Traditional Culture Encyclopedia - Photography and portraiture - Brief introduction of Wegener granuloma
Brief introduction of Wegener granuloma
2 English references Wegener granulomatosis
3 disease alias Wegener granuloma
4 disease code ICD:M3 1.3
5 disease classification respiratory medicine
6 disease overview Wegener (Wegener? Granulomatosis (WG) is a systemic necrotizing vasculitis disease with complicated clinical manifestations and poor prognosis, characterized by granulomatous changes in the whole respiratory tract, including systemic necrotizing vasculitis and glomerulonephritis. The ratio of male to female is 3∶2, and the peak age of onset is 30 ~ 50? Years old. The onset is slow, and the general symptoms are general weakness, fatigue, anorexia, emaciation and fever. Fever is often accompanied by upper respiratory tract infection, especially secondary infection of paranasal sinuses, and can also occur in patients who have no obvious active infection but are the main symptoms of the disease. About two thirds? 10 The first symptoms were nose, pharynx and mouth symptoms and fever.
7 disease description Wegener (Wegener? Granulomatosis (WG) is a systemic necrotizing vasculitis disease with complicated clinical manifestations and poor prognosis, characterized by granulomatous changes in the whole respiratory tract, including systemic necrotizing vasculitis and glomerulonephritis. Klinger( 193 1) reported a case for the first time, which was dissected as "borderline nodular polyarteritis". Wegner? At 1936? Annual report 3? For example 1939? Report again 18 in? According to the data of biopsy and autopsy, the disease was named "rhinogenic granuloma", which mainly involved arteries and kidneys, and was named Wegener granuloma. To 1950? Goldman? With Churg? The disease was expounded in detail and systematically from the pathological aspect. 1973? Fauci? With Wolff? Further observation of WG? Treatment and prognosis.
The male-female ratio of symptoms and signs is 3∶2, and the peak age of onset is 30 ~ 50? Years old. The onset is slow, and the general symptoms are general weakness, fatigue, anorexia, emaciation and fever. Fever is often accompanied by upper respiratory tract infection, especially secondary infection of paranasal sinuses, and can also occur in patients who have no obvious active infection but are the main symptoms of the disease. About two thirds? The first symptoms of these patients are nose, pharynx and mouth symptoms and fever, and joint pain, orbital tumor, skin, lung and ear involvement are rare. Nephritis is an early manifestation occasionally, and there are no other symptoms of system involvement. Some patients take unexplained high fever as the first symptom. 2/3? The primary lesions of the above patients are in nasopharynx and oral cavity. Primary tumors of joints, skin, lungs and eyes are rare. According to pathological features, morphology and clinical manifestations, the disease can be divided into general type and limited type (incomplete type), and the latter can be divided into three types. A subtype.
1. Whole body type
(1) Respiratory system: Most patients started with intractable upper respiratory symptoms. The typical clinical manifestation is the continuous increase of nasal secretions or long-term purulent nasal discharge, which can cause nasal mucosal ulcer and sinus pain at the same time. The typical onset mode is persistent upper respiratory tract infection or sinusitis, which can last for weeks to months. It can also be manifested as severe nasal congestion, nosebleeds and nasal pain. Gangrenous rhinitis can occur after the destruction of nasal mucosa. In addition, erosion and necrosis of nasal mucosa, destruction of cartilage and bone can also occur, which often leads to perforation of nasal septum or saddle nose due to the destruction and collapse of nasal bone and cartilage. Some patients had no symptoms of upper respiratory tract at first, but showed symptoms of lower respiratory tract such as cough, excessive phlegm, hemoptysis, shortness of breath, chest pain and chest discomfort. Individual patients presented with intercostal muscle pain and severe asthma, accompanied by eosinophilia and transient pulmonary infiltration. During auscultation, both lungs have dry and wet rales, which are wandering.
(2) Skin: About half patients have skin damage, which is one of the early manifestations of this disease. Clinical manifestations vary from purpura and ecchymosis caused by allergic vasculitis to papules, blisters, ischemic ulcers and subcutaneous nodules. Subcutaneous nodules are typical features of necrotizing granulomatous vasculitis. Sometimes the skin lesions show exudative erythema multiforme, telangiectasia and bleeding spots. The above lesions are mostly located on the face and limbs, especially on the extension side of joints. Older people may have pigmentation and scar formation.
(3) Urinary system has different degrees of renal damage, which is a common manifestation of systemic disease. Although some patients may have no obvious symptoms of renal disease, once renal damage occurs and is not treated in time, it can usually develop into rapid progressive renal failure. Patients without clinical and urine characteristics of nephritis were found to have histological changes of focal nephritis by renal biopsy. Renal damage is characterized by hematuria and proteinuria, and some patients have the characteristics of nephrotic syndrome, accompanied by a large number of red blood cell casts, transparent casts and granular casts. After these changes, oliguria or anuria may occur, accompanied by a sharp drop in creatinine clearance rate and other laboratory changes of renal insufficiency.
(4) Nervous system: about 1/3? Some patients may have nervous system manifestations, which are caused by vasculitis or granuloma injury, such as coma, hemiplegia, subarachnoid hemorrhage, cerebral palsy, cerebrospinal meningitis, dyskinesia and brain stem lesions. Peripheral nerve involvement is the same as typical polyarteritis nodosa, and it is also an asymmetric compound neuritis with motor and sensory disorders, which is caused by neurovascular malnutrition.
(5) five senses: about 2/3? % patients have ocular symptoms, and their clinical features range from mild keratitis to severe scleritis. Some patients show granulomatous sclera and uveitis, which can cause scleral softening holes. Secondary ptosis may also occur, which is caused by the spread of sinusitis or primary orbital granulomatous vasculitis. Retinal artery thrombosis, nasolacrimal duct obstruction, corneal ulcer and severe eye pain may also occur. Serous otitis media is also a common manifestation of this disease, which is usually secondary to Euclidean duct obstruction, but granulomatous destruction of ear structures such as tympanic membrane can also occur. Deafness in some patients may be the first symptom of this disease.
(6) Others: Some patients may have gastric and duodenal ulcer, granuloma formation, abdominal pain, hematemesis and bloody stool. There may be hepatomegaly and splenomegaly with abnormal liver function. About 15% of patients may have heart involvement, manifested as pericarditis, panpericarditis and coronary arteritis, and may be accompanied by heart failure, myocardial infarction and intractable arrhythmia. Most patients may have joint pain and joint cavity effusion. Joint symptoms reflect the activity of the lesion. A few patients may also suffer from mumps, orchitis and prostatitis.
2. Limited types
(1) respiratory and pulmonary diseases above type I are the main diseases. The onset is swelling and pain in the pharynx, and multiple tumors can appear in the posterior pharynx, showing different degrees of dysphagia, pain and bleeding. Blocky shadows or nodular shadows can appear on both lungs, which are manifested as cough, excessive phlegm, hemoptysis and chest pain. There is no kidney disease in this type.
(2) Type II is mainly nose, pharynx, oral cavity or eye diseases. Upper respiratory symptoms, sinusitis or eye diseases are often the first symptoms. The eye diseases are orbital tumor, exophthalmos and corneal ulcer. Clinicopathologically, it is easy to be misdiagnosed as "orbital inflammatory pseudotumor". There are two kinds of eye diseases: ① Proximity type: most of them are upper respiratory tract diseases that spread to orbit to form granuloma and severe exophthalmos, including paraoptic edema, fundus hemorrhage and venous dilatation. ② focus type: typical bilateral latent ulcer around cornea, caused by ciliary vascular atresia caused by necrotizing vasculitis, often accompanied by corneal lesions.
(3) Type III: The first symptom of this type is central nervous system, skin damage or reticuloendothelial system hyperplasia, and it is characterized by coma, urinary incontinence, rash, high fever, hepatosplenomegaly, systemic lymphadenopathy, cardiac symptoms or simple nephritis symptoms.
The cause of this disease is unknown. In Chlad? And HLADQW7? Frontal feather stare of WG patients? There is a high incidence: because most patients often get sick in winter and spring, accompanied by changes in respiratory system, the disease may be related to infections such as bacteria, viruses and mycoplasma, but no evidence has been found.
10 pathophysiology The discovery of antineutrophil cytoplasmic antibody (ANCA) and immunopathological research prove that this disease is an autoimmune disease. 2/3? The positive of rheumatoid factor in the above patients also suggests that it is an immune complex formed by autoimmune reaction, which activates a series of inflammatory reactions mediated by complement. ANCA? The corresponding antigens are protein kinase 3(PR3) and peroxidase. According to the phenotype of cell staining, the former is called CANCA and the latter is called PANCA. Zhongkanka? It has high specificity. Conca? It can also react with intracellular or cell surface substances of vascular endothelial cells, polymorphonuclear cells and CD4+ lymphocytes, and can pass TNFa? And soluble interleukin -2? Cells with receptors above * * * further indicate that this disease is vasculitis caused by immunopathological process. The main pathological features are total respiratory necrotizing granuloma, systemic necrotizing vasculitis and focal nephritis. The histological changes of granuloma are the infiltration of megakaryocytes, epithelioid cells, lymphocytes, neutrophils and eosinophils, and there is no caseous necrosis or granuloma layered structure as seen in tuberculosis lesions. But there is necrosis in the center of the lesion, similar to tuberculosis. Nonspecific granulomatous lesions are systemic, accompanied by necrotizing or granulomatous vasculitis, involving arterioles, arterioles and veins. In the acute stage of vasculitis, there may be full-thickness and cellulose-like necrosis of diseased blood vessels, accompanied by neutrophil infiltration; In the recovery period, the necrotic vascular wall is organized and the vascular lumen is embolized, which can lead to compensatory lumen reconstruction. The pathological change of kidney was focal nephritis. Immunopathology of kidney found that IgG existed in glomerular lesions. There are lymphocytes and megakaryocytes infiltrating in granuloma. Almost all patients have extensive superficial ulcers in trachea and bronchus; Extensive superficial ulcers and granulomas can occur in nasopharynx, sinuses, soft palate and glottis. Lesions often spread to the surrounding cartilage and bone tissues, and they are destroyed and corroded. Granuloma can also occur in the middle ear and orbit, and can also destroy the bone tissue around the lesion. There are persistent granulomatous lesions in the lung, which can be unilateral or bilateral, often accompanied by central necrosis and liquefaction, and sometimes granulomatous lesions in the lung are millet-shaped, mostly located around the bronchi. The incidence of pathological changes in each system is as follows: nasopharynx 90%, sinus 95%, lung 95%, kidney 80%, joint 57%, skin 47%, eye 60%, ear 35%, heart 29% and nerve 24%. Traditional Chinese medicine believes that the disease is caused by deficiency of qi and blood, yin deficiency of liver and kidney, invasion of heat and toxin, obstruction of meridians and blood stasis.
1 1 Diagnosis: The diagnosis of this disease depends on the clinical and histopathological manifestations: ① There is typical necrotizing granulomatous vasculitis in the whole respiratory tract; ② Necrotizing vasculitis of lung and skin; ③ Focal necrotizing glomerulonephritis. Localized Wegener's granuloma can't be diagnosed only by tissue biopsy, because it is easy to be misdiagnosed as chronic inflammation, and it must be judged comprehensively by combining clinical manifestations. The following pathological examinations can be made for suspicious cases: ① chronic rhinitis, sinusitis with mucosal erosion or granulation tissue hyperplasia; ② Ulcer, necrosis or granuloma of eye and oral mucosa; ③ Wandering shadows or cavities can be seen in the lungs; ④ The skin has purpura, erythema, necrosis or ulcer; ⑤ Renal biopsy was positive. From this, a definite diagnosis can be made. 1990? The classification diagnostic criteria of American Rheumatology Association had high application value in (table 1).
Laboratory examination:
1. Blood routine and erythrocyte sedimentation rate? 1/3? % patients have moderate anemia; Mild to moderate leukocytosis, sometimes the total number of leukocytes can reach (10 ~ 20) × 109/L, the differential count of neutrophils is obviously increased, and occasionally leukopenia occurs. There may be thrombocytopenia. But in the active phase of the disease, platelets increase. Occasionally, eosinophilia occurs. The erythrocyte sedimentation rate (ESR) of all patients increased to varying degrees.
2. Urine routine? Visible proteinuria, hematuria, tubular urine.
3. Routine fecal occult blood test is positive occasionally.
4. Biochemical examination? Some patients have abnormal liver function. When uremia occurs, blood urea nitrogen? Elevated, uremia and other blood biochemical abnormalities. Protein electrophoresis showed 7? Globulin is elevated.
5. Immunological examination? More than half of the patients were positive for rheumatoid factor. See more IgA? Elevated, there may be an increase in IgE. When the complement is normal or slightly elevated, the immune complex and C- reactive protein can be detected as positive. Nearly 1/3? Hepatitis B surface antigen carriers. Positive. Lupus cells are negative. A few patients are positive for antinuclear antibody, anti-SSA and SSB? Antibody positive. Antineutrophil plasma antibody (ANCA) against WG? The diagnosis is specific, among which CANCA? This is especially true. More than 90% of active WG? Can be positive. Can the remission period after treatment make ANCA? Turn negative, so you can surpass ANCA? Objective to detect the activity and curative effect of the disease as an observation index
Other auxiliary inspections:
X-ray examination shows that there is usually no abnormality in the lungs during the onset period, and some cases always have no X-ray. Change the line. More than half of the patients may have pulmonary interstitial texture enhancement and single or multiple nodules and masses of different sizes due to pulmonary vasculitis and granuloma, with diameters ranging from several millimeters to several centimeters. The outline of the mass can be clear and regular, similar to metastatic tumor, or it can be blurred and irregular due to surrounding inflammation. Voids are quite common, even in 1/3 ~ 1/2? In 90% cases, the cavity can be reduced with the improvement of the disease, and it can continue to increase when the disease recurs. When the cavity begins to form, the wall thickness and inner wall are irregular, and then it can develop into a thin-walled cavity, which looks like a thin-walled cyst. These manifestations have more diagnostic reference value. CT? Examination: Typical manifestations are multiple nodules with different sizes on both sides, with smooth or slightly blurred edges, about 1/3 ~ 1/2? It is a thick-walled cavity with rough and irregular inner wall. After treatment, the cavity can become thinner or even disappear completely. About 20% patients show solitary nodules, which can show huge cavity changes. Endobronchial lesions may lead to obstructive pneumonia or atelectasis. In addition, a small amount of pleural effusion may occur, and hemopneumothorax may also be caused by rupture of necrotic lesions. In patients with pulmonary hypertension, hilar vessels are enlarged. A few cases of hilar lymph node enlargement. In patients with myocardial lesions or pericardial effusion, the shadow of the heart will generally increase, which, like other rheumatism, has no characteristics. Other x? X-ray manifestations were nasal soft tissue mass, sinusitis changes and nearby bone destruction. Tomography can show granuloma of larynx and trachea.
The differential diagnosis of 12 must be differentiated from other diseases such as granulomatous inflammation and vasculitis.
1. Pulmonary hemorrhagic nephritis syndrome? Pathological examination showed that anti-glomerular basement membrane antibody and fluorescent antibody were used to detect linear IgG, which was different from Wegener granuloma.
2. lymphoma-like granuloma? In addition to no upper respiratory tract involvement, renal biopsy showed glomerular lymphatic infiltration, which can be differentiated from this disease.
3. Idiopathic midline granuloma? It is a local destruction disease of face and upper respiratory tract, which can be differentiated from this disease by renal biopsy.
4. Other Wegener granulomas? With eosinophilia, we should also pay attention to distinguish it from many primary diseases that cause eosinophilia, especially from allergic granuloma, which is characterized by fever, paroxysmal asthma and eosinophilia. The histopathological changes were mainly eosinophil infiltration, and the epithelioid cells around the lesion were arranged radially. The blood vessels involved are small and medium-sized arteries, arterioles, veins and capillaries, and there is no clinical manifestation and X? Line features. In addition, the pulmonary symptoms and X-ray features of Wegener granuloma are obviously different from allergic granuloma.
13 treatment plan when the primary site of the lesion is in the upper respiratory tract, X? Local irradiation can control local injury. Glucocorticoid can relieve symptoms and prolong the life of patients, and its dosage, administration mode and drug types are the same as those of typical nodular polyarteritis. In recent years, immunosuppressants have achieved good results in the treatment of this disease, especially in renal failure, combined with azathioprine 200mg/ day? And cyclosporine (cyclosporine A)? 0.5mg/d, it is reported that the effect is better. Some people also use trimethoprim (compound sulfamethoxazole) to treat WG with upper respiratory tract inflammation. Good curative effect has been achieved. Combined chemotherapy with alkaloids such as vincristine and alkylating agent cyclophosphamide can relieve symptoms faster than glucocorticoid alone, and the recurrence is slower after drug withdrawal. In addition, the combination of glucocorticoid and cyclophosphamide is much better than glucocorticoid alone in the active stage of the disease. Other anti-rheumatic drugs, such as aspirin, phenylbutazone, anti-rheumatic spirit, etc. It can also be used as adjuvant therapy of hormones or cytotoxic drugs. Attention must be paid to the secondary infection caused by chemotherapy. When the sinus is infected, the maxillary sinus should be punctured in time and effective antibiotics should be given to control the infection.
1. western medicine treatment
(1) Corticosteroid hormone: Prednisone is commonly used (1 ~ 2 mg/kg daily). After the symptoms are relieved, take it the next morning for maintenance, which is suitable for local WG. Examples, such as glomerulonephritis, or sensitive person, are treated with immunosuppressants or immunosuppressants without hormone alone.
(2) immunosuppressant: ① cyclophosphamide: 1 ~ 2mg/kg/ day; ② Azathioprine: 2 mg/kg per day; ③ Combined medication: Prednisone+cyclophosphamide+azathioprine combined with sequential application. Matters needing attention in immunosuppressant treatment: ① Check the blood picture regularly, and stop taking the medicine if the white blood cell is lower than 3× 109/L; ② Immunosuppressants should be used before renal failure. Once renal failure occurs, hemodialysis and kidney transplantation are still needed. ③ Cases with effective immunosuppressants need maintenance treatment 1? You can gradually stop taking drugs after a few years.
(3) trimethoprim: According to individual authors, trimethoprim can make WG? Long-term remission may be a factor to help control infection, but some people think that it can be applied in selected situations and should not be widely recommended.
2. Chinese medicine treatment
Treatment principle: heat toxin blocks collaterals, and it is advisable to clear away heat and toxic materials, promote blood circulation and remove blood stasis; Deficiency of qi and blood, blood stasis blocking collaterals, should benefit qi and nourish blood, eliminate evil and dredge collaterals; Qi stagnation and blood stasis, promoting qi and promoting blood circulation; Yin deficiency of liver and kidney, hyperactivity of liver yang, should nourish yin and subdue yang, promote blood circulation and remove blood stasis. Commonly used prescriptions: ① Jiawei Simiao Yong 'an Decoction; ② Shenqi Guizhi Wuwu Decoction is ambiguous; ③ Xuefu Zhuyu Decoction; ④ The experience in diagnosis and treatment of modified Zhengan Xifeng Decoction is as follows. ① Huiyang Jianzhongfang: The main drugs are Radix Aconiti Lateralis Preparata (decocted first), Radix Angelicae Sinensis, Radix Paeoniae Alba, Radix Salviae Miltiorrhizae, Atractylodis Rhizoma, Poria, Rhizoma Chuanxiong, Pericarpium Citri Tangerinae, Caulis Spatholobi, Fructus Lycii, Cortex Magnolia Officinalis, Radix Angelicae Pubescentis and Radix Aucklandiae; ② Wenyang Yiqi recipe: the main drugs are aconite, cinnamon, codonopsis pilosula, dodder, dogwood, Pseudostellaria heterophylla, Radix Glycyrrhizae Preparata, Angelica sinensis, Chuanxiong, Carthami Flos, Dioscorea opposita, Scrophularia, Carthami Flos, peach kernel, Salvia Miltiorrhiza, Adenophora adenophora, Ophiopogon japonicus, magnet, Radix Paeoniae Alba, Rhizoma Cyperi, Zingiberis Rhizoma, Schisandra chinensis, Asarum and Astragalus. Many clinical reports think that WG? At the same time, glucocorticoid and/or immunosuppressant are used, and the curative effect of traditional Chinese medicine is significantly improved.
Step 3: Nursing
(1) nursing problems:
① Pain and infection.
② Eye injury.
③ Other systems are damaged.
(2) Nursing objectives:
① Relieve pain and control infection.
② Prevention and relief of eye discomfort.
③ Strengthen nutrition and physique.
(4) Prevent other systems from being damaged.
(3) Nursing measures:
① Give supportive therapy, strengthen nutrition, transfuse blood, enhance physical fitness and control infection.
② According to the infection situation, different antibiotics were used to control the infection. Physical therapy methods such as local hot compress, ultrashort wave and infrared ray can be used to promote inflammation regression and improve symptoms. In order to relieve the symptoms of sinusitis, head-down drainage can be used to promote secretion drainage and control infection. Methods: First, 1% ephedrine saline was dripped into the nose, which made the mucosa contract, the ostium of sinus unobstructed and convenient for drainage. The patient takes a sitting position, his lower limbs are separated, his upper body leans downward, and his head hangs close to his knees, which is convenient for pus in the sinus to be discharged into the nasal cavity.
③ Check your eyesight regularly to understand the eye involvement. Pay attention to eye cleaning and remove inner canthus secretion in time. People with exophthalmos should pay attention to avoid corneal dryness, injury and infection. Wear protective glasses for outdoor activities to avoid sandstorms. Wash conjunctival sac and eye drops frequently, and apply eye ointment and eye mask before going to bed.
④ Clinical observation to prevent other systems from being damaged.
Complications of 14 can occur nasal mucosa erosion and necrosis, cartilage and bone destruction, and often lead to nasal septum perforation or saddle nose due to nasal bone and cartilage collapse. It can also be papules, blisters, ischemic ulcers and subcutaneous nodules. Subcutaneous nodules are necrotizing granulomatous vasculitis. It may also be accompanied by joint cavity effusion. A few patients may also have gills.
Adenositis, orchitis and prostatitis.
15 prognosis and preventive prognosis: the mortality rate was very high in the past. Since the combination of glucocorticoid and cyclophosphamide, the remission rate has reached more than 90%. The annual survival rate is 85%, and our treatment rate is 1? A patient survived 16? I still lived a normal life in 2008. Most patients died of renal failure, or secondary infection and hemoptysis. Early diagnosis and treatment have a great influence on the prognosis. It is reported that the disease is mostly malignant if it is not treated, and 82% patients are in 1? Died during the year, with an average survival time of 5? Last month. It is also reported that the survival time of 75% patients is 5-8 years. Year, the longest is 10? Yu Nian
Prevention:
1. Primary prevention
(1) Strengthen nutrition and physical fitness.
(2) Prevention and control of infection and improvement of autoimmune function.
(3) Avoid cold, humidity, fatigue, alcohol, tobacco and spicy food.
(4) Protect your eyes, goggles and nose when you are outdoors.
2. Secondary prevention? Early diagnosis, understanding of eye and nose infection, clinical observation, early detection of various system damage and early treatment are mainly to control eye and nose infection.
3. tertiary prevention? Pay attention to lung, kidney, heart and skin lesions, and pay attention to the occurrence of secondary Staphylococcus aureus infection. In addition, the nervous system and digestive system may also be involved, and the application of traditional Chinese medicine can regulate immunity, clear away heat and toxic materials, promote blood circulation and remove blood stasis.
16 epidemiology 20? Century 50? Little was known about Wegener's granuloma before 1990s. 193 1? Heinz, a medical student at the University of Berlin in Germany? Klinger? It is the first time to report two patients who died of septicemia due to inflammation of vascular wall involving the whole body. 1936? Year and 1939? Frederick? Wegner? Doctor description 3? A case of syndrome with necrotizing granuloma of upper and lower respiratory tract as the main symptom. 1954? Goldman? Dr. Chulg reported seven more cases. The clinical and pathological features of the disease were reported in detail. Thus people have a preliminary understanding of this syndrome, which is also caused by Friedrich? Wegner? Named after the doctor. 1973, National Institutes of Health (NIH) Fauci? With Wolff? Yes 18? A patient with Wegener's granuloma was relieved after treatment with hormone and cyclophosphamide, which marked a new era in the treatment of Wegener's granuloma. 1990? The American Rheumatology Association (ACR) established the diagnostic criteria of Wegener's granuloma in 1996. The typical Wegener's granuloma triad refers to the lesions involving the upper respiratory tract, lung and kidney, and those without kidney involvement are called localized Wegener's granuloma. The disease is slightly more common in men than in women, and can be seen at any age from children to the elderly, but it mostly occurs in middle-aged people, and 85% of patients are more than 15? Years old, 40 ~ 50? The peak period of this disease is years old, and the average age of patients is 4 1? Years old. The age range reported recently is 5 ~ 9 1? Between the ages of two. According to Gary, Wegener granuloma can occur in all races? Hoffman? Research, WG? The incidence rate is every 3? Ten thousand to five? Per 10,000 people 1? Of these patients, 97% were white, 2% were black, and 1% were of other races. There is no statistical data on the incidence of Wegener's granuloma in China. The ratio of male to female is 3∶2, and the peak age of onset is 30 ~ 50? Years old.
Effect of Tanreqing injection, a Chinese patent medicine for treating Wegener granuloma, on cough latency in mice and mice induced by sulfur oxide: inhibiting xylene-induced granuloma in rats and ear swelling in mice. Adaptability of Tanreqing injection ...
Effect of Longbishu Capsule on contraction of deltoid muscle of bladder in animals. 3. It can inhibit the formation of cotton granuloma in rats, that is, it has anti-inflammatory effect. 4. Increase urine nitrogen 2 hours after animal administration. ...
The ketone extract of Qianliekang tablets can inhibit foot swelling and filter paper granuloma caused by croton oil and ovalbumin. 3. Regulating immune function: improving cellular immunity. ...
Injury effect of Wuren Pill: The pepsin hydrolysate of monarch drug almond has obvious inhibitory effect on inflammatory edema and granulation tissue proliferation. Peach kernel extract can inhibit inflammation. ...
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