liu.seSearch for publications in DiVA
Change search
ReferencesLink to record
Permanent link

Direct link
Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Neurology.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion.
Show others and affiliations
2003 (English)In: Multiple Sclerosis, ISSN 1352-4585, Vol. 9, no 3, 239-245 p.Article in journal (Refereed) Published
Abstract [en]

Objective: The aim of this study was to evaluate if multiple sclerosis (MS) is associated with vitamin B12 (cobalamin) deficiency. Methods: We measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), plasma homocysteine (tHcy) and also cerebrospinal fluid (CSF) MMA and tHcy in 72 patients with MS and 23 controls. Results: The mean plasma tHcy level was significantly increased in MS patients (11.6 ╡mol/L) compared with controls (7.4╡mol/L) (P = 0.002). Seven patients showed low serum vitamin B12 levels but only one of them had concomitant high plasma tHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. We found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MCV), haemoglobin concentration, CSF tHcy or CSF MMA between patients and healthy subjects. There were no correlations between CSF and serum/plasma levels of MMA or tHcy. Serum vitamin B12, serum MMA, plasma tHcy, CSF Hey or CSF MMA were not correlated to disability status, activity of disease, duration of disease or age. Conclusions: The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. Our findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. Analysis of CSF MMA and CSF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.

Place, publisher, year, edition, pages
2003. Vol. 9, no 3, 239-245 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-25194DOI: 10.1191/1352458503ms918oaLocal ID: 9633OAI: diva2:245521
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2011-01-13

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Vrethem, MagnusLandtblom, Anne-MarieKågedal, Bertil
By organisation
Faculty of Health SciencesDepartment of Neuroscience and LocomotionDepartment of NeurologyClinical ChemistryDepartment of Clinical Chemistry
In the same journal
Multiple Sclerosis
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 19 hits
ReferencesLink to record
Permanent link

Direct link