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Extrinsic allergic alveolitis

  Extrinsic allergic alveolitis (extrinsicallergicalveolitis) is an allergic alveolitis caused by repeatedly inhaling certain antigenic organic dust, often involving the terminal bronchioles simultaneously. The term hypersensitivity pneumonitis is commonly used in American literature. In China, the main reported conditions include farmer's lung, bagasse worker's lung, mushroom worker's lung, parrot breeder's lung, and humidifier lung, among others. Although there are many causes, the pathology, clinical symptoms, signs, and X-ray manifestations are extremely similar.

 

Table of Contents

What are the causes of extrinsic allergic alveolitis?
What complications can extrinsic allergic alveolitis easily lead to?
What are the typical symptoms of extrinsic allergic alveolitis?
How should extrinsic allergic alveolitis be prevented?
What laboratory tests are needed for extrinsic allergic alveolitis?
6. Diet recommendations and禁忌 for patients with exogenous allergic alveolitis
7. Conventional methods of Western medicine for the treatment of exogenous allergic alveolitis

1. What are the causes of the onset of exogenous allergic alveolitis

  Exogenous allergic alveolitis has many causes. Common ones include organic dust containing actinomycetes and fungal spores, animal and plant proteins, bacteria and their products, insect antigens, and certain chemical substances. Some dusts have not yet been clearly identified in terms of their antigenic nature. It is generally believed that the cause of farmer's lung is primarily Actinomyces viscosus. In recent years, Chinese scholars have successively reported another strain of actinomycete associated with farmer's lung, Streptomyces thermophillus. Among many antigens, thermophilic actinomycetes are the most common and important, especially Microsporum thermophiles, followed by Actinomyces viscosus. This bacterium has the morphology of fungi but belongs to bacteria. It thrives in moist, warm, and moldy organic matter, and there are large amounts of the bacterium in compost, soil, food, and polluted water. Farmers who inhale moldy hay, grains, and sugarcane dust are often prone to the disease. The air in the environment where mushrooms are grown contains a lot of thermophilic actinomycetes, mainly Actinomyces viscosus, and inhalation can lead to mushroom worker's lung. Poultry keeper's lung (such as pigeon keeper's lung, parrot keeper's lung, etc.) is caused by bird serum, bird feces, bird feather powder, and bird eggs. Some believe that the powder on pigeon feathers is a keratin particle antigen about 1 μm in size, which is more pathogenic than bird serum and feces. There are also reports from China of silk reeling workers developing allergic alveolitis by inhaling the dust of mulberry silk in the workshop air (possibly silk glue protein). The cause of humidifier and air conditioner lung is white thermophilic actinomycetes. The inhalation of toluene diisocyanate and phthalic anhydride, widely used in the chemical industry, may also cause allergic alveolitis due to their haptenic action. The antigenic nature of diseases such as tobacco grower's disease and tea grower's disease has not been fully clarified.

2. What complications can exogenous allergic alveolitis easily lead to

  Exogenous allergic alveolitis has many causes, common ones include organic dust containing actinomycetes and fungal spores, animal and plant proteins, bacteria and their products, insect antigens, and certain chemical substances. Some dusts have not yet been clearly identified in terms of their antigenic nature. In the late stage, exogenous allergic alveolitis usually complicates respiratory failure and pulmonary heart disease.

3. What are the typical symptoms of exogenous allergic alveolitis

  Allergic alveolitis is a group of non-asthmatic allergic pulmonary diseases caused by different allergens, with a low incidence in children. The pulmonary symptoms of exogenous allergic alveolitis are non-specific. The diagnosis of this disease should be based on a history of exposure, typical clinical symptoms, pulmonary signs, chest X-ray findings, serum precipitation antibody testing, bronchoalveolar lavage, pulmonary function tests, and other comprehensive analyses to make an accurate diagnosis.

  1. Acute type caused by short-term inhalation of high concentrations of antigens

      The onset of the disease is acute, usually occurring 4 to 12 hours after exposure to the antigen. It begins with dry cough, chest tightness, followed by fever, chills, and shortness of breath, often accompanied by sinus tachycardia. Fine moist rales are heard in both lungs, and about 10 to 20% of patients may have asthma-like wheezing. The total white blood cell count increases, mainly neutrophils, and symptoms usually disappear a few days to a week after discontinuing exposure.

  2. The chronic type is caused by repeated inhalation of antigens in small amounts or continuously.

      The onset is insidious, but dyspnea progresses progressively, and severe cases have dyspnea at rest. In the late stage, there are irreversible histological changes due to diffuse pulmonary interstitial fibrosis. Patients have exertional dyspnea, weight loss, diffuse fine moist rales in both lungs, accompanied by respiratory failure or pulmonary heart disease.

4. How to prevent exogenous allergic alveolitis

  Exogenous allergic alveolitis is an allergic alveolitis caused by repeated inhalation of certain antigenic organic dust, often involving terminal bronchioles simultaneously. The most fundamental preventive and treatment measure is to completely avoid contact with pathogenic organic dust.. Improve the production environment, pay attention to dust-proof ventilation, and strictly follow the operational procedures, such as drying the hay and grain after sunbathing before storage. Keep the places where poultry are raised clean and properly handle bird droppings. Keep the water in humidifiers and air conditioning systems clean to avoid contamination. Workers in organic dust-polluted environments should undergo regular medical surveillance. People with obvious chronic respiratory diseases such as chronic asthmatic bronchitis, bronchial asthma, chronic obstructive pulmonary emphysema, and those with allergic constitution should not engage in jobs that require close contact with organic dust.

5. What laboratory tests should be done for exogenous allergic alveolitis

  Exogenous allergic alveolitis is a group of non-asthmatic allergic pulmonary diseases caused by different allergens, which are organic dust particles containing fungal spores, bacterial products, animal proteins, or insect antigens. The following examinations need to be done:

  First, imaging

  The chest X-ray examination may be normal or show diffuse interstitial fibrosis. There are often bilateral plaques or nodular infiltrates, thickening of bronchopulmonary markings, or small acinar changes, suggesting pulmonary edema. Lymph node enlargement at the hilum and pleural effusion are rare. CT, especially high-resolution CT, is of high value in judging the type and extent of the lesion.

  1. The CT manifestations of acute allergic pneumonia show bilateral ground-glass changes; widespread patchy, mass-like, and cloud-like lung consolidation shadows with blurred edges, uneven density and distribution, more common in the middle and lower lungs, with significant changes in lesion location and mobility in a short period of time. The pathological basis of the imaging manifestations of acute allergic pneumonia is the infiltration of neutrophils and eosinophils in the lung parenchyma and inflammation of small blood vessels, leading to diffuse pulmonary congestion, edema, and the exudation of protein fluid in alveoli.

  2. The CT manifestations of subacute allergic pneumonia show diffuse distribution of small lobular central nodular shadows with unclear edges; patchy ground-glass shadows; atelectasis signs and lung cystic changes. The pathological basis of the imaging manifestations of subacute allergic pneumonia: small lobular central nodular shadows are the manifestation of cellular bronchiolitis; ground-glass shadows are the manifestation of diffuse lymphocytic interstitial pneumonia; atelectasis signs and lung cystic changes are the result of bronchiolitis, inflammation, and obstruction. Small lobular central nodular shadows and ground-glass changes are characteristic changes of allergic pneumonia, and small lobular central nodular shadows are characteristic changes of subacute allergic pneumonia.

  3. CT manifestations of chronic allergic pneumonia can show reticular and honeycomb fibrous streak shadows, indicating pulmonary interstitial fibrosis. In severe cases, atelectasis, emphysema, and pleural thickening can be seen.

  Second, pulmonary function

  Mostly restrictive, with reduced lung volume, decreased carbon monoxide diffusion, abnormal ventilation/perfusion ratio, and hypoxemia. Airway obstruction is rare in acute cases, but it can occur in chronic cases. Eosinophils are normal.

  Third, bronchoscopy

  Bronchoalveolar lavage is a sensitive method to determine the presence or absence of alveolitis. Generally, lymphocytes are visible, especially T cells increase, with CD8+ (cytotoxic suppressor) T cell subsets as the main group. The value of bronchoscope biopsy is very limited, as the specimen is too small and can cause misdiagnosis.

6. Dietary taboos for patients with extrinsic allergic alveolitis

  Patients with extrinsic allergic alveolitis should avoid eating known allergenic foods, and be careful with foods that have not been eaten or whose methods have changed. However, food allergy is not necessarily lifelong, and food allergy is more common in children, which can disappear with age. For adults, after avoiding allergenic foods for several years, the degree of allergy can decrease significantly or disappear. Pay attention to allergies to nuts, peanuts, fish, and shellfish, and less common allergy disappearance phenomena.

7. Conventional methods for the treatment of extrinsic allergic alveolitis in Western medicine

  The first attack of allergic pneumonia is easy to be confused with viral pneumonia, and attention should be paid to differentiation. Once infected, immediate separation from the environment of contact, lying in bed and rest should be ensured. Oxygen therapy should be provided to those with significant difficulty breathing and cyanosis. Acute patients should be treated with symptomatic treatment and short-term high-dose hormone therapy. Prednisone 60mg/d, oral for 4 weeks, and then gradually reduced until discontinued. In addition, it should be avoided to re-expose to known pathogenic antigens. Hormones can also be tried in the chronic phase, but the efficacy is often not ideal.

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