STUDY OBJECTIVES: Sarcoidosis is a granulomatous disorder with heterogeneous clinical manifestations, which are potentially reflective of a syndrome with different etiologies leading to similar histologic findings. We examined the relationship between environmental and occupational exposures, and the clinical phenotype of sarcoidosis. DESIGN: We performed a cross-sectional study of incident sarcoidosis cases that had been identified by A Case Control Etiologic Study of Sarcoidosis. Subjects were categorized into the following two groups: (1) pulmonary-only disease; and (2) systemic disease (with or without pulmonary involvement). Logistic regression was used to examine the associations of candidate exposures with clinical phenotype. SETTING: Ten academic medical centers across the United States. PATIENTS: The current study included 718 subjects in whom sarcoidosis had been diagnosed within 6 months of study enrollment. Patients met the following criteria prior to enrollment: (1) tissue confirmation of noncaseating granulomas on tissue biopsy on one or more organs within 6 months of study enrollment with negative stains for acid-fast bacilli and fungus; (2) clinical signs or symptoms that were consistent with sarcoidosis; (3) no other obvious explanation for the granulomatous disease; and (4) age > 18 years. MEASUREMENTS AND RESULTS: Several exposures were associated with significantly less likelihood of having extrapulmonary disease in multivariate analysis, including agricultural organic dusts and wood burning. The effects of many of these exposures were significantly different in patients of different self-defined race. CONCLUSIONS: The differentiation of sarcoidosis subjects on the basis of clinical phenotypes suggests that these subgroups may have unique environmental exposure associations. Self-defined race may play a role in the determination of the effect of certain exposures on disease phenotypes.
STUDY OBJECTIVES:Sarcoidosis is a granulomatous disorder with heterogeneous clinical manifestations, which are potentially reflective of a syndrome with different etiologies leading to similar histologic findings. We examined the relationship between environmental and occupational exposures, and the clinical phenotype of sarcoidosis. DESIGN: We performed a cross-sectional study of incident sarcoidosis cases that had been identified by A Case Control Etiologic Study of Sarcoidosis. Subjects were categorized into the following two groups: (1) pulmonary-only disease; and (2) systemic disease (with or without pulmonary involvement). Logistic regression was used to examine the associations of candidate exposures with clinical phenotype. SETTING: Ten academic medical centers across the United States. PATIENTS: The current study included 718 subjects in whom sarcoidosis had been diagnosed within 6 months of study enrollment. Patients met the following criteria prior to enrollment: (1) tissue confirmation of noncaseating granulomas on tissue biopsy on one or more organs within 6 months of study enrollment with negative stains for acid-fast bacilli and fungus; (2) clinical signs or symptoms that were consistent with sarcoidosis; (3) no other obvious explanation for the granulomatous disease; and (4) age > 18 years. MEASUREMENTS AND RESULTS: Several exposures were associated with significantly less likelihood of having extrapulmonary disease in multivariate analysis, including agricultural organic dusts and wood burning. The effects of many of these exposures were significantly different in patients of different self-defined race. CONCLUSIONS: The differentiation of sarcoidosis subjects on the basis of clinical phenotypes suggests that these subgroups may have unique environmental exposure associations. Self-defined race may play a role in the determination of the effect of certain exposures on disease phenotypes.
Authors: Hiroe Sato; Felix A Woodhead; Tariq Ahmad; Jan C Grutters; Paolo Spagnolo; Jules M M van den Bosch; Lisa A Maier; Lee S Newman; Sonoko Nagai; Takateru Izumi; Athol U Wells; Roland M du Bois; Kenneth I Welsh Journal: Hum Mol Genet Date: 2010-08-03 Impact factor: 6.150
Authors: Matthew McPeek; Anagha Malur; Debra A Tokarz; Kvin Lertpiriyapong; Kymberly M Gowdy; Gina Murray; Christopher J Wingard; Michael B Fessler; Barbara P Barna; Mary Jane Thomassen Journal: Am J Respir Cell Mol Biol Date: 2019-09 Impact factor: 6.914
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Authors: Konstantinos Loupasakis; Jessica Berman; Nadia Jaber; Rachel Zeig-Owens; Mayris P Webber; Michelle S Glaser; William Moir; Basit Qayyum; Michael D Weiden; Anna Nolan; Thomas K Aldrich; Kerry J Kelly; David J Prezant Journal: J Clin Rheumatol Date: 2015-01 Impact factor: 3.517
Authors: Matthew McPeek; Anagha Malur; Debra A Tokarz; Gina Murray; Barbara P Barna; Mary Jane Thomassen Journal: Biochem Biophys Res Commun Date: 2018-06-15 Impact factor: 3.575