formation.

At present, it is apt to think that exogenous allergic alveolitis is initially mediated by type III allergy, and then turns to type IV allergic reaction, while macrophage activation and the resulting inflammatory response can be shared through non-immune pathways. Causes lung damage, but many details are unclear.


Exogenous allergic alveolitis prevention

Completely avoid contact with pathogenic organic dust is the most fundamental prevention and control measures, improve the production environment, pay attention to dust, ventilation, and strictly abide by the operating procedures such as harvested hay and grain should be dried and put into the warehouse; places where poultry are kept are often cleaned and properly disposed of. Bird manure; the water in the humidifier and air conditioning system is kept clean and avoids pollution; for operators in the environment polluted by organic dust, it is advisable to have regular medical monitoring, and there are obvious chronic respiratory diseases such as chronic asthmatic bronchitis and bronchi. Asthma, chronic obstructive emphysema and allergic constitutions should not be engaged in close contact with organic dust.


Exogenous allergic alveolitis complications Complications, respiratory failure, pulmonary heart disease

In advanced cases, there are usually respiratory failure and pulmonary heart disease.


Exogenous allergic alveolitis symptoms common symptoms pulmonary interstitial fibrosis dyspnea tachycardia allergic cough dry cough chills respiratory failure labor dyspnea impotence chest tightness

The pulmonary symptoms of exogenous allergic alveolitis are not specific. The diagnosis of this disease should be based on exposure history, typical clinical symptoms, lung signs, chest X-ray findings, serum sedimentation antibody determination, bronchoalveolar lavage, and lung function. Check and other comprehensive analysis to make a correct diagnosis.

(1) Acute short-term inhalation of high-concentration antigen, rapid onset, often after 4 to 12 hours of inhalation of antigen, onset, first dry cough, chest tightness, followed by fever, chills and shortness of breath, cyanosis, often accompanied by sinus Sexual tachycardia, the two lungs heard the fine wet rales, about 10 to 20% of patients may have asthma-like wheezing, the total number of white blood cells increased, mainly neutrophils, usually disappeared within a few days to one week after dissociation .

(2) Chronic type caused by repeated small or continuous inhalation of antigen, the onset is concealed, but the difficulty in breathing is progressively worsened. In severe cases, there is difficulty in breathing at rest, and the irreversible histological changes in diffuse pulmonary fibrosis in the advanced stage. The patient developed labor dyspnea, weight loss, and the two lungs smelled of diffuse fine wet rales accompanied by respiratory failure or pulmonary heart disease.


Exogenous allergic alveolitis

(1) X-ray varies according to the disease stage and disease degree. Early or mild patients may have no abnormal findings, sometimes the clinical manifestations and X-ray changes are not consistent. Typical cases are in the middle stage, and the lower lungs are seen in diffuse lung texture. Thickening, or small, blurred edges of the nodules, lesions can be reversed, a few weeks after the contact with the shadow absorption, chronic late, the lungs are widely distributed reticulated nodular shadows, with lung volume reduction, often Multiple small cystic transparent areas, showing a honeycomb lung.

(2) Typical changes in lung function are restrictive ventilatory disorders, forced vital capacity and total lung volume are reduced, 1 second rate is increased, carbon monoxide diffusion and lung compliance are reduced, and arterial oxygen saturation is reduced in severe and advanced patients, chronic phase patients Pulmonary dysfunction is mostly irreversible.

(3) Serological examination The positive reaction of precipitated antibody suggests that the human body has been exposed to the corresponding antigen. If there is a corresponding history of contact, symptoms and signs, X-ray findings, positive reaction is very helpful for diagnosis.

(4) Bronchoalveolar lavage in bronchoalveolar lavage fluid of exogenous allergic alveolitis, the proportion of lymphocytes increased, and the ratio of IgG and IgM also increased. In recent years, many authors believe that bronchoalveolar lavage fluid is exogenous. The diagnosis of sacral alveolitis is of great value and can be exempted from lung biopsy, which helps early treatment and prevents the development of the disease.

(5) Inspiring the test, such as clinical suspected diagnosis of the disease, and patients with negative serological tests, can be used as a challenge test, some authors use the moldy hay extract for peasant lungs for nebulization, most patients have reactions, such as fever, leukocytosis The ventilation per minute increased, but the control group did not respond. Because the exogenous allergic alveolitis challenge test was not standardized, it is not suitable for the antigen that has definitely caused pulmonary symptoms, especially the lung function damage. Serious.


Diagnosis and diagnosis of exogenous allergic alveolitis

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

Viral pneumonia, miliary tuberculosis, sarcoidosis, idiopathic pulmonary fibrosis, bronchial asthma, exogenous allergic alveolitis and bronchial asthma must be distinguished from exogenous allergic alveolitis.

Exogenous allergic alveolitis exogenous bronchial asthma specific mass mostly without histological changes alveolar and interstitial lymphocytes infiltrating bronchial wall edema and eosinophil infiltration lesions alveolar and interstitial bronchial pathological exposure antigen After 4 to 6 hours of episodes of exposure to antigen, rapid onset of systemic symptoms have fever, chills and fatigue, and so on. There is almost no sign of fine wet rhythm wheezing X-ray. The acute phase is fine nodular shadow or normal lung inflation or normal lung function. Changes in restrictive ventilatory disorders, diffuse dysfunction, obstructive ventilatory disorders, serological examination, precipitation of antibody-positive IgE, normal IgE, and precipitation of antibody-negative major allergic reaction type III IV type I.

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