Extrinsic Allergic Alveolitis

  • Samuel P. Hammar


The lung is the site of a variety of complex inflammatory reactions. In many instances the inflammation is a normal reaction against various infectious agents, such as bacteria and viruses, or is a response to necrotic tissue, such as infarcted lung parenchyma or degenerating tumor. In extrinsic allergic alveolitis, the inflammatory reaction characteristic of this condition is thought to represent a hypersensitivity process mediated by immunoglobulins, lymphokines, and immune effector cells. Although the four immunologic responses described by Gell and Coombs1 (Fig. 18-1) are often used in characterizing various inflammatory reactions in the lungs, the immunopathogenesis of extrinsic allergic alveolitis remains poorly understood. Extrinsic allergic alveolitis, also referred to as hypersensitivity pneumonitis or microgranulomatous hypersensitivity reaction, is a predominantly chronic inflammatory disease of the peripheral gas-exchanging portion of the lung resulting from sensitization and subsequent exposure to a variety of organic dusts. The condition was first described in 1932 in farmers exposed to moldy hay.2 Initially it was considered a mycotic process.3,4 Pepys and colleagues5,6 elucidated some of the initial immunologic mechanisms though to be operative in the disease. Williams7,8 demonstrated that the disease could be produced in sensitized farmers by the inhalation of extracts of moldy hay. Farmer’s lung disease was found to result from a hypersensitivity reaction against a species of thermophilic actinomyces, Thermoactinomyces vulgarus, that proliferated as the hay became overheated in the process of becoming moldy.9,10 Numerous organic antigens have now been recognized as causing hypersensitivity reactions in the lung, and these are usually named after the occupation in which the patient was exposed to the organic antigen. The term extrinsic allergic alveolitis was coined by Pepys11 to refer to the entire group of similar reactions to organic dusts.


Idiopathic Pulmonary Fibrosis Bronchoalveolar Lavage Fluid Hypersensitivity Pneumonitis Open Lung Biopsy Organic Dust 
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© Springer Science+Business Media New York 1994

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  • Samuel P. Hammar

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