Journal
NEUROLOGY
Volume 75, Issue 18, Pages 1617-1622Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181fb449e
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Funding
- Dutch Foundation of Multiple Sclerosis Research
- Bayer Schering Pharma
- Biogen Idec
- Merck Serono
- Teva Pharmaceutical Industries Ltd.
- Genzyme Corporation
- Novartis
- Innogenetics
- Institute of Clinical and Experimental Neurosciences
- The Netherlands Organisation for Scientific Research (NWO)
- European Union
- Dutch Foundation for MS Research
- Koninklijk Wilhelmina Fonds/Dutch Cancer Society
- Dutch MS Research Foundation
- GlaxoSmithKline
- UCB
- European Community (EEC)
- Dutch Multiple Sclerosis Society
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Objectives: Chronic cerebrospinal venous insufficiency (CCSVI) has been suggested to be a possible cause of multiple sclerosis (MS). If the presumed mechanism of venous stasis-related parenchymal iron deposition and neurodegeneration were true, then upregulation of intrathecal iron transport proteins may be expected. Methods: This was a cross-sectional (n = 1,408) and longitudinal (n = 29) study on CSF ferritin levels in patients with MS and a range of neurologic disorders. Results: Pathologic (>12 ng/mL) CSF ferritin levels were observed in 4% of the control patients (median 4 ng/mL), 91% of patients with superficial siderosis (75 ng/mL), 73% of patients with a subarachnoid hemorrhage (59 ng/mL), 10% of patients with relapsing-remitting MS (5 ng/mL), 11% of patients with primary progressive MS (6 ng/mL), 23% of patients with secondary progressive MS (5 ng/mL), and 23% of patients with meningoencephalitis (5 ng/mL). In MS, there was no significant change of CSF ferritin levels over the 3-year follow-up period. Conclusion: These data do not support an etiologic role for CCSVI-related parenchymal iron deposition in MS. Neurology (R) 2010;75:1617-1622
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