Pulmonary amyloidosis

Introduction to pulmonary amyloidosis Amyloidosis refers to a group of clinical syndromes with different manifestations, all of which are characterized by extracellular amyloid deposition. In 1854, Virchow first called the disease amyloidosis. This is because the deposited amyloid (amyloid) showed a similar staining reaction with starch when it encountered iodine and sulfuric acid, and it was amorphous under the light microscope. Yihong. The amyloids of different proteins have the same shape and are stained with Congo red to form a specific green or yellow birefringent under polarizer. Amyloid deposition can cause organ parenchymal cells to shrink, interfere with the mechanical function of the organ, or affect vasoconstriction and cause bleeding. Amyloidosis can invade multiple or individual organs, and all parts of the respiratory system can be affected. Amyloid deposits on the tongue can cause obstructive sleep-disordered breathing; deposition in the tracheobronchial can cause airflow obstruction or hemorrhage; diffuse deposition of interstitial lung can lead to ventilation dysfunction and respiratory failure; pleural or diaphragmatic deposition can lead to Thoracic exudate or respiratory muscle weakness. basic knowledge The proportion of illness: the incidence rate is about 0.004%-0.005% Susceptible people: no special people Mode of infection: non-infectious complication:

Causes of pulmonary amyloidosis

(1) Causes of the disease

The etiology of bronchopulmonary amyloidosis has not been fully elucidated. It is currently believed that the majority of focal tracheobronchial and pulmonary nodular amyloidosis in this disease are mainly A1 type, and the amyloid is mainly derived from immunoglobulin. Over-deposition of amyloid in the bronchopulmonary may be related to the following factors:

1. An abnormal immune response occurs in bronchial-associated lymphoid tissue (BALT). Plasma cells derived from B lymphocytes are excessively monogenic and metamorphosed locally, producing excessive normal immunoglobulins and fragments that are structurally abnormal or beyond the body's ability to clear. The degradation products form corresponding light chain fragments, which are deposited as amyloid in bronchopulmonary tissues. Some authors believe that macrophages are important sites for the conversion of immunoglobulin polypeptide precursors into amyloid structures, so the amyloid peripheral regions are often Cases with plasma cell and macrophage infiltration, plasmacytoma, lymphoma complicated with amyloidosis support this theory, and clinical cases of plasmacytoma or lymphoma conversion to amyloid tumor are still seen.

2. Due to the inflammatory lesions in the lungs, the vascular permeability is increased, and the related protein precursors in the circulating blood leak out from the blood vessels. The deposition and activation of the phage cells in the lungs, plasma cells and phagocytic cells reflect local inflammatory reactions. In some cases, Bronchopulmonary amyloid serum-containing monoclonal protein supports this theory. The formation and deposition of amyloid is regulated by T lymphocytes. The innate immune function of thymic dysplasia is prone to amyloidosis. Inducing amyloidosis in animals, the time required is significantly shorter than normal animals, local T lymphocyte function is reduced and B lymphocyte function is hyperthyroidism, pH value is reduced, which is conducive to amyloid deposition.

Diffuse pulmonary interstitial or alveolar septal amyloidosis can be derived from AL, AA protein or thyroxine transport protein, as one of the manifestations of systemic amyloidosis, its etiology and pathogenesis have the following possibilities:

3. Primary systemic amyloidosis or combined with multiple myeloma, malignant hyperplasia of bone marrow plasma cells (plasma cell disease), leading to subclinical or clinical multiple myeloma with AL fibrosis deposition.

4. Secondary to chronic infection (tuberculosis, suppurative osteomyelitis, leprosy), chronic inflammation (rheumatoid arthritis, Crohn's disease) or malignant tumor (Hodgkin's disease, kidney cancer), etc., relatively rare, At this time, serum acute response protein was significantly increased, and serum amyloid-associated (SAA) protein was also continuously elevated. AA protein was a degradation product of SAA protein, causing secondary or inflammation-related amyloidosis, and AA protein was reported. Mainly from the stimulated macrophages, there are traces of blood in normal people, the molecular weight is about 8500, and can be produced in large quantities in chronic infections and inflammatory diseases.

5. Family autosomal dominant hereditary and senile amyloidosis, amyloid mainly from plasma thyroxine transporter, its structure is mutated, valine is substituted by methionine, and thus has amyloidogenicity, thyroxine 95% of the carrier protein is derived from the liver, mainly deposited in the central nervous system, myocardium and interstitial lung. It is believed that diffuse interstitial amyloidosis is mainly caused by leakage of circulating blood-related protein precursors from blood vessels, and part of inflammation Related to increased vascular permeability, the leaked protein fragments are degraded and bound to the extracellular matrix to form amyloid fibrils. The precursors of the monoclonal proteins can be found in the blood of the patients, and the lesions can be infiltrated without plasma cells. An argument.

(two) pathogenesis

Under electron microscope, 95% of the amyloid is composed of uniform crystalline fibrils, and the remaining 5% is a pentagonal hollow "fried doughnut"-like structure. The fibrils are different types of proteins or polypeptides, and the diameter is about 10-15 nm, and the length is not 1. At about 8000 nm, the fibrils are observed by X-ray diffraction and consist of two subunits arranged in a -pleated sheet, which explains the confolars after being stained by Congo red. Depending on the orientation of the polarizer and the crystal axis, and the chemical and physical properties of the "fried doughnut"-like structure are the same in various amyloid changes, which are derived from soluble circulating plasma proteins, called soluble amyloid proteins. (SAP), a product of hepatocyte synthesis, may be the scaffold structure of amyloid.

All kinds of protein fibrils of amyloid are derived from their soluble precursors. Once deposited in tissues, they become insoluble under physiological conditions and are not hydrolyzed by proteases. Although the morphology is consistent, 15 kinds of amyloid fibrils have been elucidated. The chemical structure, systemicity and most of the local amyloidosis are derived from three precursor proteins, namely immunoglobulin light chain (AL), amyloid-associated protein (AA protein) or transthyretin (thyroxin transporter) , transthyretin, TTR, formerly called thyroxine-binding prealbumin, TBPA), AL is the most important one, and some immunoglobulin light chain variable regions (especially lambda) have potential amyloidosis Original, after proteolytic hydrolysis, the variable region in the light chain is separated from the constant region, which then forms amyloid fibrils and is deposited in the tissue. The molecular weight of the AL protein is 5,000 to 250 million, which is less common. The source of renal dialysis-related amyloidosis of 2 microglobulin, elderly patients with Waldheimer's disease and atrial amyloid protein and atrial natriuretic peptide, with medullary thyroid carcinoma, amyloidosis, procalcitonin, II Lesions of islet amyloid polypeptide islet cells and the like.

Laryngeal tracheal bronchial amyloidosis can be a single nodule, multiple nodules or diffuse type, the ratio of single to multifocal is about 2:5, the common histological feature of amyloidosis is extracellular homogeneous eosinophil Deposited in irregular mass or flake, can be dyed purple by periodic acid-Schiff (PAS) reagent, is fungic to Congo red, dyed orange under light microscope, under polarizer It is an apple green or yellow birefringent. There are often different numbers of lymphocytes and plasma cell infiltration and multinucleated giant cell reaction around the sediment. The lesions are mostly located under the mucosa, which can reach the cartilage and invade the vascular wall or serous mucosa basement membrane. Or wrapped around the mucous gland, can be transparent ring in adipose tissue, about 14% of bone or cartilage metaplasia, ossification abnormalities in some cases, the formation of secondary tracheobronchopathia ossific deposits (tracheobronchopathia ossific deposits), The mucosal epithelium of the lesion is intact, and squamous metaplasia can be seen.

Pulmonary nodular lesions are mostly located in the subpleural area around the lungs, showing gray bright nodules, varying in size. The larger ones are 8 cm in diameter, which can cause significant compression of the lung parenchyma. The smaller ones are less than 1 cm, and some contain chalky spots or Forming lumps, amyloid deposits in or adjacent to small vessel walls and alveolar septa, peripheral lymphocytes, plasma cells and tissue cells in an irregular flaky infiltration and macrophage response (phagocytic amyloid), 25 Calcification, ossification or cartilage metaplasia can be seen in % of cases, cavities are formed in about 5% of cases, miliary lesions are widely distributed in the interstitial and blood vessels of the lungs, and are small nodules or strips. The vascular lesions mainly involve the lungs. The muscular layer of the muscular blood vessel may also be accompanied by calcification and ossification. The pulmonary interstitial diffuse type (bubble septum type) shows that the lungs are enlarged in volume, gray, and the texture is rubbery. The lesion is mainly located in the alveolar septum and small. Around the veins, under the electron microscope, the amyloid is most common in the accumulation of collagen fibers, which can lead to thickening of the alveolar septum and capillary occlusion, and mild fibrous tissue hyperplasia, alveolar septum (ie alveolar epithelium and pulmonary capillaries) Endothelium The area where the basement membrane is fused as one is less involved.

Lung amyloidosis prevention

Active treatment can induce the primary disease of this disease is the most important preventive measure. In recent years, it has been complicated by tuberculosis, and it has been rare for people with suppurative disease, indicating that prevention of primary disease is effective.

Lung amyloid complication Complication

Can be secondary to lung infection, systemic failure.

Symptoms of pulmonary amyloidosis common symptoms cyanosis, repeated atelectasis, difficulty breathing, shortness of breath, respiratory failure, calcification

The clinical manifestations of bronchopulmonary amyloidosis are diverse due to the type of lesion and the organ involved, and the following are described by organ:

1. Laryngeal amyloidosis is the most common site of focal amyloidosis in the respiratory tract. It is reported to account for about 75%. Laryngeal amyloidosis accounts for about 1% of benign laryngeal tumors. More than 250 cases have been reported so far. ~90 years old (average 48 years old), the ratio of male to female is 1:1, false voice band is the most commonly affected part, vocal cords and epiglottis are often involved, the main symptoms are hoarseness, may be associated with bleeding, and even cause fatal upper respiratory tract bleeding, Severe cases may have inhalation dyspnea, throat and other upper respiratory tract obstruction symptoms, diffuse mucosal hypertrophy through the laryngoscope, uneven or accompanied by a smooth and hard polypoid mass, lower airway amyloidosis and invasion of the throat It is not uncommon, accounting for about 12% to 40%. Occasionally, other organs such as lacrimal glands, lymph nodes, stomach or skin amyloidosis are involved in the throat. Lewis et al reported 22 cases of laryngeal amyloidosis, of which 7 cases were combined with tracheal amyloid. In 22 cases, immunohistochemical staining revealed 12 cases of light chain positive, 5 cases, light chain positive, only 3 cases were negative, and the amyloid fibrils of throat amyloidosis were mainly light chain.

2. Tracheal bronchial amyloidosis tracheal bronchial amyloidosis has been reported in nearly 200 cases, the age of onset is 16 to 76 years old (average 53 years old), male to female ratio of 1:1, most of the no underlying disease, clinical multifocal mucosa The lower plaque is the most common (about 85%), followed by the single tumor tumor mass, the diffuse infiltration type is the least common, the lesion generally does not extend beyond the bronchial wall, common symptoms are difficulty breathing or wheezing (54%), Cough (49%), hemoptysis (46%) and hoarseness (24%), etc., due to airway stenosis secretions often have secondary infections, cough is persistent, with cough and sputum, may have fever, lung Department of dry and wet sputum and white blood cells increased, bronchial obstruction can cause lobes or atelectasis of the lungs, patients may have shortness of breath after activity, difficulty breathing, lung volume reduction sign and local breath sound reduction, blood vessel wall amyloidosis leading to blood vessels Increased fragility and decreased contractility, and this disease is often accompanied by coagulation mechanism, so hemoptysis is quite common, X examination can show obstructive pneumonia, atelectasis and airway focal or diffuse stenosis, about 1/4 patient X-ray Seen in the normal range, high-resolution CT bronchography Clearer display of trachea, thickening of the bronchial wall and prominent nodules in the cavity, and some with calcification, bronchoscopy can be seen in the airway wall multi-fog or single-potential bulge or general hypertrophy, stenosis, bulge is smooth and pedicle Nodules, ranging in size (up to 1cm in large), covered with intact pale epithelium, sometimes completely obstructed by bronchi, easy to bleed, and have been reported to have died of tracheobronchial amyloidosis in 20 cases (both multifocal or diffuse) Lesions), the main causes of death were hemorrhage, infection and respiratory failure, 7 patients died of bleeding, 4 patients died of massive bleeding due to bronchoscopy, and 2 patients died of diffuse lesions confirmed by primary systemic autopsy. Amyloidosis, according to 15 years of observation at Boston University Hospital, 30% of tracheobronchial amyloidosis died within 7 to 12 years after diagnosis. The prognosis of proximal airway disease is worse than that of distal lesions, and the mortality rate is high.

Some scholars have treated 1 case of bronchial amyloidosis. The patient, male, 50 years old, was admitted to hospital due to intermittent fever, cough, cough and phlegm and shortness of breath after 4 months of repeated treatment. The sound is reduced, blood leukocytes, blood gas, immunoglobulin, etc. are in the normal range; is repeatedly tested for acid-fast bacilli, chest radiograph shows a slight thickening of the lungs, and the right heart has a triangular density increase, and the heart shadow is contoured. Fuzzy signs, lateral shadows in the middle lobe, middle bronchial obstruction signs, pulmonary function tests showed mild obstructive ventilatory dysfunction, bilateral bronchoscopy showed bilateral leaves, segmental bronchus generally hypertrophic deformation, visible polypoid swelling The object and the unevenness were easy to bleed, the right middle lobe was completely obstructed, the right lower lobe and the left lingual bronchus were obviously narrow, the mucosa was congested, and the biopsy was taken at the bronchial bulge on both sides. The bronchial amyloid was confirmed by Congo red staining. Change, the symptoms of antibiotic treatment are alleviated, the right middle lobe is absorbed and partially absorbed, but the basal segment of the right lower lobe appears blurred, and it is treated with antibiotics and low dose cyclophosphamide. After the symptoms were completely relieved, the shadow of the right lower lobe was mostly absorbed. The bronchoscopy showed that the mucosal hypertrophy was relieved, the color was pale, the polypoid prominence was slightly flattened, and the bronchial opening was still narrow. The diagnosis was bronchial amyloidosis with right middle and lower lobe. Obstructive pneumonia and right middle lobe atelectasis.

3. Lung amyloidosis pulmonary amyloidosis has been reported to date more than 160 cases, as mentioned above, pulmonary amyloidosis can be expressed as a single nodular (can evolve into multiple nodules), multinodular, miliary ( With fusion nodular type) or pulmonary interstitial (alveolar septum) diffuse type, the age of onset is 37 to 95 years old (average 65 years old).

Single nodular type has been reported in 47 cases, multi-nodular type in 56 cases; male to female ratio of 1.4 to 1.5:1, only 25% of single nodular type and 50% of multiple nodular type have symptoms, the main symptoms are cough, no sputum or Less sputum, hemoptysis and shortness of breath after activity, hemoptysis is mostly intermittent small amount or blood in the sputum, lung function is generally not damaged, lesions are often found by chest X-ray or CT examination, chest radiograph shows a clear boundary Or multiple circular shadows, mostly located in the surrounding subpleural area, ranging from 1 to 8 cm in diameter, may have mild lobulation, calcification and cavity formation, sometimes difficult to distinguish from primary or metastatic tumors, the prognosis is better, there are Case reports have a survival of 20 years, with few single nodular (2%) and multiple nodular (7%) combined with systemic amyloidosis.

32 cases of miliary or fusion nodular have been reported, the ratio of male to female is 1:1. About 90% of this type has symptoms, mainly dyspnea, shortness of breath, cough, coughing a small amount of white sticky sputum and hemoptysis. Can be heard dry and wet voice, lung function test can show restrictive ventilation disorder, X-ray chest radiographs are diffuse miliary or small nodular shadow, can also be reticular nodules, can be associated with hilar lymphadenopathy Large (lymphoid amyloidosis), CT film can more clearly show the shape and location of the lesion, clinical diagnosis has certain difficulties, about half of the reported cases are post-mortem autopsy diagnosis, the rest is bronchoscopy lung biopsy or thoracotomy Lung biopsy diagnosis, more common pulmonary infection, at this time often have fever and respiratory heart rate, the lungs appear wet voice or the original dry and wet voice increased significantly, white blood cells can rise, ESR increased, about 16% combined Systemic amyloidosis, the lesions are chronic progressive, and the prognosis is worse than the nodular type.

There are 31 cases of diffuse pulmonary interstitial, all cases have symptoms, progressive shortness of breath, the most frequent respiratory distress, other cough, cough, blood in the sputum, etc., patients with repeated pulmonary infection, frequent fever and cough Purulent sputum, check the two lungs can be heard cracking sounds, late cyanosis and hypoxemia, pulmonary function tests have diffuse reduction and restrictive ventilation disorders, chest X-ray signs and miliary nodules are difficult to distinguish, also Nodular or reticular nodular shadow, sometimes similar to pulmonary edema, often associated with hilar mediastinal lymphadenopathy, may have a single or double pleural effusion, high-resolution CT helps to suggest diffuse pulmonary interstitial In addition to the reticular and flaky shadows, the interlobular septal thickening can be seen. The middle and lower lobe are scattered in small nodules with a clear boundary of 1 to 4 mm in diameter. Some of them can be fused, and calcification is visible in the middle and lower parts. Pathological histological examination of lung biopsy, 64.5% of the 31 cases reported have systemic or cardiac amyloidosis, the disease progresses rapidly, the patient died of respiratory failure, secondary infection or systemic failure, and very few cases are chronic progressive. Survival period is about 3 5 years.

Some scholars have observed a systemic amyloidosis with both pulmonary miliary nodule and alveolar septum. The male patient, 74 years old, was admitted to hospital due to progressive dyspnea, cough, cough, loss of appetite, 3 years ago. Ulcerative colitis, prolonged unhealed, 2 years ago chest radiograph found two lungs increased in texture and mesh shadow, physical examination of shortness of breath, 30 times / min, low lung breath sounds, lower lung scattered in wet voice, blood biochemistry There was no obvious abnormality in the immunological examination. The chest radiograph showed diffuse reticular nodular shadows of both lungs, with a small density of small calcifications, a small amount of pleural effusion on the right side, and increased heart shadow. No tumor cells were found in pleural effusion. Oxygen therapy, anti-infective and corticosteroids and immunosuppressive agents were not effective, dyspnea and hypoxemia were progressively aggravated. The patient died after 3 months, and multiple organs were found at autopsy. Loss, lung damage is the most serious, the two lungs are covered with gray nodules, the texture is hard and sandy, and histology shows that the nodules contain unstructured eosin, with calcification in the center, Congo red staining and polarized light. Mirror observation confirmed as amyloid, mainly invading the pulmonary vascular wall Interstitial lung, and pleural surrounding alveolar septa are also involved, heart, liver, spleen, adrenal, colon and thyroid have amyloidosis.

So far, 14 cases of pleural amyloidosis have been reported, mostly a manifestation of systemic amyloidosis. There are also some cases involving simple pleural effusion. The pathology shows inflammatory reaction in the pleura. The lesions involve small blood vessels and lymphatic vessels, and amyloid deposits. Between the deep layer of dense collagen and the surface layer of granulation tissue, the surface of the pleura is often covered with cellulite exudate, and the pleural fluid is mostly exudative. Because amyloid fibrils often block the lymphatic vessels, causing back absorption disorder, after the chest fluid is removed There is a clear tendency to relapse, a small amount of pleural fluid is leaking, mainly due to heart failure, the diagnosis needs to rely on common pleural biopsy, thoracoscopic guided or open chest pleural biopsy confirmed, in addition, there are reports of a few diaphragmatic amyloid myopathy Amyloidosis of the diaphragm can cause a decrease in trans-sacral pressure, muscle weakness and respiratory failure, and is mostly one of the manifestations of systemic amyloidosis.

The above-mentioned amyloidosis can be combined, and the respiratory amyloidosis can be part of the systemic amyloidosis. About 20% of patients have other underlying diseases, the most common being tuberculosis, hypergammaglobulinemia , Sjogren's syndrome, rheumatoid and other connective tissue diseases, nephrotic syndrome, malignant tumors and syphilis, etc., also secondary to allergic alveolitis and pneumoconiosis, such clinical symptoms of secondary amyloidosis are often not obvious, More than chest X-ray examination or bronchopulmonary biopsy or even autopsy, therefore, patients with respiratory amyloidosis should be examined to determine the presence or absence of underlying disease, so as not to delay the treatment of the latter.

Bronchopulmonary amyloidosis is rare, clinical manifestations vary, can involve multiple systems, organs, secondary symptoms are often confused with the underlying disease, it is easy to miss diagnosis or misdiagnosis, therefore, improve the awareness and alertness of the disease, Familiar with a variety of clinical manifestations, it is very important, detailed medical history and serious physical examination is still the first step of correct diagnosis, especially for patients with chronic inflammation, tumor patients or family history, such as a multi-issue Sexual myeloma patients have fatigue during treatment, difficulty breathing after exercise, chest radiographs found limited or diffuse shadows, no signs of infection, C-reactive protein does not increase, you should suspect the disease and carry out corresponding examination.

It is often seen in chest X-ray or fiberoptic bronchoscopy that many patients are asymptomatic, especially pulmonary nodular type. The chest radiograph has an important suggestive effect on lung amyloidosis, which can show the extent of the lesion and Type, bronchoscopy can visualize the morphological changes of the tracheobronchial tree and take a biopsy. Patients with lung lesions should also perform this test to determine whether there is airway damage. The high-resolution CT and bronchoscopy of the lungs can be more clear. The lesions and details are displayed. The lung function and blood gas examination only play an auxiliary role. Most patients have normal results, and amyloid deposition is a morphological change. Therefore, histopathological examination is the gold standard for the diagnosis of this disease. The specimens in place are the key to histological examination. Laryngeal and tracheobronchial specimens can be taken more than once or more to increase the positive rate. It is feasible for bronchoscopy lung biopsy (TBLB) for diffuse lung lesions. The nodular type can be chest X-ray biopsy under X-ray or ultrasound guidance. In recent years, thoracoscopic TV-guided pleural and lung biopsy can clearly observe the adjacent pleura. In the case of a large piece of tissue specimen, the damage and complications are less than that of open lung biopsy, but certain equipment and operation skills are required, and the cost is high. The most reliable specimen can be obtained by open lung biopsy. Generally, the above examination cannot be performed. To determine the implementation of the diagnosis, regardless of the type of biopsy, should pay attention to the problem of combined bleeding, in advance to prepare for anti-bleeding, the operation is as soft and accurate as possible.

Once the bronchopulmonary amyloidosis is diagnosed, other organs should be examined for bone marrow biopsy, abdominal subcutaneous fat biopsy, skin biopsy, rectal mucosal biopsy or renal biopsy to determine whether it is systemic amyloid. change.

Examination of pulmonary amyloidosis

Amyloid fibril type can be identified by immunofluorescence and immunohistochemistry. Immunoperoxidase staining can identify lambda () light chain and kappa () light chain in amyloid and plasma cells. AL, AA protein and thyroxine transporter monoclonal antibody can determine the type of most patients, can also use potassium permanganate to eliminate Congo red staining to distinguish between AA protein (can be eliminated) and AL (can not be eliminated), amyloid chemical extraction After the amino acid sequencing, the type can be determined more accurately.

X-ray films have an important role in the amyloidosis of the lungs, showing the extent and type of lesions. Bronchoscopic examination can visualize the morphological changes of the tracheobronchial tree and take biopsy. Patients with lung lesions should also perform this examination. To determine whether there is airway damage, high-resolution CT and bronchoscopy of the lungs can clearly show the lesions and details. Pulmonary function and blood gas examination only play an auxiliary role. Most patients have normal results, and amyloid deposition is Morphological changes, so histopathological examination is the gold standard for the diagnosis of this disease. Obtaining sufficient specimens is the key to histological examination. Throat and tracheobronchial specimens can be taken more than once or more to increase the positive rate. Transbronchial lung biopsy (TBLB) is feasible for diffuse lung disease. Thoracic wall lung biopsy can be performed by X-ray or ultrasound guided chest wall biopsy. Can clearly observe the lesions adjacent to the pleura, take larger pieces of tissue specimens, less damage and complications than open lung biopsy, but need certain equipment and operation skills And expensive, open lung biopsy specimens can obtain the most reliable, the general purposes of the above checks can not be determined at the time of diagnosis.

Once the bronchopulmonary amyloidosis is diagnosed, other organs should be examined for bone marrow biopsy, abdominal subcutaneous fat biopsy, skin biopsy, rectal mucosal biopsy or renal biopsy to determine whether it is systemic amyloid. change.

Diagnosis and differentiation of pulmonary amyloidosis

As mentioned above, the suspected diagnosis of this disease mainly lies in the familiarity and alertness of the clinician. For the underlying diseases that may be complicated by amyloidosis, there is no obvious incentive for shortness of breath, hoarseness, cough or hemoptysis after activity. Fiberoptic laryngoscopy or bronchoscopy see airway patchy hypertrophy or nodular bulge, chest radiograph showing isolated nodules or reticular nodules in the lungs or repeated atelectasis, should consider the disease, and actively related Histopathological examination to confirm the diagnosis.

Laryngeal amyloidosis must be differentiated from larynx, malignant tumor and recurrent laryngeal nerve palsy, both of which have hoarseness symptoms, but it is not difficult to identify with this disease. Laryngeal tumor can be confirmed by biopsy histopathology, recurrent laryngeal nerve Paralysis has no local mucosal hypertrophy or polypoid changes. Indirect laryngoscopy and fiber laryngoscopy can be seen on one side of the vocal cord paralysis, can not be closed, chest radiograph can show mediastinal lymphadenopathy, resulting in recurrent laryngeal nerve compression, mostly due to lymph node metastasis of lung cancer .

Tracheal bronchial amyloidosis should be differentiated from bronchial tuberculosis and tumors, bronchial tuberculosis often accompanied by tuberculosis, more irritating cough, fever, night sweats and other symptoms of tuberculosis, bronchoscopy can be seen mucosal congestion, caseous necrosis or ulcer formation, and the disease The mucous membrane is completely pale and completely different. The acid-fast bacilli can be found in the brush or lavage fluid. The bronchial cancer progresses rapidly, and the obstructive symptoms appear earlier. The mucosal mass is obvious under bronchoscopy, which may be accompanied by epithelial damage, bleeding, erosion or dishing. The pattern can be covered with white moss-like necrosis. The above manifestations can be identified with the disease. The final diagnosis depends on the results of histopathological examination.

Pulmonary nodular amyloidosis should be differentiated from lung, malignant or metastatic cancer, diffuse miliary or alveolar septal amyloidosis and pulmonary interstitial fibrosis, sarcoidosis, allergic alveolitis and other diffuse Interstitial disease and hemosiderin deposition, alveolar microlithiasis and other depositional diseases are identified, and various necessary biopsy methods are needed to actively obtain specimens and confirm the diagnosis by pathological examination.

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