Background: Anti-CD20 B-cell-depleting therapies, including rituximab and ocrelizumab, have demonstrated their efficacy in patients with relapsing–remitting multiple sclerosis (RRMS).

Objectives: Herein we report a series of patients with RRMS treated with anti-CD20 monoclonal antibodies (mAb) who developed a de novo spondyloarthritis (SpA).

Methods: Following the presentation of an index case, we collected all cases of de novo SpA in the anti-CD20-treated RRMS cohort of our institution’s referral center.

Clinical, biochemical, and imaging characteristics of the cases were identified through a clinical assessment. Information was collected via a standardized form to obtain key characteristics on the onset and type of disease development at baseline and on outcomes up to 12 months. All patients had a magnetic resonance imaging (MRI) of the sacroiliac joints and, depending on the clinical presentation, a spine MRI and/or a musculoskeletal grayscale and power Doppler (PD) ultrasound (US) examination.

Results: De novo SpA developed in 6 of 480 patients with RRMS treated with anti-CD20 mAb, accounting for an incidence of 1.25%. All but one received rituximab treatment. The median time from the last anti-CD20 mAb infusion to SpA onset was 1.5 months [IQR: 1-4]. At the time of SpA emergence, the RRMS activity was controlled.

The most frequent clinical SpA phenotype identified was peripheral SpA (4/6), with Power Doppler ultrasound-detected synovitis. The 2 patients with axial SpA phenotype had bilateral sacroiliitis on MRI. Five of the 6 patients had a personal or family history of psoriasis, whereas the prevalence of psoriasis in the entire RRMS cohort was 3.33% (16/480). No other extra-articular manifestation was observed. All patients were HLA B27 negative and fulfilled at least one classification criteria of SpA. None required hospitalization and the SpA onset did not affect the management of MS. The 2 patients with axial SpA were successfully treated with NSAIDs. Among the patients with peripheral SpA, 3 of four had inadequate response to NSAIDs, 2 were treated with methotrexate and 1 with leflunomide. Only one patient required initiation of an IL-17 inhibitor to control the SpA activity.

Conclusion: We report a pattern of patients with MS successfully treated with B cell-depleting drug developing axial or peripheral SpA, predominantly HLA-B27 negativity and associated with psoriasis.

Disclosure of Interests: None declared