Vitamin D3 Concentration Correlates with the Severity of Multiple Sclerosis

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Abstract

Background:

To investigate the possible association between serum 25(OH) vitamin D ₃ concentration and the severity of disease in Iranian patients with multiple sclerosis (MS) and to compare this concentration with a matched control group.

Methods:

This was an analytical cross-sectional study performed at Jondishapour Neurology Clinic in Tehran, Iran. Patients with relapsing–remitting MS were categorized by disease severity: mild [0≤ Expanded Disability Status Scale (EDSS) ≤3], moderate (3.5≤EDSS≤5.5), and severe (6≤EDSS). Serum concentrations of 25(OH) vitamin D ₃, calcium, phosphorus, magnesium, and parathyroid hormone were measured in 98 MS patients and 17 healthy age- and sex-matched controls. Fisher's exact, Kruskal–Wallis, Mann–Whitney U test, and independent t and Spearman rank correlation tests were used.

Results:

Serum 25(OH) vitamin D ₃ concentration was significantly lower in patients with MS, especially in the severe MS subgroup, compared with healthy controls ( P=0.047). There was a statistically significant inverse correlation between 25(OH) vitamin D ₃ concentration and EDSS score ( P=0.049, R=−0.168 by Spearman rank correlation test), which was observed in women only ( P=0.044, R=−0.199).

Conclusions:

Our findings not only further disclose the lower level of vitamin D in MS patients in comparison with healthy controls, but also support the association between vitamin D and disease severity in MS.

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Most cited references 24

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Vitamin D as an immune modulator in multiple sclerosis, a review.

Joost Smolders, Jan Damoiseaux, Paul. Menheere … (2008)

The role of vitamin D in calcium homeostasis is well known. More recently vitamin D has become a topic of interest in immune regulation and multiple sclerosis. The main reason for this is the observed geographical distribution of multiple sclerosis. Areas with high sunlight exposure, the principal inducer of vitamin D synthesis, have a relatively low prevalence of multiple sclerosis and vice versa. Furthermore, low levels of the principal vitamin D metabolite (25-hydroxy vitamin D) in the circulation are associated with a high incidence of multiple sclerosis. Other epidemiological evidence also supports the view that vitamin D metabolites have an immune and disease modulating effect in multiple sclerosis. Experimental research in vitro and in animal models has further clarified the interaction of vitamin D metabolites with the immune system. The evidence obtained from these studies strongly supports a model in which vitamin D mediates a shift to a more anti-inflammatory immune response, and in particular to enhanced regulatory T cell functionality. In the current review we link the basic knowledge on vitamin D and immune regulation with the vitamin D related observations in multiple sclerosis. We conclude that there is a sound basis on which to initiate double-blind placebo-controlled trials that not only address the effect of vitamin D on the clinical outcome of multiple sclerosis, but also on the regulatory T cell compartment.

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1,25-Dihydroxyvitamin D3 reversibly blocks the progression of relapsing encephalomyelitis, a model of multiple sclerosis.

Margherita T. Cantorna, W Hayes, Stephanie H. DeLuca (1996)

Experimental autoimmune encephalomyelitis (EAE) is an autoimmune disease believed to be a model for the human disease multiple sclerosis (MS). Induced by immunizing B10.PL mice with myelin basic protein (MBP), EAE was completely prevented by the administration of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. 1,25-(OH)2D3 could also prevent the progression of EAE when administered at the appearance of the first disability symptoms. Withdrawal of 1,25-(OH)2D3 resulted in a resumption of the progression of EAE. Thus, the block by 1,25-(OH)2D3 is reversible. A deficiency of vitamin D resulted in an increased susceptibility to EAE. Thus, 1,25-(OH)2D3 or its analogs are potentially important for treatment of MS.

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Vitamin D3 confers protection from autoimmune encephalomyelitis only in female mice.

Karen M. Spach, Helen Hayes (2005)

The prevalence of multiple sclerosis (MS) increases significantly with decreasing UV B light exposure, possibly reflecting a protective effect of vitamin D(3). Consistent with this theory, previous research has shown a strong protective effect 1,25-dihydroxyvitamin D(3) in experimental autoimmune encephalomyelitis (EAE), an MS model. However, it is not known whether the hormone precursor, vitamin D(3), has protective effects in EAE. To address this question, B10.PL mice were fed a diet with or without vitamin D(3), immunized with myelin basic protein, and studied for signs of EAE and for metabolites and transcripts of the vitamin D(3) endocrine system. The intact, vitamin D(3)-fed female mice had significantly less clinical, histopathological, and immunological signs of EAE than ovariectomized females or intact or castrated males. Correlating with reduced EAE, the intact, vitamin D(3)-fed female mice had significantly more 1,25-dihydroxyvitamin D(3) and fewer CYP24A1 transcripts, encoding the 1,25-dihydroxyvitamin D(3)-inactivating enzyme, in the spinal cord than the other groups of mice. Thus, there was an unexpected synergy between vitamin D(3) and ovarian tissue with regard to EAE inhibition. We hypothesize that an ovarian hormone inhibited CYP24A1 gene expression in the spinal cord, so the locally-produced 1,25-dihydroxyvitamin D(3) accumulated and resolved the inflammation before severe EAE developed. If humans have a similar gender difference in vitamin D(3) metabolism in the CNS, then sunlight deprivation would increase the MS risk more significantly in women than in men, which may contribute to the unexplained higher MS incidence in women than in men.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Prev Med

Journal ID (iso-abbrev): Int J Prev Med

Journal ID (publisher-id): IJPVM

Title: International Journal of Preventive Medicine

Publisher: Medknow Publications & Media Pvt Ltd (India )

ISSN (Print): 2008-7802

ISSN (Electronic): 2008-8213

Publication date (Print): May 2013

Volume: 4

Issue: 5

Pages: 585-591

Affiliations

[1]Jondishapour Neurology Clinic, Tehran, Iran

[1 ]Shaheed Beheshti University of Medical Sciences and Health Services (SUMS), Tehran, Iran

[2 ]Firoozgar Clinical Research Development Center (FCRDC), Tehran University of Medical Sciences (TUMS), Tehran, Iran

[3 ]Jondishapour Neurology Clinic, Tehran, Iran

[4 ]Tehran University of Medical Sciences (TUMS), Tehran, Iran

[5 ]Jondishapour Neurology Clinic, Tehran, Iran

Author notes

Correspondence to: Dr. Seyed-Mohammad Fereshtehnejad, Firoozgar Hospital, Beh Afarin St., Valiasr Square, Tehran, Iran. E-mail: sm_fereshtehnejad@ 123456yahoo.com

Article

Publisher ID: IJPVM-4-585

PMC ID: 3733190

PubMed ID: 23930170

SO-VID: eb8333aa-44dd-4d7b-a8fb-94a6fb1bc9c4

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.