From pathogenesis and research to the treatment of secondary progressive multiple sclerosis in clinical practice: switching from anti-CD20 monoclonal antibody therapy to siponimod (clinical case)

Abstract

The pathogenesis of multiple sclerosis is multifaceted and not fully investigated, but it is now clear that each patient has their own ratio of inflammation and neurodegeneration severity. Given the available evidence base, understanding of the pathogenesis underlying secondary progression, and accumulated clinical experience, it is important not only to make a timely diagnosis and prescribe adequate therapy, but also to monitor for continued progression in order to revise treatment with the aim of preventing patient disability. This publication describes a clinical case of a patient with secondary progressive multiple sclerosis (SPMS) who received therapy with an anti-CD20 monoclonal antibody infusion. The patient showed complete suppression of activity and no exacerbations, but despite this, there was a gradual progression on the EDSS scale from 4.5 to 6.0 points over 3 years of therapy. In this regard, the patient was transferred to therapy with siponimod, against which a decrease to 5.5 points was noted within a few months. At the time of publication, this indicator has remained stable for 3 years, indicating that the main goal of therapy for SPMS – preventing secondary progression – has been achieved.

Therefore, when treating patients with SPMS and ongoing secondary progression, even with complete suppression of activity and no exacerbations, including against the background of infusion therapy with anti-CD20 monoclonal antibody drugs, it is necessary to consider switching to siponimod therapy.