To PLEX or not to PLEX in natalizumab-associated PML.

Abstract

Natalizumab (NTZ) is one of the most effective therapies available for the treatment of relapsing multiple sclerosis (MS).1 The most important adverse effect of treatment is the development of progressive multifocal leukoencephalopathy (PML), with ∼700 cases having been reported since 2005.2 The incidence of NTZ-PML in patients with MS varies from as high as 1.3% among individuals who are JC virus (JCV) antibody–positive, have a history of prior immunosuppressant therapy, and have received more than 4 years of NTZ treatment, to less than 0.1% in those with none of these risk factors.3 PML results from reactivation of latent JCV and subsequent infection and death of oligodendrocytes leading to demyelination. There is currently no treatment of proven efficacy for PML; however, interventions that facilitate restoration of immunocompetence reduce disability and enhance survival. This is clearly seen in patients with HIV-associated PML, in whom prognosis improved dramatically after the introduction of highly active antiretroviral therapy.4 It is logical to assume that reversal of the NTZ-induced immunodeficiency state would be the most effective therapeutic option for patients with NTZ-PML.