A granulomatous lung disease was first recognized in beryllium workers in the 1940s (1-3). Clinicians and researchers noted the strong clinical and pathologic similarities between the chronic form of beryllium disease and sarcoidosis. The clinical overlap was so strong that Harriet Hardy, in first describing chronic beryllium disease (CBD), referred to it as “Salem Sarcoid” after the town in which the first cluster of cases was identified. Until the 1980s, discriminating between the two had been quite difficult. Past approaches relied on epidemiologic evidence of beryllium exposure, measurement of beryllium in affected organs, and compatible clinical findings. However, our improved understanding of the immunopathogenesis of CBD and the development of reliable and specific immunologic tests now allows for a confident diagnosis in the majority of patients. More importantly, use of immunologic assays allows detection of CBD at an early stage, sometimes before the patients develop symptoms or any physiologic or radiographic abnormalities (4-6). Furthermore, the use of immunologic assays of beryllium sensitization has opened the door for research into the interactions among cellular immunology, genetics, and environmental exposure (7-12). Studies using beryllium disease as a model of granulomatous disease due to known antigen may help us understand granulomatous diseases for which the antigens are not yet known, i.e., sarcoidosis. This paper will compare sarcoidosis and beryllium disease, with emphasis on both the similarities that may help us unravel the immunopathogenesis of sarcoidosis, and the differences that allow us to clinically separate these diseases. The paper will emphasize the comparison between CBD and sarcoidosis, since a more acute form of beryllium disease is now seen rarely.
|Original language||English (US)|
|Title of host publication||Sarcoidosis|
|Number of pages||24|
|ISBN (Print)||0824759265, 9780824759261|
|State||Published - Jan 1 2005|
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