Background Although B cells are not commonly associated with the pathogenesis of ankylosing spondylitis (AS), some findings corroborate their potential role in this chronic inflammatory rheumatic disease. Dense infiltrations of B cells are found in the spine of patients with active inflammation. Furthermore, tumor necrosis factor-blocker treatment naïve AS patients showed a good treatment response to B cell depletion with Rituximab. As B-cell activating factor (BAFF) is a potent B cell survival and maturation factor, we analyzed BAFF serum levels in AS patients before and after TNF-alpha inhibition.

Objectives To determine whether levels of BAFF are elevated or relate to disease activity and response to treatment in patients with ankylosing spondylitis.

Methods Serum samples were obtained from 49 patients with definite AS as well as from 35 healthy controls. TNF-alpha inhibition with infliximab (n=20) or adalimumab (n=15) was initiated in a proportion of patients with BASDAI >4, according to the decision of the treating rheumatologist and serum was obtained again after 3 months in these subjects. BAFF levels were assessed by enzyme-linked immunosorbent assay (R&D Systems).

Results Baseline BAFF levels were lower in AS patients compared with healthy controls (median 1.1 ng/ml [5th-95th percentile: 1–1.9] vs 1.5 ng/ml [5th-95th 0.8–2.0] respectively; p=0.002). Only in 3/49 AS patients BAFF levels exceeded slightly the upper cutoff limit of 2.1 ng/ml (corresponding to the mean +2SD of the normal sera). Baseline BAFF levels did not correlate with BASDAI, CRP, HLA-B27 positivity, disease duration or co-medication with DMARDS. The median BAFF levels increased modestly 3 months after initiation of anti-TNF treatment, from 1.06 ng/ml to 1.38 ng/ml (Wilcoxon paired sign rank test 95% CI of increase: +0.09;+0.39, p=0.003) and nearly reached levels observed in healthy controls.

Conclusions BAFF levels are not elevated in AS patients and do not correlate with disease activity parameters. These findings do not support the use of BAFF-targeted treatment strategies in AS patients not responding adequately to conventional treatment or TNF-alpha inhibition.

Disclosure of Interest F. Niederer: None Declared, A. Scherer: None Declared, G. Tamborrini: None Declared, B. Michel: None Declared, R. Gay: None Declared, S. Gay: None Declared, D. Kyburz: None Declared, A. Ciurea Grant/Research support from: Abbott