Is maraviroc useful in multiple sclerosis patients with natalizumab-related progressive multifocal leukoencephalopathy?

2017 ◽  
Vol 378 ◽  
pp. 233-237 ◽  
Author(s):  
Cristina Scarpazza ◽  
Luca Prosperini ◽  
Chiara R. Mancinelli ◽  
Nicola De Rossi ◽  
Alessandra Lugaresi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Multiple Sclerosis Patients

Blood miRNA expression pattern is a possible risk marker for natalizumab-associated progressive multifocal leukoencephalopathy in multiple sclerosis patients

2014 ◽  
Vol 20 (14) ◽  
pp. 1851-1859 ◽  
Author(s):  
M Muñoz-Culla ◽  
H Irizar ◽  
T Castillo-Triviño ◽  
M Sáenz-Cuesta ◽  
L Sepúlveda ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Differential Expression ◽  
Expression Pattern ◽  
Mirna Expression ◽  
Disease Biomarkers ◽  
Mirna Expression Pattern ◽  
Increased Risk ◽  
Relapsing Remitting ◽  
Multiple Sclerosis Patients

Background: Natalizumab has shown its efficacy in reducing multiple sclerosis (MS) relapses and progression of disability; however, it has been associated with an increased risk of developing progressive multifocal leukoencephalopathy (PML). The differential expression of microRNA (miRNA), the small non-coding RNAs that regulate gene expression, in natalizumab-treated patients has been reported and miRNA have also been described as good candidates for disease biomarkers. Objective: To characterize the effect of natalizumab therapy on the miRNA expression pattern and to search for miRNAs that can predict PML on an individual basis. Methods: The expression of 754 microRNAs was measured in blood samples from 19 relapsing–remitting MS patients at three time points during natalizumab therapy, using TaqMan OpenArray panels. Two patients included in this study developed PML after more than 2 years of therapy. Results: We found that the expression level of three miRNAs (let-7c, miR-125a-5p and miR-642) was affected after 6 months of therapy (t6). Furthermore, we observed a differential expression of another three miRNAs (miR-320, miR-320b and miR-629) between the PML and non-PML groups after 12 months of treatment (t12); and a positive correlation was found between therapy time and the expression of miR-320. Conclusions: Natalizumab modified the expression levels of three miRNAs after a 6-month treatment. We suggest miR-320, miR-320b and miR-629 as possible biomarkers for individual PML risk assessment.

Longitudinal JCV serology in multiple sclerosis patients preceding natalizumab-associated progressive multifocal leukoencephalopathy

2015 ◽  
Vol 21 (12) ◽  
pp. 1600-1603 ◽  
Author(s):  
Anke Vennegoor ◽  
Johannis A van Rossum ◽  
Chris H Polman ◽  
Mike P Wattjes ◽  
Joep Killestein
Keyword(s):  
Multiple Sclerosis ◽  
Risk Factor ◽  
Progressive Multifocal Leukoencephalopathy ◽  
High Serum ◽  
Saturation Level ◽  
Antibody Index ◽  
John Cunningham Virus ◽  
Multiple Sclerosis Patients

The presence of anti-John Cunningham Virus (JCV) antibodies is a risk factor for the development of progressive multifocal leukoencephalopathy (PML) in MS patients treated with natalizumab. It has been suggested that an increase in serum anti-JCV antibody index precedes the development of PML. We here describe extensive longitudinal serum anti-JCV antibody indexes of four MS patients who developed PML. Anti-JCV antibodies were measured using the STRATIFY JCV™DxSelect™ test. All four patients had rather stable high anti-JCV antibody indexes in all samples obtained before developing PML. Possibly caused by reaching the saturation level of the assay, no increase in anti-JCV antibody indexes was seen just before the diagnosis of PML. This study confirms that high serum anti-JCV antibody indexes precede natalizumab-associated PML.

Serum neurofilaments increase at progressive multifocal leukoencephalopathy onset in natalizumab‐treated multiple sclerosis patients

2019 ◽  
Vol 85 (4) ◽  
pp. 606-610 ◽  
Author(s):  
Gloria Dalla Costa ◽  
Vittorio Martinelli ◽  
Lucia Moiola ◽  
Francesca Sangalli ◽  
Bruno Colombo ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Multiple Sclerosis Patients

scholarly journals Progressive multifocal leukoencephalopathy in dimethyl fumarate-treated multiple sclerosis patients

2020 ◽  
pp. 135245852094915 ◽  
Author(s):  
Allison LM Jordan ◽  
Jennifer Yang ◽  
Caitlyn J Fisher ◽  
Michael K Racke ◽  
Yang Mao-Draayer
Keyword(s):  
Multiple Sclerosis ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Immune Cell ◽  
Dimethyl Fumarate ◽  
The Central Nervous System ◽  
Immune Cell Migration ◽  
Absolute Lymphocyte Counts ◽  
Adhesive Molecules ◽  
Multiple Sclerosis Patients ◽  
Relapsing Multiple Sclerosis

Dimethyl fumarate (DMF), a fumaric acid with antioxidant and immunomodulatory properties, is among the most commonly used oral therapies for relapsing multiple sclerosis (MS). Progressive multifocal leukoencephalopathy (PML) has been associated with several disease-modifying therapies (DMTs), including DMF in treating MS. We present detailed clinical characteristics of nine PML cases and show that the PML incidence in DMF-treated patients is 0.02 per 1000 patients. In addition to persistent severe lymphopenia, older age appears to be a potential risk for PML. However, younger patients without lymphopenia were also observed to develop PML. DMF-associated PML has occurred in patients with absolute lymphocyte counts (ALCs) above the guideline threshold, suggesting that changes in specific subsets might be more important than total ALC. Furthermore, since DMF has been found to decrease immune cell migration by decreasing the expression of adhesive molecules, the cerebrospinal fluid (CSF) immune profile may also be useful for assessing PML risk in DMF-treated patients. This review provides an up-to-date assessment of PML cases occurring in DMF-treated patients and discusses other potential considerations in light of our current understanding of DMF’s mechanism of action on the immune system in the periphery and in the central nervous system (CNS).

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