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Natalizumab-associated progressive multifocal leukoencephalopathy is not preceded by elevated drug concentrations

920 journals.sagepub.com/home/msj Progressive multifocal leukoencephalopathy (PML) is an opportunistic, demyelinating infection of the brain caused by the neurotropic JC polyomavirus (JCPyV). Within the central nervous system (CNS), PML-type JCPyV variants can cause a lytic infection. Around 80% of cases occur in AIDS and around 10% in patients with haematological disorders. In 2005, PML was first described in three patients with multiple sclerosis (MS) treated with the IgG4 monoclonal antibody natalizumab.1,2 Owing to its efficacy, natalizumab is still available for the MS indication, despite 698 (695 MS, 3 Crohn’s disease; Biogen, Safety Update 12/2016) confirmed cases of PML. While the risk of PML has initially been estimated to be around 1/1000 patients treated, it has significantly increased during the past decade and can reach up to 1%–2% if certain risk factors are present.3,4 The rising risk prompted development of measures to stratify patients based on treatment duration, prior immunosuppressive therapy, and exposure to the virus as assessed by JCPyV serology.5