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• W2022110359 abstract "Abstract The etiologic spectrum of diffuse infiltrative lung disease is extremely broad and presents a formidable challenge to the clinician in recognition and diagnosis. An ever-increasing number of agents are being identified in our environment that are capable of eliciting a response in the lung, either of a transient or permanent type. These include bacterial, fungal, viral, or parasitic infectious diseases, disorders related to the inhalation of vapors such as chlorine and nitrogen dioxide; disorders related to the inhalation of inorganic dusts such as silicon dioxide and beryllium; and the immunologically mediated diseases resulting from the inhalation of organic dusts and certain reactive organic chemicals. Since the clinical response produced by the inhalation of organic dusts and chemicals may be variable, recognition of these diseases, particularly in the occupational environment, may be extremely difficult. Often the problem becomes evident only because of the occurrence of a cluster of cases in a particular industry. A variety of organic dusts derived from fungal, bacterial, or serum protein sources have been identified as etiologic agents of hypersensitivity pneumonitis (HP). Typical examples are Micropolyspora faeni in farmer's lung and the thermophilic actinomycetes in bagassosis and humidifier lung. In general, the manifestations are similar regardless of the organic dust inhaled and the hypersensitivity pneumonitides should be considered as a syndrome with a spectrum of clinical features. The patient with HP may present with one of three difficult types of response. The most typical, an acute form of the disease, resembles an acute viral or bacterial infection and usually results from intermittent exposure to an organic dust. Symptoms include chills, fever, chest tightness, nonproductive cough, and dyspnea without wheezing, which develop 4 to 8 hr after exposure. This delayed response may result in failure to recognize the relationship of an environmental exposure and the occurrence of symptoms. The symptoms generally will resolve spontaneously in 12 to 24 hr, only to recur on re-exposure. With prolonged low-level exposure to antigen, a small number of patients show the more insidious subacute form of the disease, manifested by a productive cough, dyspnea, fatigue, and weight loss. Acute attacks, although infrequent, can be precipitated by heavy exposure. Long-term avoidance of exposure and administration of corticosteroids result in the resolution of signs and symptoms of the disease. Prolonged and intense exposure to an organic dust can lead to the chronic form of the disease. Pulmonary fibrosis is the predominant feature and can lead to the gradual development of disabling respiratory symptoms with irreversible physiologic changes. It is therefore imperative to recognize the problem before the chronic stage of the disease has been reached when there is little chance of reversibility. The roentgenographic and physiologic changes in the various clinical forms of HP will be discussed." @default.
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• W2022110359 date "1982-07-01" @default.
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• W2022110359 title "Infiltrative lung disease hypersensitivity pneumonitis" @default.
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• W2022110359 doi "https://doi.org/10.1016/0091-6749(82)90201-9" @default.
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