Interstitial lung disease eight: epidemiology and clinical manifestations of allergic pneumonia

Navigation:Home > Respiratory Medicine > Pneumonia > Interstitial lung disease eight: epidemiology and clinical manifestations of allergic pneumonia

Interstitial lung disease eight: epidemiology and clinical manifestations of allergic pneumoniaHypersensitivity pneumonitis (HP), also known

Content

Interstitial lung disease eight: epidemiology and clinical manifestations of allergic pneumonia

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis (EAA), refers to individuals susceptible to repeated inhalation of organic dust induced lung inflammation after antigen in lung diseases, interstitial mononuclear cell inflammatory cell exudation and bronchioles and scattered characteristic changes in the distribution of pathology non caseating granuloma.

1 epidemiology: HP showed big differences in the prevalence of different populations, and is closely related to occupation, such as the Scotland agricultural area farmer's lung prevalence rate is 2.3%~8.6%, the United States of Wisconsin contact with the hay group the prevalence rate of male 9%~12%. The different HP risk and dangerous season are not the same, the peak incidence of farmer's lung in late winter and early spring, with them in the cold and wet climate using store hay and feed animals, and the Japanese HP summer peak is in warm and humid regions in June to September, and in multiple occupation women. Interestingly, the 80%~95% of HP patients are non smokers, the possible reason is that smoking affects the formation of serum antibodies, inhibit the immune response of the lung.

Common types and causes of allergic pneumonia

2 pathogenesis and pathology: the pathogenesis of HP includes type III and type IV immune response, mainly IV, characterized by granuloma formation. In patients with inhalation of antigen to stimulate the redistribution of peripheral blood lymphocytes to the lungs, local lymphocyte proliferation, and decreased lymphocyte apoptosis led to increased lung lymphocytes. In a few days after antigenic stimulation, the local immune response to T cell alveolitis mainly, which accounted for 60%~70% and naive lymphocytes; macrophages into epithelioid cells and multinucleated giant cell granuloma formation.

Acute and subacute HP clinical diagnosis is not difficult, but the chronic HP misdiagnosis rate is very high, because the HP will disappear from the antigen contact granuloma at 3~4 months after bronchiolitis, performance is not obvious, but only left some nonspecific interstitial pneumonitis and fibrosis is, some patients may and honeycombing changes are often misdiagnosed as IPF.

3 clinical manifestations: common and characteristic HP manifestations of acute HP, usually 2~9 hours occupation or environmental antigen contact clear began to appear after a similar "flu" symptoms such as chills, fever, malaise and chest tightness, dyspnea and cough, the most typical 6~24 in the hours after the onset of symptoms. Check two lungs can smell and fine fine rales or crackles. The severity of the reaction or the severity of the clinical manifestations was related to the amount of inhaled antigen and exposure time. Can be recovered in the detachment after antigen contact 24~72 hours, but if you continue to contact the antigen will be repeated due to acute attacks within a few weeks or months of progressive dyspnea accompanied with the progressive development of cough, subacute form of performance. If long-term exposure to low intensity antigen, may be a chronic form of HP, the performance of the hidden development of dyspnea with cough and weight loss, the bottom of the lungs can be heard and inhale the end of small burst sound, very similar to IPF.

4 imaging: acute forms of typical imaging findings are characteristic, namely the bilateral middle and lower lung field mainly diffuse evenly distributed unclear fine nodules, patchy ground glass opacity or with real variable (Figure 1). After the cessation of antigen exposure 4~6 weeks after the abnormal nodules or ground glass shadow can disappear, so after acute exacerbation of chest X-ray can be no abnormal. CT in addition to small nodules, there will be a patchy ground glass and alveolar hyperinflation staggered to form a mosaic sign (Figure 2), the formation of this phenomenon is due to the HP pathological bronchiolitis, slight concentric bronchial stenosis in the expiratory phase when the bronchioles collapse after the occlusion of alveolar excessive gas retention inflatable. In addition to the characteristics of acute HP, subacute HP findings may also include the presence of a thin line of the pleura and the nodules, as well as an uneven distribution of small nodules (Figure 3). The main manifestations of chronic HP septal and intralobular interstitial thickening, honeycombing tractional bronchi or bronchioles, which mixed with patchy ground glass opacity. In particular, to be reminded that 50% of patients with chronic HP will appear in the honeycomb lung, easy to confuse with the IPF, the identification point is the chronic HP of the cellular lung generally does not affect the angle of the ribs, and the probability of pulmonary fibrosis will be more.

Figure 1. Chest CT of acute allergic pneumonia showing diffuse and small nodules in the lungs of two.

Figure 2. Chest CT findings of acute allergic pneumonia

Figure 3 subacute HP irregular small nodules and shadow

Figure 4. The presence of a mesh and a honeycomb lung in chronic HP

 

www.Cure001.comwww.Cure999.com

Cerebral Vascular Disease,Acne,Heart Disease,Deaf,Headache,Std,Condyloma Acuminatum,Fibroid,Pneumonia,Brain Trauma,。 Rehabilitation Blog 

Rehabilitation Blog @ 2017