Sarcoid arthropathy and the association with the human leukocyte antigen. The Icelandic Sarcoidosis Study.

To access publisher's full text version of this article. Please click on the hyperlink in Additional Links field. The aim of the present study was to evaluate whether certain HLA antigens were risk factors for developing sarcoid arthritis and whether HLA antigens appear to account for the pheno...

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Main Authors: Petursdottir, Dyrleif, Haraldsdottir, Sigridur Olina, Bjarnadottir, Kristjana, Jonsson, Thorbjorn, Gislason, Thorarinn, Gudmundsson, Sveinn, Gudbjornsson, Bjorn
Other Authors: Landspitali Univ Hosp, Ctr Rheumatol Res, IS-101 Reykjavik, Iceland Landspitali Univ Hosp, Dept Resp Med, IS-101 Reykjavik, Iceland Landspitali Univ Hosp, Iceland Blood Bank, IS-101 Reykjavik, Iceland Univ Iceland, Fac Med, Reykjavik, Iceland
Format: Article in Journal/Newspaper
Language:English
Published: Clinical And Experimental Rheumatology S.A.S 2014
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Online Access:http://hdl.handle.net/2336/317146
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Summary:To access publisher's full text version of this article. Please click on the hyperlink in Additional Links field. The aim of the present study was to evaluate whether certain HLA antigens were risk factors for developing sarcoid arthritis and whether HLA antigens appear to account for the phenotype and the resolution of the arthritis condition in an unselected nationwide cohort. The Icelandic Sarcoidosis Study (ISS) contains all tissue-verified cases of sarcoidosis in Iceland since 1981. Of a total of 234 cases, 39 patients were identified with arthritis and of those 36 delivered a biosample for the study. The patient cohort has previously been described in detail. DNA was isolated from EDTA blood and HLA antigen typing was performed. A total of 544 Icelandic stem cell donors acted as controls. HLA-B8 and HLA-B14 antigens were more common among those who suffered from sarcoid arthritis (24% vs. 11%, p<0.01; 6.5% vs. 2.4%, p<0.05). DRB1*03 was also found more frequently in patients with sarcoid arthritis compared to controls (28% vs. 11%, p<0.001), while DRB1*04 was less frequently reported (5.6% vs. 17%, p<0.01). No differences were found in the HLA-A distribution between the groups. A higher proportion of patients with chronic arthritis had HLA-A11 than those with resolving joint problems (60% vs. 3.8%). Our nationwide study of patients with sarcoid arthritis further supports the conclusion that genetics may strongly influence the development and the clinical course of the disease. Furthermore, some HLA antigens may even be protective for the disease. Thus, classification of the major histocompatibility complex may have clinical implications. Icelandic Society for Rheumatology University Hospital Research Fund