scholarly journals Anti-CD20 monoclonal antibody in multiple sclerosis therapy: the results of phase 3 clinical studies on relapsing and primary progressive multiple sclerosis

2015 ◽  
Vol 15 (3) ◽  
pp. 150-154
Author(s):  
Maciej Maciejowski ◽  
2019 ◽  
Vol 12 (5) ◽  
pp. e229080 ◽  
Author(s):  
Sydney Feldman ◽  
Salman Aljarallah ◽  
Shiv Saidha

Cobalamin (vitamin B12) deficiency often manifests with neurologic symptoms and may rarely mimic multiple sclerosis (MS) among other neurological disorders. However, MRI changes associated with cobalamin deficiency are typically spinal predominant and distinct from MS-related changes. We report a case of a patient with cobalamin deficiency who was recommended by her primary neurologist to commence treatment with ocrelizumab, a potent anti-CD20 B-cell depleting monoclonal antibody, after being diagnosed with primary progressive MS. However, cervical spine MRI demonstrated changes classical of cobalamin deficiency including ‘inverted V sign’ signal hyperintensity and following parenteral cobalamin supplementation her neurological symptoms quickly and dramatically improved.


The Lancet ◽  
2016 ◽  
Vol 387 (10023) ◽  
pp. 1075-1084 ◽  
Author(s):  
Fred Lublin ◽  
David H Miller ◽  
Mark S Freedman ◽  
Bruce A C Cree ◽  
Jerry S Wolinsky ◽  
...  

2017 ◽  
Vol 23 (12) ◽  
pp. 1636-1641 ◽  
Author(s):  
Jerry S Wolinsky

The last several decades have witnessed considerable progress in our understanding of the pathogenesis, refining diagnostic criteria, and identifying therapies of value for modifying the course of relapsing forms of multiple sclerosis. While the pace of progress has lagged for those with progressive phase disease, this now seems to be changing. This review considers those characteristics of patients with primary progressive multiple sclerosis that may contribute to phase 3 trial success and identifies some of the thorny issues that remain ahead. The larger of the studies conducted thus far have sequentially informed our understanding of “pure” primary progressive disease, and also challenge both phase 3 and especially phase 2 trial designs and participant selection for investigations going forward. This may have particular relevance for testing therapeutics directed at neuroprotection and repair in the face of ongoing progression regardless of trial participant categorization using current conventional disease phenotypes.


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