Current location - Training Enrollment Network - Mathematics courses - Brief introduction of allergic pneumonia
Brief introduction of allergic pneumonia
Directory 1 Overview 2 Disease Name 3 English Name 4 Alias Allergic Pneumonia 5 Classification 6 ICD 7 Epidemiology 8 Etiology 9 Pathogenesis 10 Clinical Manifestations of Allergic Pneumonia 10.654 38+0 Acute Allergic Pneumonia 10.2 Subacute Allergic Pneumonia 10.3 Chronic Allergic Pneumonia/KLOC-0. Kloc-0/ Allergic pneumonia complications 12 laboratory examination 12 function examination 12.3 inhalation provocation test 12.4 skin allergy test 12.5 bronchoalveolar lavage is helpful for diagnosis 13 auxiliary examination 15. Treatment of allergic pneumonia 17 prognosis 18 prevention of allergic pneumonia 19 related drugs 20 related tests Attachment: 1 allergic pneumonia related drugs This is a redirected entry, * * * Enjoy the content of allergic pneumonia. For the convenience of reading, allergic pneumonia in the following article has been automatically replaced by allergic pneumonia. You can click here to restore the original appearance, or you can use the remarks to explain that allergic pneumonia is a group of non-asthmatic allergic lung diseases caused by different allergens, with diffuse interstitial inflammation as the pathological feature. It is an allergic reaction caused by inhaling organic dust particles (diameter < 10μ) containing fungal spores, bacterial products, animal proteins or insect antigens, so it is also called exogenous allergic alveolitis.

Allergic pneumonia represents a group of diseases with different etiology, but similar pathogenesis, pathology, clinical manifestations, treatment and prognosis, so it can also be called symptom group. This disease is characterized by a group of fine organic dust particles, which are very small and can penetrate most of the parenchyma around the lung, causing alveolitis. The following conditions often occur in this group of diseases, which should be paid attention to:

1. Most patients have been exposed to organic dust particles small enough before onset, which can enter the most distal lung parenchyma.

2. Paroxysmal dyspnea occurs within a few hours after contact with antigen, accompanied by symptoms such as dry cough, fever and fatigue.

3. The auscultation of both lungs can fill sonic boom, especially the basal segment of both lungs.

4. Acute chest X-ray showed diffuse nodules or reticular nodules in both lungs.

5. The pulmonary function is characterized by FVC and carbon monoxide diffusion function and static lung compliance decrease, but some patients also show airway obstruction.

6. Subcutaneous injection of appropriate antigen can cause delayed hypersensitivity. Allergic alveolitis caused by antigen inhalation into alveoli. It belongs to type ⅲ immune response mediated by immune complex, but there is non-caseous granuloma in histopathology, which accords with type ⅳ immune response. Therefore, most scholars believe that allergic pneumonia is a dual immune process mediated by immune complex and cellular immunity.

7. After inhaling all kinds of organic dust, there are immune complexes deposited on the basement membrane of alveoli and capillaries, and corresponding antigen precipitates can also be detected in blood, and some can produce IgE antibodies, causing asthma.

8.BALF can reflect the basis of immune pathogenesis. In BALF, lymphocytes account for more than 60%, and the absolute values of CD8 and CD4 both increase, but CD8 is more obvious than CD4, so the ratio of CD4∶CD8 can be reversed.

9. After inhaling antigen for several hours, symptoms and chest X-ray are abnormal without abnormal lung function. If you get out of contact in time, X-ray abnormalities and symptoms can disappear, but some patients have persistent symptoms, abnormal lung function and fibrosis.

10. Lung biopsy showed the formation of bronchiolitis, interstitial pneumonia and granuloma.

The diagnosis of allergic pneumonia depends on the history (including environmental factors, living habits and hobbies), symptoms, signs and changes in lung function. X-ray changes and immunological examination, especially the specific precipitation of sensitive antigens found in serum, are helpful for diagnosis. Patients should avoid contact with allergens immediately. Such as extensive lung lesions, hormone therapy. Early diagnosis and early exposure from antigen have a good prognosis.

2 disease name allergic pneumonia

3 English name allergic Europe

4. allergic pneumonia; ; Allergic pneumonia; Loffler syndrome; Allergic pneumonia; Allergic pneumonia

5 classification respiratory department > infectious diseases > other pneumonia.

6 ICDNo。 J 18.8

Epidemiological allergic pneumonia is mostly occupational, but it may also be caused by various fungal pollution on walls, floors, ceilings, humidifiers, air conditioners and buildings in homes and offices, as well as chemical pollutants used in indoor furniture decoration. Therefore, in the diagnosis of allergic pneumonia, it is very important to collect the medical history in detail and understand the living and working environment of patients, and even the air pollution status of patients. In three places in Britain, local farmers were investigated. The chest radiograph is normal, and there is no precipitation in the blood, but there are typical clinical symptoms, hypoxemia and decreased diffusion function. Lung biopsy confirmed the diagnosis. There are also reports of allergic pneumonia in farmers' lungs and bird feeders. The chest radiograph is normal and the T lymphocytes in alveolar lavage fluid are significantly increased.

8 Causes of allergic pneumonia The occurrence of allergic pneumonia is mainly caused by organic dust as immunogen. Its particles should be less than 5 ~ 6 μ m, because particles larger than this diameter are mostly deposited in the upper respiratory tract or bronchi, only when reactants enter the small airways and alveoli and enter the surrounding lung tissue can alveolitis be caused. When the reactive particles entering the alveoli reach a certain amount, the lung tissue produces a strong immune response, causing allergic alveolitis. Lacey estimated that when farmers inhale air polluted by moldy hay, 750,000 particles can be deposited on alveolar walls every minute, causing diseases. Every 1mg of moldy bagasse contains 500 million fungal spores. According to statistics, at least 40 kinds of organic dust are known as antigens that can cause allergic pneumonia, and their common antigens and sources are listed in table 1.

9 Pathogenesis Symptoms and signs of human contact with allergens. At present, the research mainly focuses on type ⅲ immune complex reaction and type ⅳ cell-mediated immune mechanism. Immune complex reactive diseases generally begin to show symptoms 4 to 6 hours after exposure to allergens. Most of them are related to antibodies. Allergic pneumonia can often detect the existence of IgG, IgA and IgM antibodies by immunoprecipitation or enzyme-linked immunosorbent assay. After continuous contact, the antibody titer increased, but after leaving antigen contact, the antibody titer decreased and the symptoms were alleviated. The positive rate of precipitation reaction in allergic pneumonia varies from report to report. Pepys and Jenkins reported that 90% of farmers were positive for antibody precipitation in their lungs, while Graff observed that only 50% of farmers had antibody precipitation in their lung serum. Through the comparative analysis of clinical manifestations and laboratory tests, it is found that the positive precipitation reaction is related to the severity of acute attack of clinical symptoms. Farmers' lungs were divided into acute and chronic groups according to clinical symptoms. The results showed that most of the precipitate reaction in acute attack group was positive, while only half of the chronic patients were positive. At present, it has been made clear that precipitants only reflect the exposure of organic dust, and the more serious the exposure, the more antibody precipitates. Most people are positive after exposure to organic dust, but they may not have symptoms. For example, 30% ~ 40% of pigeon breeders have positive antigen precipitation without any symptoms, and 18% ~ 50% of healthy farmers produce antibodies after contact with moldy hay. 10% ~ 15% asymptomatic workers exposed to fermented malt had positive serum reaction. The reaction to the precipitation of bagasse extract was positive not only in the serum of bagasse lung patients, but also in all healthy workers who inhaled bagasse. Therefore, it can be concluded that the existence of sediment is no longer of diagnostic value for allergic pneumonia. Precipitin often exists in asymptomatic patients, which leads some authorities to conclude that precipitin does not play a role in the pathogenesis of allergic pneumonia. Lee et al. (1983) reported that 48 parakeet breeders in Australia continued to observe the serum precipitant level after stopping contact. It is found that half of the people with decreased serum precipitin have no better symptoms than those with continuously increased serum precipitin, which also shows that precipitin does not play an important role in the pathogenesis of allergic pneumonia. Although the antigen-antibody reaction is controversial, there is indeed type ⅲ allergic reaction in the pathogenic process of allergic pneumonia, at least there are histological changes related to it.

1. Immunofluorescence examination confirmed that the antigen-antibody complex was deposited on the bronchiole wall and along the alveolar capillaries.

2. Both farmers' lungs and birds' lungs have delayed skin reaction, and skin biopsy also confirmed the deposition of immunoglobulin and complement, accompanied by complement consumption.

3. Arthur reaction can be used as a diagnostic test.

4. Inhalation of allergen extract can induce positive reaction in provocation test, which can produce two kinds of reactions:

(1) immediate reaction: bronchospasm, and fever will be relieved within 3 ~ 4 hours.

(2) Delayed reaction: it occurs after 4-6 hours and relieves after 24-48 hours. Although some patients have bronchospasm, their lung function is still restricted ventilation disorder. Systemic reactions include fever, chills, weakness and anorexia. The provocation test not only makes the acute allergic pneumonia positive, but also can make the recessive patients positive.

Recent studies on alveolar lavage fluid of animals and patients have confirmed that type ⅳ allergic reaction or delayed allergic reaction also plays a role in the pathogenesis of allergic pneumonia.

A group of studies confirmed that 18 patients with bird lung had cellular immune response, and the serum dilution of pigeons and parakeets could inhibit the migration of phagocytes. Many experiments show that this pathological change is a cell-mediated immune response. Lymphocytes in alveolar lavage fluid of farmers' lungs and pigeons' lungs increased significantly. In the early stage of antigen-induced alveolitis, neutrophils predominate, and lymphocytes increase in the later stage. However, CD4 is the main lymphocyte increase in sarcoidosis and CD8 is the main lymphocyte increase in allergic pneumonia, but the lymphocyte classification in peripheral blood is normal. Another group of studies found that mast cells in alveolar lavage fluid of patients with allergic pneumonia were 1000 times more than those in normal control group, suggesting that degranulation of mast cells in this disease has a certain regulatory effect on the number of lung immune cells.

In short, the development of allergic pneumonia, the local immune regulation mechanism is in the lungs rather than in the peripheral circulation blood. Lymphocytes in alveolar lavage fluid of farmer's lung and pigeon's lung exposed to antigen increased, suggesting that the disease is a cellular immune-mediated disease.

Although there are many pathogens of allergic pneumonia, the histological changes are very similar, and most of them can not be identified from histomorphology. Only a few exceptions, such as fungi of maple disease, plant fiber of bagasse lung and cork powder of cork, were found in diseased tissues as evidence for identification. Pathological characteristics depend on the degree of allergen exposure, and partly on whether the course of the biopsy is early or late. After 36 hours of exposure to moldy hay, farmers' lungs became bloodshot with capillaries, and neutrophils, eosinophils and lymphocytes infiltrated around alveoli and small airways and around the walls of medium-sized blood vessels. The study of fluorescence immunity shows that IgM, IgG and complement C3 are deposited in the above blood vessels, so some people think that they represent vasculitis. These pathological changes may be related to Arthus reaction. In the late stage of acute disease, bronchiolitis and alveolitis are accompanied by granuloma formation. In addition to alveolitis, there is inflammatory cell infiltration in the stroma, mainly lymphocytes with histiocytes, plasma cells, neutrophils and eosinophils. Inflammatory infiltration is patchy, and there are often foam phagocytes around the affected bronchi and alveolar cavities, which may be secondary bronchiolitis obliterans. About 2/3 cases have damage to alveolar epithelium and capillary endothelium. Among them, neutrophils mixed with protein-like substances or loose connective tissue masses in alveolar cavity may be the early stage of mature collagen and alveolar fibrosis. 66% ~ 70% have granulation tissue formation. Irregular appearance, no fibrosis around granuloma and unclear boundary. Bronchitis is also a common manifestation.

Due to the severity of the disease and the frequency of patients' exposure to allergens, lung injury can be fibrosis in different degrees. In the early stage of acute inflammation, mild fibrosis is patchy, and fibrosis can only be seen under the microscope, but it may develop into a large lesion visible to the naked eye in the later stage, showing fibrous scar and honeycomb lung. If out of contact, granuloma can disappear. One group reported 10 cases of active peasant lung, and 5 cases of lung biopsy had granuloma. After the symptoms disappeared, lung biopsy was performed again and the granuloma disappeared.

Only a few people exposed to organic dust suffer from allergic pneumonia. It is suggested that the patient is susceptible, which may be related to human leukocyte antigen (HLA). HLA may be the decisive factor of genetic immune response and play a role in this disease. This is only confirmed in the lungs of farmers and pigeon breeders, but this relationship has not been found in other patients with allergic pneumonia.

The clinical manifestations of 10 allergic pneumonia can be divided into three types: acute, subacute and chronic according to the number, frequency and duration of contact with antigens and the responsiveness of the host.

10. 1 acute allergic pneumonia inhaling a large amount of antigen in a short time often causes acute symptoms. Four hours after exposure to antigen, symptoms such as shortness of breath, cough, chills, fever, headache, fatigue, cold sweat and nausea may occur. Most patients are related to the living and working environment, and some have wheezing symptoms within a few minutes after contact, and are often misdiagnosed as asthma or go home from work. Occupation-related people often attack the working environment from home, such as farmers entering grain depots and barns where moldy hay is stored. The symptoms of immediate attack are mostly dry cough without phlegm and chest tightness. Relieve after leaving the environment, touch again, and have another attack. In severe cases, cyanosis may occur, and sonic boom may appear in the lungs. Because it belongs to type III reaction, it can occur 4 ~ 6 hours after contact, so it can occur after contact at work and at work after family contact.

10.2 subacute allergic pneumonia subacute allergic pneumonia is mostly caused by acute. Or mild multiple attacks, the symptoms last for several days or weeks. Dry cough, dyspnea, loss of appetite, weight loss. Because of dry cough, fever and general weakness, it is easy to be misdiagnosed as pneumonia. Stop the air conditioner or humidifier, the symptoms will be improved, and the moldy particles will stop releasing and spreading. Some people cough and have short breath at the beginning of each week because of professional contact, and the symptoms will be fine if they rest at home for two days on weekends. Some rest days are aggravated and work is getting better. They may come into contact with pets at home, and the decoration at home is an allergen.

An important finding is that in 1977, Werren reported 18 cases of allergic pneumonia, including 13/ 15(73%) men and 3/3 women (100%). They Before and after this, several similar reports showed that smoking had a short-term effect on the removal of human tracheal secretions. Harris( 1975) found that smoking can interfere with several aspects of immune response, such as the formation of macrophage antibodies and the inhibition of immune activity of T lymphocytes and B lymphocytes. Therefore, allergic pneumonia is more likely to occur in non-smokers.

10.3 chronic allergic pneumonia is caused by repeated attacks or continuous contact with antigens or a small amount of contact. It can only be diagnosed as chronic when the onset is hidden until the late stage of the disease, and some of them eventually develop into chronic and bilateral pulmonary fibrosis due to misdiagnosis. Pulmonary fibrosis in the upper part of both lungs is obvious, and compensatory emphysema in the lower part of both lungs is obvious.

Recent studies have found that allergic pneumonia is related to abdominal diseases. It was found that patients with villous atrophy of jejunum were highly sensitive to avian antigen and antibody. It is estimated that alveolar allergy may be caused by absorbing undercooked bird eggs as antigen substances. The incidence of asthma in patients with intestinal diseases is high. In recent years, there are more and more reports about intestinal diseases and chronic bronchial diseases, and lung and intestinal diseases in farmers are also common. The relationship between intestinal diseases and respiratory diseases is also a newly discovered problem in recent years.

1 1 Complications of allergic pneumonia Patients with allergic pneumonia may have honeycomb lung in the later stage.

12 Laboratory examination 12. 1 Blood examination During acute attack, the peripheral blood picture showed leukocytosis15×109 ~ 25×109/L (1509/L

12.2 pulmonary function examination is a very useful means to estimate the degree of lung injury and can also be used to observe the therapeutic effect. In acute and subacute allergic pneumonia, the vital capacity decreased, and the forced vital capacity (FVC), 1 sec forced expiratory volume (FEV 1), total lung capacity (TLC) and lung compliance (CL) all decreased, and the rate of 1 sec was always normal, showing restrictive ventilation disorder. Generally, the changes of lung function are consistent with extensive bronchiolar obstruction, so it is best to carry out the above examination within 4 ~ 8 hours after onset, because/kloc-0 can return to normal after 2 ~ 24 hours. Blood gas analysis, oxygen saturation, oxygen partial pressure and carbon dioxide partial pressure have slight changes. In chronic phase, FVC, TLC, DLCO, arterial oxygen partial pressure and blood oxygen saturation all decreased. Antibodies against allergens can be detected in serum. The corresponding antibodies can be detected in farmers' lungs, mushroom lungs, sugarcane pneumoconiosis and pigeon breeders' lungs. 40% of asymptomatic antigen contacts detected corresponding precipitated antibodies. Precipitated antibodies only represent contact with these antigens.

12.3 Inhalation of the antigen extract for provocation test can produce a positive reaction within several hours. It is characterized by fever, cough and shortness of breath. The objective index is pulmonary dysfunction, FEV 1 decrease, and sometimes bronchospasm occurs. Positive reaction helps to find out the original allergic reaction. The lung function of patients who have been diagnosed with an antigen or have found specific precipitated antibodies in serum is obviously decreased, and it is not suitable for severe patients to do provocation test.

12.4 skin allergy test There are many positive reactions and false positives in skin allergy test, which are not suitable as the basis for diagnosing diseases.

12.5 bronchoalveolar lavage is helpful for diagnosis. In the BALF of normal non-smokers, macrophages account for more than 85% ~ 90%, lymphocytes account for 6% ~ 10%, and neutrophils account for less than 1% ~ 2%. However, within 24 hours of allergic pneumonia, neutrophils temporarily increased, followed by lymphocytes. The total number of cells in BALF is 3 ~ 5 times of normal. Among them, lymphocytes account for 60%, mainly T lymphocytes, and B lymphocytes account for a minority. Among them, the suppressor T cells (CD8) are dominant, so the CD4/CD8 ratio is reversed. BALF immunoglobulin increased, and the main IgG and IgA increased, which was 4 times higher than that of asymptomatic patients. In the acute phase, the white blood cells in the blood occasionally move to the left, the total number is not high, and the eosinophils in the blood rarely rise.

13 auxiliary examination acute early chest film can not show obvious abnormalities. It is reported that pathological biopsy confirmed allergic pneumonia, but chest X-ray examination was completely normal. In addition, 26 cases of mushroom lung have typical clinical symptoms, and only 8 cases have abnormal chest radiographs. The other group reported that 99 cases (93%) of farmers' lungs had diffuse lung shadows on chest X-rays. The number of shadows is not necessarily parallel to lung function, BAL and the severity of clinical symptoms. Chest x-ray findings are mostly diffuse nodules in both lungs. Nodules vary in diameter from 1 mm to several millimeters, with unclear boundaries or ground glass shadows. Some shadows are reticular or reticular nodules. Although there is no special tendency in the distribution of lesions, there are few pulmonary apex and basal segments. Fine reticular and nodular types are mostly subacute manifestations. Fraser and others have seen farmers' lungs, mushrooms' lungs and pigeons' lungs. It is more common that two alveolar shadows appear in a short time after acute exposure to severe antigens. Alveolar shadow is often caused by small airway occlusion of bronchiolitis obliterans, which makes the contents in alveoli form an image with increased density. Persistence of diffuse reticular or reticular nodule shadow and glandular bubble in acute exacerbation.

Allergic alveolitis, common hilar and mediastinal lymphadenopathy in mushroom lung, and some farmers also have lymphadenopathy.

Chest x-rays often have flaky shadows, which may represent alveolar consolidation. Thickening of interlobular septa at the recess of costal diaphragm angle may represent a high load of lymphatic drainage.

The patient is out of allergen contact within 10 days to several weeks, and the shadow on chest film can fade and return to normal. The prognosis depends on the frequency, severity and duration of allergen exposure. The key lies in early diagnosis and elimination of allergens. In acute or subacute stage, diffuse nodular shadow in lung is replaced by diffuse interstitial fibrosis, and becomes medium or coarse reticular and reticular nodular shadow. When honeycomb lesions appear, the lung volume can be reduced, forming cicatricial atelectasis. But the unaffected lung forms compensatory emphysema. Such cases are also difficult to recover from contact and active treatment. Hargreave reported that 4 1 pigeon eaters had 20 cases of atelectasis with lobes, and 17 cases of atelectasis occurred in the upper lobe. In the late stage, there are annular shadows with a diameter of 5 ~ 8 mm, and some of them are honeycomb lungs, which tend to be distributed in the upper lobe. Sometimes it is difficult to distinguish hypersensitive pneumonia from idiopathic pulmonary fibrosis.

The diagnosis of most patients should be based on clinical manifestations, because only a few patients have abnormal chest radiographs. However, the chest X-ray examination results of a few patients are completely consistent with the manifestations of allergic pneumonia without any clinical symptoms.

High resolution tomography (HRCT) is one of the main methods to diagnose allergic pneumonia. Chest x-ray examination of patients with early allergic pneumonia is normal, and HRCT can find early pulmonary interstitial lesions. HRCT can find some important features, such as diffuse reticular nodules or cystic light transmission area between lung medulla and cortex in ground glass shadow. It is considered that this is the characteristic of allergic pneumonia, which is caused by allergic pneumonia complicated with bronchiolitis obliterans. Another feature of allergic pneumonia is that there is a part of normal lung tissue between shadows, sandwiched between ground glass or nodules and reticular shadows. The above two manifestations can only be found by HRCT, and these changes are often concealed by volume effect on conventional CT or chest radiograph. The manifestations of HRCT are as follows: 1. There are patches, nodules or reticular shadows on both sides or one side.

2. Polishing glass shadows.

3. The above two cystic light-transmitting areas coexisting between shadow or normal lung tissue have reference value for the diagnosis of this disease.

4. The manifestations of pulmonary interstitial fibrosis may have honeycomb lung in the late stage.

The diagnosis of 14 allergic pneumonia is mainly based on antigen contact history, clinical symptoms and signs, chest radiograph, serological examination, antibody precipitation and bronchoalveolar lavage. There are also some cases that are difficult to diagnose and misdiagnosed as other diseases, and allergens are often found through repeated attacks. Individual patients were diagnosed by inhalation provocation test. A few patients need lung biopsy.

15 The differential diagnosis of acute allergic pneumonia should be differentiated from viral lung infection, bronchial asthma, pulmonary eosinophilic infiltration, allergic bronchopulmonary aspergillosis, pulmonary edema caused by chemical drugs, etc. (Tables 2 and 3). Chronic stage should be distinguished from patients with idiopathic pulmonary fibrosis and sarcoidosis stage III (Table 4).

Treatment 16 allergic pneumonia has no allergen, and the acute attack can be relieved naturally. Those with obvious symptoms should be treated symptomatically. If the symptoms persist and worsen with cyanosis, oxygen should be inhaled and prednisone should be given 30 ~ 60 mg/d, and the maintenance dose should be given 20 ~ 30 mg/d 1 week after the condition is stable. After the symptoms disappear completely, the dosage should be reduced and the drug should be stopped gradually. Most of the chest HRCT ground glass shadow lesions were absorbed and improved after glucocorticoid treatment. When the shadows are mostly honeycomb shadows, the therapeutic effect of glucocorticoid is poor.

17 Prognosis Early diagnosis of allergic pneumonia, early separation from antigen exposure and good prognosis. Detect the antigen in time after the onset of acute phase to avoid the symptoms of contact disappearing quickly. When the patient is hiding or on the run and recognizes the antigen, the onset time has been long, and it has become subacute or chronic allergic pneumonia, and the lesion has changed from inflammatory infiltration to fibroplasia. At this time, although active treatment may leave lung dysfunction. According to the survey in the United States, if people leave contact with birds before the age of 45 and the respiratory symptoms exist for less than 2 years, the damage of restrictive ventilation function can be significantly reduced. Brown followed up 92 cases of farmers' lungs, and found that 36/92(39%) had chest X-ray manifestations of pulmonary interstitial diseases, and 39/92 (42%) had PAO 2 < 70 mmHg, suggesting that the lungs had substantial damage. Monkary followed up the lungs of 86 farmers for 5 years, and found that the clinical improvement was mainly in 1 month, and there was almost no progress after 6 months. Five years after the onset, 65% still have symptoms, 45% have lung function damage, and 32% have persistent X-ray shadow. The proliferation degree of BALF lymphocytes can not predict the prognosis of the disease.

18 prevention of allergic pneumonia Avoiding inhalation of antigen is the best preventive measure for allergic pneumonia. Farmers need to dry their grain and store it to prevent mildew. When raising poultry, pigeons and all kinds of birds, it is necessary to keep the breeding shed clean, deal with feces and fallen feathers in time, wear protective masks when working, and often clean humidifiers and air conditioners to prevent mildew or other pollution.

19 related drugs oxygen, malt, collagen, carbon dioxide, prednisone

20 correlation detection of plasma cells, oxygen saturation, oxygen partial pressure, carbon dioxide partial pressure.

Carbamazepine capsule poisoning, peripheral neuritis, acute uremia, thromboangiitis, allergic pneumonia and acute intermittent porphyria can cause hypothyroidism. Yes. ...

Nabumetone capsules, dizziness, bullous rash, urticaria, dyspnea, asthma, allergic pneumonia, proteinuria, hematuria and angioneurotic edema. Taboo work ...

High dose amiodarone hydrochloride capsules (0.8 ~ 1.2g daily). It mainly produces allergic pneumonia and fibrosis alveolitis. Discovered symptoms: alveoli and interstitial bubbles. ...

A large dose of amiodarone hydrochloride for injection (0.8 ~ 1.2g per day). It mainly produces allergic pneumonia and fibrosis alveolitis. The lesions showed air bubbles in alveoli and interstitium. ...

Amiodarone hydrochloride tablets