Therapeutic potential of hydroxychloroquine on serum B-cell activating factor belonging to the tumor necrosis factor family (BAFF) in rheumatoid arthritis patients

Abstract

Objective

To assess the serum B-cell activating factor belonging to the tumor necrosis factor family (BAFF) level in rheumatoid arthritis (RA) patients in view of different treatment regimens received and evaluate its relation with disease activity.

Patients and methods

Ninety female RA patients were included. Sixty were on disease modifying anti-rheumatic drugs (DMARDs); 34 on hydroxychloroquine (HCQ) plus methotrexate (MTX), 26 on leflunomide (LFN) plus MTX and 30 newly diagnosed cases not yet on any treatment. Thirty age and gender matched healthy subjects served as controls. Full history taking, clinical examination and relevant laboratory investigations were performed. Disease activity score, in 28 joints (DAS-28), was calculated.

Results

Serum BAFF level was significantly higher in patients (1.82 ± 0.91 ng/ml) compared to control (0.71 ± 0.33 ng/ml; p < 0.001). There was a significantly lower BAFF and disease activity in patients receiving DMARDs (1.55 ± 0.73 ng/ml and 3.08 ± 0.73) compared to new cases (2.36 ± 1.02 ng/ml and 3.46 ± 0.82) (p < 0.001 and p = 0.036, respectively). Those receiving HCQ + MTX had a lower BAFF level (1.29 ± 0.51 ng/ml) compared to those receiving LFN + MTX (1.94 ± 0.85 ng/ml; p = 0.002). The BAFF level significantly correlated with the presence of anti-CCP antibodies, DAS28 and MTX dose in all RA patients (r = 0.24, p = 0.02; r = 0.504, p < 0.001; r = 0.51, p < 0.001, respectively). Only DAS28 and MTX dose would highly influence the BAFF level (p = 0.015 and p = 0.001, respectively).

Conclusion

Elevated level of BAFF in RA has been confirmed with a notable relation to disease activity making it a promising marker. The beneficial effect of hydroxychloroquine in dampening BAFF level throws light on the importance of considering it in combination among the newly developed biologics that also target B-cells.