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Natalizumab is a disease-modifying therapy (DMT) used in relapsing-remitting multiple sclerosis (RRMS), licenced for use in patients with highly-active disease. It is an α4-integrin receptor antagonist that decreases activated T cell migration across the blood-brain barrier.1 Natalizumab carries a risk of progressive multifocal leucoencephalopathy (PML)—a risk that increases with duration of treatment; John Cunningham Virus (JCV) seropositivity and higher index values; prior use of immunosuppression.1 Patients may choose to withdraw from natalizumab to mitigate PML risk, or less commonly when natalizumab fails to control disease activity, or is poorly tolerated. Fingolimod has been commonly used as an option in those making the switch from natalizumab, but is associated with high rates of breakthrough clinical and/or radiological disease activity, although the risks may be lower with shorter washout periods.2 Rituximab has been suggested as an alternative to fingolimod in patients discontinuing natalizumab due to high PML risk, however, rituximab is not licenced for the treatment of RRMS and is not available in some countries for this indication.3
Alemtuzumab is a monoclonal antibody that binds to the CD52 surface protein on T and B lymphocytes, resulting in their depletion with subsequent repopulation, with comparable efficacy to natalizumab.1 Switching to alemtuzumab might be an alternative to fingolimod in patients stopping natalizumab but there is a paucity of clinical and safety data to guide this transition. Here, we present a single-centre experience in switching from natalizumab to alemtuzumab in RRMS.
Methods
We retrospectively identified patients from the National Hospital for Neurology and Neurosurgery who switched from natalizumab to alemtuzumab from May 2015 to February 2018. We extracted data from the medical records: demographic characteristics, duration of natalizumab use, drug washout period, cerebrospinal fluid (CSF) examination results, JCV serology, clinical …
Footnotes
Contributors NJ and WJB planned the study. NJ and AC were involved in data acquisition. NJ completed data analysis and drafted the manuscript. WJB provided key edits to the manuscript. The final manuscript was reviewed and edited by AC, WJB and JC. The guarantor for the content of the manuscript is JC.
Competing interests WJB has received speaker honoraria for educational activities for Merck Serono, Roche and Sanofi Genzyme. JC has received support from the Efficacy and Mechanism Evaluation Programme and Health Technology Assessment Programme (NIHR); UK Multiple Sclerosis Society and National Multiple Sclerosis Society; National Institute for Health Research University College London Hospitals (NIHR-UCLH) Biomedical Research Centre (BRC) and University College London. In the last three years, he has been a local principal investigator for trials in multiple sclerosis funded by: Receptos, Novartis and Biogen Idec, and has received an investigator grant from Novartis outside this work. He has taken part in Advisory Boards/consultancy for Apitope, Roche, Merck, MedDay, Biogen and Celgene.
Patient consent for publication Not required.
Ethics approval The study was approved by the Queen Square Quality and Safety Committee, National Hospital for Neurology and Neurosurgery.
Provenance and peer review Not commissioned; externally peer reviewed.