chronic eosinophilic pneumonia
Introduction
Introduction to chronic eosinophilic pneumonia Chronic eosinophilic pneumonia (CEP) is also known as persistent eosinophilia and chronic erythrocytic pneumonia (CEP). The disease has a longer course than simple eosinophilia, usually 2 to 6 months, or even more than 1 year, and the symptoms are more serious. basic knowledge The proportion of illness: 0.005% Susceptible people: between 30 and 40 years old Mode of infection: non-infectious Complications: respiratory failure
Cause
Causes of chronic eosinophilic pneumonia
Causes:
The cause of CEP may be similar to that of simple eosinophilia, or it may be an autoimmune disease caused by the synergistic effect of type III and IV allergies, or by type II allergy, despite the exact immune pathogenesis. The mechanism is still unclear, but there is much evidence that eosinophils play an initial important role in lung tissue damage. Before the onset of clinical symptoms, the number of eosinophils in peripheral blood and bone marrow has increased, in BALF. Eosinophil-derived granule protein (EDGP) was also observed on the lung parenchyma and microvessels. EDP was also increased in BALF of patients with CEP, including type II tissue phase. BALF-derived eosinophil expression activation markers, including soluble antigens, are also elevated, although these are not clear in the regulation of eosinophil activation and degranulation in CEP, indicating that these eosinophils are activated. Increased expression of eosinophils derived from type II tissue-soluble antigens and other activating markers in BALF but not in the blood indicates that the immune inflammatory response is localized in the lungs. In vitro, immunoglobulins amplify eosinophil chemotaxis and degranulation, and elevated immune cycle complexes and IgE titers are associated with clinical onset of disease, so far, eosinophil activation and immunoglobulin The relationship between them is still unclear.
Pathogenesis:
Lung damage manifested as infiltration of eosinophils in alveolar and interstitial cells, and associated macrophages and small to moderate lymphocytes and occasional plasma cells, destruction of alveolar wall structure, and localized edema of capillary endothelium Focal type II epithelial hyperplasia, alveolar protein exudation and multinuclear tissue cell infiltration, 1/3 of cases with hyperplastic obstructive bronchiolitis, can also see mild non-necrotic microangiitis, the main effect Small veins, a small number of cases (less than 20%) showed obvious necrosis, eosinophilic microabscess, or non-caseous granuloma, lymphatic biopsy specimens in the mediastinum showed lymphatic hyperplasia and eosinophil infiltration.
Prevention
Chronic eosinophilic pneumonia prevention
1. Increase outdoor activities to enhance the child's immune function, especially the respiratory disease resistance.
2, room ventilation, even in winter, regular ventilation, to keep indoor air fresh, reduce the concentration of pathogenic microorganisms.
3, eat more foods rich in vitamin A, can promote the health of the respiratory mucosa.
4, prevention of respiratory infections, winter and spring, especially during the flu epidemic to avoid taking children to public places. Infected with influenza, measles and other diseases should cause pneumonia.
Complication
Chronic eosinophilic pneumonia complications Complications, respiratory failure
Can be complicated by severe respiratory failure or ARDS.
Symptom
Chronic eosinophilic pneumonia symptoms Common symptoms Cough with wheezing wheezing night sweating night sweats low fever
The disease can occur at any age, but the peak age is 30 to 40 years old, women are almost twice as many as men, most cases are Caucasian, and 1/3 to 1/2 patients have a history of allergic rhinitis or nasal polyps. In addition, 2/3 of the patients have adult episodes of asthma or other respiratory symptoms, showing subacute clinical manifestations, common symptoms are low fever, excessive sweating at night, moderate weight loss, cough, a little sticky, about 2/9 patients had a small amount of hemoptysis, and the patient eventually developed progressive dyspnea, which was associated with paroxysmal asthma. A small number of patients presented with acute severe respiratory failure or ARDS.
Examine
Examination of chronic eosinophilic pneumonia
Leukocytosis >10 × 109 / L, 60% ~ 90% of patients with peripheral blood eosinophilia (> 6%), but the lack of peripheral blood eosinophils can not rule out the disease, you can find more Eosinophils, increased erythrocyte sedimentation rate (>20mm/h), and elevated blood IgE in 1/3 of cases.
Abnormalities and severity of lung function are related to the stage of the disease, typically moderate to severe restrictive ventilatory dysfunction, and decreased DLCO.
An elevation of the alveolar-arterial oxygen gradient, if accompanied by asthma, has an obstructive change.
The X-ray showed a progressive density-enhanced infiltrating shadow with respect to the pleura. The margin was unclear and non-segmented. The distribution of sub-segments and leaves was mostly located 2/3 of the periphery of the lung, and the hilar was more transparent. For "pulmonary edema reverse shape", the shadow is easy to recur in the original place, and the shadow is quickly absorbed after prednisone treatment. Contrary to Loffler' syndrome, the lung infiltration of CEP is non-migratory, with little pleural effusion, atypical X-ray findings include nodular infiltration and diffuse ground-glass-like alveolar filling.
Chest CT examination can be used for CT examination in clinically suspected cases with atypical X-ray findings. The performance of CT, in the first few weeks of symptom onset, is mostly characterized by typical density zone, local alveolar consolidation, when symptoms persist More than 2 months, there is a strip of opaque area, and see the mediastinal lymph nodes.
Diagnosis
Diagnosis and identification of chronic eosinophilic pneumonia
According to the medical history, the course of the disease, asthmatic sounds in both lungs, peripheral blood eosinophils and chest X-ray shadow can be diagnosed clinically, atypical, pathological examination by lung biopsy to confirm the diagnosis, if necessary, prednisone Experimental treatment to aid diagnosis.
The differential diagnosis of CEP includes infection, especially tuberculosis and fungi, especially cryptococcal infection, sarcoidosis, Loeffler's syndrome and the like.
