Immunological Mechanism of Action and Clinical Profile of Disease-Modifying Treatments in Multiple Sclerosis

被引:0
作者
Renaud A. Du Pasquier
Daniel D. Pinschewer
Doron Merkler
机构
[1] Centre Hospitalier Universitaire Vaudois,Service de Neurologie, Département des Neurosciences Cliniques, BT
[2] University of Basel,06
[3] Geneva University Hospital,Division of Experimental Virology, Department of Biomedicine
[4] University of Geneva,Division of Clinical Pathology
[5] University Medical Center Göttingen,Department of Pathology and Immunology
来源
CNS Drugs | 2014年 / 28卷
关键词
Multiple Sclerosis; Experimental Autoimmune Encephalomyelitis; Progressive Multifocal Leukoencephalopathy; Alemtuzumab; Natalizumab;
D O I
暂无
中图分类号
学科分类号
摘要
Multiple sclerosis (MS) is a life-long, potentially debilitating disease of the central nervous system (CNS). MS is considered to be an immune-mediated disease, and the presence of autoreactive peripheral lymphocytes in CNS compartments is believed to be critical in the process of demyelination and tissue damage in MS. Although MS is not currently a curable disease, several disease-modifying therapies (DMTs) are now available, or are in development. These DMTs are all thought to primarily suppress autoimmune activity within the CNS. Each therapy has its own mechanism of action (MoA) and, as a consequence, each has a different efficacy and safety profile. Neurologists can now select therapies on a more individual, patient-tailored basis, with the aim of maximizing potential for long-term efficacy without interruptions in treatment. The MoA and clinical profile of MS therapies are important considerations when making that choice or when switching therapies due to suboptimal disease response. This article therefore reviews the known and putative immunological MoAs alongside a summary of the clinical profile of therapies approved for relapsing forms of MS, and those in late-stage development, based on published data from pivotal randomized, controlled trials.
引用
收藏
页码:535 / 558
页数:23
相关论文
共 706 条
[51]  
Zhang X(2012)Risk stratification for progressive multifocal leukoencephalopathy in patients treated with natalizumab Mult Scler 18 143-79
[52]  
Niu X(2012)Risk of natalizumab-associated progressive multifocal leukoencephalopathy N Engl J Med 366 1870-1704
[53]  
Zang YC(2013)Best practice in the use of natalizumab in multiple sclerosis Ther Adv Neurol Disord 6 69-245
[54]  
Mirandola SR(2011)Clinical outcomes of natalizumab-associated progressive multifocal leukoencephalopathy Neurology 76 1697-1643
[55]  
Hallal DE(2012)Pathology of immune reconstitution inflammatory syndrome in multiple sclerosis with natalizumab-associated progressive multifocal leukoencephalopathy Acta Neuropathol 123 235-1151
[56]  
Farias AS(2012)Switching therapy from natalizumab to fingolimod in relapsing–remitting multiple sclerosis: clinical and magnetic resonance imaging findings Mult Scler 18 1640-411
[57]  
Oliveira EC(2008)Postwithdrawal rebound increase in T2 lesional activity in natalizumab-treated MS patients Neurology 70 1150-395
[58]  
Brandao CO(2010)Considerations on discontinuing natalizumab for the treatment of multiple sclerosis Ann Neurol 68 409-191
[59]  
Ruocco HH(2010)Natalizumab drug holiday in multiple sclerosis: poorly tolerated Ann Neurol 68 392-399
[60]  
Prinz M(2011)Immune reconstitution inflammatory syndrome in patients with multiple sclerosis following cessation of natalizumab therapy Arch Neurol 68 186-664