Background Joint involvement in systemic lupus erythematosus (SLE) is one of the earliest manifestation of the disease (1).Only 2–5% of the cases develop a deforming and non-erosive type of arthritis, known as Jaccoud Arthropathy (JA). Until now, there is no serum autoantibodies marker for it (2).The chemokine CXC ligand 13 protein (CXCL13) is one of the most potent B-cell chemo attractants and is constitutively expressed in the B-cell follicles of secondary lymphoid organs (3). Its seric level has been associated to the degree of synovitis in patients with rheumatoid arthritis as studied by ultrasonography (US).
Objectives To perform the first detailed US analysis of hands and wrists of SLE patients, with and without JA, and to correlate those findings with the levels of CXCL13,other clinical and laboratory features and disease activity
Methods 64 patients with SLE were included, being 32 with JA and 32 without JA paired by age and disease duration. The definition of JA was based on clinical criteria recently described by Santiago (4).Patients and controls underwent a high-resolution US exam of wrists and hands. Synovial hypertrophy,tenosynovitis and erosions were evaluated according a semi-quantitative grading system according definitions provided by OMERACT (5). Serum concentrations of CXCL13 were quantified in both groups utilizing a commercially available kit. Autoantibodies such as antinuclear antibody (ANA), anti-dsDNA,anti-Sm,anti-SSA, anti-SSB were also tested. US findings were correlated with seric levels of CXCL13, other serological parameters and SLEDAI score.
Results In the JA group, the mean age was 46.2 years and the mean duration of the disease was 17.3 years. Synovitis on US was found in 25 patients and tenosynovitis in 14. All of these findings were more frequent in SLE with JA, particularly tenosynovitis with difference statistically significant (p=0.002). In JA patients the median levels of CXCL13 was 23.21 pg/ml as compared to 11.48 pg/ml in SLE without JA group (p=0.08). There was an association between tenosynovitis and higher levels of CXCL13 in the JA group (p=0.026). Patients with active disease were more common in the JA group (p=0.004) and had increased serum levels of CXCL13 compared to patients with disease inactive (p=0.008).
Conclusions In conclusion, the present study is one of a few to describe US findings in SLE patients with JA and it confirms that synovitis and tenosynovitis are common features in the majority of these patients. In addition, CXCL13 may be regarded as a biomarker for tendon inflammation in JA.
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Disclosure of Interest None declared