Exogenous allergic alveolitis

Overview of exogenous allergic alveolitis (extrinsic allergic alveolitis) is repeated inhalation of certain antigens of organic dust caused by allergic alveolitis. Chang also extended terminal bronchiole. American literature with more allergic pneumonia (hypersensitivity pneumonitis) name. Reported domestic farmers mainly lung, bagasse the lung, the lung mushrooms, feeding the parrots lung and humidification devices lung. Although many of its etiology, pathology, clinical symptoms, signs and X-ray performance very similar. Etiology of exogenous allergic alveolitis many causes, including the common actinomycetes and fungi spores, plant and animal proteins, and the product of bacteria, insects antigen and certain chemical substances, such as organic dust. Some dust nature of the antigen has yet clear. Generally believed that the etiology of lung farmers mainly ordinary high temperature actinomycosis. In recent years, many Chinese scholars have reported another line with the farmers on the high temperature lung actinomycosis a hot Streptomyces hygroscopicus. In many antigen, a thermophilic actinomycetes the most common and important, particularly small number of fungi, Second is the general high temperature actinomycosis. With the fungal pathogen form, with the bacteria. The humid, warm, rotten organic matter breeding, composting, soil, food and water contaminated with a large number of items. Farmers inhaling moldy hay, grain and sugar cane are often easy to end such incidence. Mushroom cultivation and fertilizer production environment present in the air more thermophilic actinomycetes, and the general high temperature actinomycete-based, growers inhalation can lead to lung mushroom workers. Poultry breeders lung (such as the lung feeding pigeons, parrots feeding of the lung, etc.) is due to bird serum, droppings guano, Toba Powder Frost and bird eggs are subject. Some people think pigeons feathers on the Powder Frost is about the size of 1 μm keratin particulate antigen, its pathogenic role than pigeon droppings in serum and more important. Another domestic reporting of silk textile workers from inhaling the air of workplace Silk Dust (possibly Sericin protein) and allergic alveolitis. Humidification devices, and air conditioners cause lung is white thermophilic actinomycetes. Chemical Industry : Application of two widely different cyanide toluene, 1,2-anhydride inhalation, hapten their role may also trigger allergic alveolitis. On tobacco growers, tea growers disease, the nature of antigen not entirely clear. Pathological changes in pulmonary lesion is located, alveolar septal, blood vessels and terminal bronchiole, the pathological changes of the period with the disease. Acute phase : alveolar wall and bronchiole wall edema, a large number of lymphocytes, plasma cells also increased significantly, still mononucleosis, cells, eosinophils and less invasive. About two weeks edema, a large number of epithelial tumor-like granuloma Langhan's giant cells. Many granuloma collagen fibers parcels. Acute pulmonary granuloma lesions typical period, the disease often occur within three weeks, in a slow year dissipated At this point with glucocorticoids may promote their absorption. Chronic : interstitial fibrosis and alveolar wall lymphocyte infiltration, collagen fiber proliferation, especially in the bronchioles and their small artery sometimes because muscle fibers and endothelial cell proliferation and thickening. Granulomatous lesions and then disappeared. As fibrosis stretch and contraction, which may eventually develop pulmonary emphysema, and even cellular, with pulmonary hypertension and right heart hypertrophy. Pathogenesis in recent years that exogenous allergic alveolitis of immune complex disease, type III allergic mechanisms are important, also involves collagen type hypersensitivity. Complement activation system has its significance, and the activation of alveolar macrophages may be the pathogenesis of the central link. (1) - mediated type III allergic sensitization has been in contact with the individual again after antigen 4 ~ 8 hours of onset. Intradermal injection of antigen 4 ~ 6 hours Arthus reaction can occur. and the reaction of the skin specimens were found IgG and complement the sediments. Most patients can be found in serum antigen corresponding to the precipitation antibody (an IgG). Application antigen for bronchial provocation test, there may be clinical and exogenous allergic alveolitis the same lung function changes. Therefore, the disease and complement-mediated allergic III, immune complex is of great significance. (2) T-lymphocyte mediated allergic type IV collagen type noted in recent years in the allergic disease plays an important role used. Patients with lung pathology caseating granulomas form, lymphocytes in vitro encountered corresponding antigen can produce macrophage migration inhibitory factor (MIF). Animal experiments showed that T lymphocytes sensitized to the animals in vivo implantation, and then inhaled antigen inspire, caused human exogenous allergic alveolitis very similar to the lung injury. Outer-derived allergic alveolitis patients with bronchoalveolar lavage fluid were also found in the lymph factor increased. Found support above collagen type hypersensitivity in the pathogenesis of role. (3) Local macrophages with the role of small and mildew Bacillus spores of bacteria can be more directly stimulate alveolar macrophages caused eggs White lyase release, the release of cracking C3 C3b. The latter with the macrophage surface of the complement receptor binding, further activating macrophages, produced including granuloma formation of lung tissue lesions. Currently inclined to think that exogenous allergic alveolitis initially by the III-mediated allergy. Later allergic to collagen type mainly, and macrophage activation and the resulting inflammatory response which can be through non-immune channels, a common cause lung injury. But many details unclear. Diagnosis of exogenous allergic alveolitis lungs without specific symptoms, the diagnosis of the disease should contact history, typical clinical symptoms and signs of the lung, chest X-ray and serum antibody measured precipitation, bronchoalveolar lavage, pulmonary function tests comprehensive analysis, and make a correct diagnosis.