Background The anti-chromatin antibody is frequently is elevated in patients with active SLE and its titer correlates with activity.

Objectives The objective of this study is to determine the diagnostic value of anti-chromatin antibodies in the assessment of clinically active SLE.

Methods A cross-sectional study with 74 patients (110 samples) diagnosed with SLE. Disease activity was evaluated by Safety of Estrogens in SLE National Assessment— SLE Activity Index (SELENA-SLEDAI) and the British Isles Lupus Activity Group 2004 (BILAG 2004) index. Serological titers of anti-dsDNA high avidity, anti-chromatin and anti-C1q antibodies were measured by enzyme-linked immunosorbent assay (ELISA) using commercially available kits INOVA Diagnostics, Inc. Complement levels by nephelometric test

Values in this study were expressed as mean ± standard deviation (SD). The chi-squared test was used for the categorical variables as needed. The Wilcoxon Rank-Sum Testwas used for comparison of SLEDAI score indices. Correlation among the levels of complements, anti-dsDNA, anti-chromatin, anti-C1q antibodies and disease activity scores was made by the nonparametric Spearman’s rank correlation test (correlation coefficient ρ [rho]). Values of p< 0.05 were considered to be of statistical significance. STATA SE-11,1 (STATA Corp®) was used.

Results The mean SLEDAI score was 3,36 ± 3,19 (0-14). 49,9% (n=54) of patients had a SLEDAI score of ≥ 4. Activity by BILAG A/B: Renal 9% (n=10), mucocutaneous 8,18 (n=9), musculoskeletal 6,5% (n=7), neuropsychiatric 1,8% (n=2), hematological 1,8% (n=2), cardiorespiratory and constitucional 0,9% (n=1). 60% of patients had activity by SLEDAI or BILAG.

Biomarkers: Anti-chromatin antibodies 64,08 ± 74,3 (1-251), anti-dsDNA 54,99 ± 77,63 (12-543), anti-C1q antibodies 14,66 ± 23,09 (2-153), C3 97,81± 30,5 (26-152) and C4 16,53 ± 8,99 (2-42). The prevalence of positive anti-chromatin, anti-dsDNA and anti-C1q antibodies in the recruited patients was 51%, 45%, and 16% respectively. Anti-chromatin antibodies and anti dsDNA antibodies were found to be positive in 70% and 72% active-SLE patients by SLEDAI ≥ 4 (p<0,0001). Anti-chromatinantibodies were found to be positive in 15,4% SLE patients lacking anti-dsDNA antibody, 53% without activity for SLEDAI o BILAG at the moment of the study.

The Wilcoxon Rank-Sum Testshowed an excellent correlation between anti-chromatin antibodies and SLEDAI score ≥ 4 (p< 0,0001). Spearman’s rank correlation test (ρ) among the levels of anti-chromatina and anti-dsDNA with disease activity scores was 0,38 (p<0,001) and 0,41 (p<0,001) respectively.

Conclusions Anti-chromatincould precede the development of lupus flares and thus has a value in predicting lupus flares and preempting treatment.

References Translational Research 2012;159:326–342. Arthritis Research & Therapy 2009, 11:R154. Ann Rheum Dis 2007;66:693–696.

Disclosure of Interest None Declared