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Annals of the Rheumatic Diseases 1998;57:503-505; doi:10.1136/ard.57.8.503
Copyright © 1998 BMJ Publishing Group Ltd & European League Against Rheumatism.
Ann Rheum Dis 1998;57:503-505 ( August )

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A study of the association of HLA DR, DQ, and complement C4 alleles with systemic lupus erythematosus in Iceland K Steinsson,a b S Jónsdóttir,c G J Arason,d H Kristjánsdóttir,b R Fossdal,e I Skaftadóttir,c A Árnasonc

a Department of Internal Medicine, Division of Rheumatology, b Icelandic Centre for Rheumatology Research, c Department of Pathology, Immunogenetics Unit, d Department of Immunology, e The Blood Bank, f Landspítalinn, National University Hospital, Reykjavík, Iceland

Correspondence to: Dr K Steinsson, Department of Internal Medicine, Division of Rheumatology, Landspitalinn National University Hospital, 101 Reykjavik, Iceland.

Accepted for publication 23 June 1998

OBJECTIVE---To perform an exploratory analysis of the relative contribution of single MHC genes to the pathogenesis of systemic lupus erythematosus (SLE) in a homogenous white population.
METHODS---MHC class II alleles and C4 allotypes were determined in 64 SLE patients and in ethnically matched controls. HLA-DR and DQ typing was performed by polymerase chain reaction amplification with sequence specific primers. C4 allotypes were determined by agarose gel electrophoresis.
RESULTS---The frequency of C4A*Q0 was significantly higher in patients than in controls (46.9% v 25.3%, p=0.002). HLA-DRB1, DQA1, and DQB1 alleles in the whole group of SLE patients were not significantly different from those of controls. On the other hand increase in DRB1*03 was observed in the group of patients with C4A*Q0, as compared with patients with other C4A allotypes (p=0.047). There was no significant correlation between severe and mild disease, as judged by the SLEDAI, and HLADR, DQ alleles and comparing the patients with C4A*Q0 with those with other C4A allotypes there was no significant difference regarding clinical manifestations.
CONCLUSION---The results are consistent with the argument that C4A deficiency contributes independently to susceptibility and the pathogenesis of SLE. C4A*Q0 in SLE patients in Iceland shows weaker linkage disequilibrium with DR3 genes than reported in most other white populations and emphasises the role of ethnicity.

Keywords: systemic lupus erythematosus; HLA; C4 allele; disease associations


© 1998 by Annals of the Rheumatic Diseases

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