Journal
RHEUMATOLOGY
Volume 50, Issue 12, Pages 2197-2205Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ker282
Keywords
B-lymphocyte activating factor; Systemic lupus erythematosus; Acute-phase reactants; Genetics
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Funding
- Norsk Revmatikerforbund
- Oslo Sanitetsforening
- Scandinavian Rheumatology Research Foundation
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Methods. The case-control study included 101 SLE patients and 111 healthy controls. Five single nucleotide polymorphisms (SNPs) in the BAFF promoter region were investigated by melting point analysis: c.-2841 (T > C), c.-2704 (T > C), c.-2701 (A > T), c.-871 (C > T) and c.-514 (A > G). BAFF mRNA levels were determined by real-time PCR (BAFF-RQ) and serum BAFF (s-BAFF) levels were measured by ELISA. Independent predictors that might be correlated with increased s-BAFF in SLE patients were analysed by multivariate regression methods. Results. Although s-BAFF levels were increased in SLE patients (1.73 vs 0.98 ng/mu l, P < 0.001), no specific BAFF genotype was found to associate with SLE. The different genotypes defined by the investigated SNPs were identified both in SLE patients and healthy controls with similar frequencies. No association was found between BAFF genotype and BAFF-RQ. s-BAFF was independent of other factors, correlated with CRP (beta = 0.40, P < 0.001) and physician's visual analogue score (R = 0.21, P = 0.046) and inversely with haemoglobin (beta = -0.32, P < 0.001) and IgA (beta = -0.33, P = 0.001). Conclusions. Increased s-BAFF levels in SLE patients are associated with the acute-phase responses, CRP and haemoglobin, but probably not dependent on BAFF genotype or expression. This indicates that s-BAFF production occurs at sites of inflammation.
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