期刊
ANNALS OF THE RHEUMATIC DISEASES
卷 70, 期 10, 页码 1752-1757出版社
B M J PUBLISHING GROUP
DOI: 10.1136/ard.2011.154104
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资金
- National Institutes of Health [R03AI076729, P20RR020143, P20RR015577, P30AR053483, R01AR042460, R37AI024717, R01AI031584, N01AR62277, P50AR048940, P01AI083194, RC1AR058621, U19AI082714, HHSN266200500026C, P30RR031152, P01AR049084, R01AR043274, R01AI063274, K08AI083790, P30DK42086]
- Lupus Research Institute
- Arthritis National Research Foundation
- American College of Rheumatology/Research and Education Foundation
- University of Oklahoma College of Medicine, Kirkland
- Alliance for Lupus Research
- US Department of Veterans Affairs
- US Department of Defense [PR094002]
- Federico Wihelm Agricola Foundation
- Instituto de Salud Carlos III [PS09/00129]
- European Union
- Consejeria de Salud de Andalucia [PI0012]
- Swedish Research Council
- Ministry for Health and Welfare, Republic of Korea [A080588]
Objective Systemic lupus erythematosus is a clinically heterogeneous autoimmune disease. A number of genetic loci that increase lupus susceptibility have been established. This study examines if these genetic loci also contribute to the clinical heterogeneity in lupus. Materials and methods 4001 European-derived, 1547 Hispanic, 1590 African-American and 1191 Asian lupus patients were genotyped for 16 confirmed lupus susceptibility loci. Ancestry informative markers were genotyped to calculate and adjust for admixture. The association between the risk allele in each locus was determined and compared in patients with and without the various clinical manifestations included in the ACR criteria. Results Renal disorder was significantly correlated with the lupus risk allele in ITGAM (p=5.0 x 10(-6), OR 1.25, 95% CI 1.12 to 1.35) and in TNFSF4 (p=0.0013, OR 1.14, 95% CI 1.07 to 1.25). Other significant findings include the association between risk alleles in FCGR2A and malar rash (p= 0.0031, OR 1.11, 95% CI 1.17 to 1.33), ITGAM and discoid rash (p= 0.0020, OR 1.20, 95% CI 1.06 to 1.33), STAT4 and protection from oral ulcers (p= 0.0027, OR 0.89, 95% CI 0.83 to 0.96) and IL21 and haematological disorder (p= 0.0027, OR 1.13, 95% CI 1.04 to 1.22). All these associations are significant with a false discovery rate of < 0.05 and pass the significance threshold using Bonferroni correction for multiple testing. Conclusion Significant associations were found between lupus clinical manifestations and the FCGR2A, ITGAM, STAT4, TNSF4 and IL21 genes. The findings suggest that genetic profiling might be a useful tool to predict disease manifestations in lupus patients in the future.
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