4.7 Article

Normal CSF ferritin levels in MS suggest against etiologic role of chronic venous insufficiency

Journal

NEUROLOGY
Volume 75, Issue 18, Pages 1617-1622

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181fb449e

Keywords

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Funding

  1. Dutch Foundation of Multiple Sclerosis Research
  2. Bayer Schering Pharma
  3. Biogen Idec
  4. Merck Serono
  5. Teva Pharmaceutical Industries Ltd.
  6. Genzyme Corporation
  7. Novartis
  8. Innogenetics
  9. Institute of Clinical and Experimental Neurosciences
  10. The Netherlands Organisation for Scientific Research (NWO)
  11. European Union
  12. Dutch Foundation for MS Research
  13. Koninklijk Wilhelmina Fonds/Dutch Cancer Society
  14. Dutch MS Research Foundation
  15. GlaxoSmithKline
  16. UCB
  17. European Community (EEC)
  18. 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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