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Vitamin D and Health

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Table 47: Meta-analysis of genetic studies on multiple sclerosis risk<br />

Study Methods Results Author’s conclusions<br />

Huang & Xie<br />

(2012)<br />

Tizaoui et al<br />

(2014)<br />

Selection criteria:<br />

Inclusion: Studies that evaluated VDR polymorphisms & risk<br />

of MS; case-control design based on unrelated individuals;<br />

<strong>and</strong> sufficient data for genotype distributions in both cases<br />

<strong>and</strong> controls.<br />

Exclusion: No control; no usable data reported<br />

Selection criteria:<br />

Inclusion: Case control studies that reported the number of<br />

individual genotypes <strong>and</strong>/or alleles for VDR polymorphisms<br />

in cases <strong>and</strong> controls. Each study had disease outcome<br />

definitions that followed accepted diagnostic guidelines.<br />

Exclusion: Cross-sectional studies, size of cases <strong>and</strong> controls<br />

not reported.<br />

Outcome measure<br />

The association of VDR polymorphisms with MS risk.<br />

11 case-control studies (2599 cases & 2816 controls). 2 studies in<br />

Asian & 9 in white populations.<br />

Apa-I polymorphism (rs7975232) 4 studies (599 cases & 878<br />

controls)<br />

Dominant model: OR=0.71 (95% CI, 0.46-1.12); p=0.14<br />

Recessive model: OR=1.09 (95% CI, 0.85-1.38); p=0.51<br />

Homozygote model: OR=0.72 (95% CI, 0.39-1.36); p=0.32<br />

Bsm-I polymorphism (rs1544410) 3 studies (352 cases & 582<br />

controls)<br />

Dominant model: OR=0.81 (95% CI, 0.36-1.80); p=0.60<br />

Recessive model: OR=1.17 (95% CI, 0.83-1.64); p=0.38<br />

Homozygote model: OR=1.48 (95% CI, 0.90-2.45); p=0.12<br />

Fok-I polymorphism (rs10735810) 6 studies (1775 cases &1830<br />

controls)<br />

Dominant model: OR=0.99 (95% CI, 0.87-1.14); p=0.93<br />

Recessive model: OR=0.89 (95% CI, 0.74-1.07); p=0.21<br />

Homozygote model: OR=0.90 (95% CI, 0.74-1.11); p=0.33<br />

Taq-I polymorphism (rs731236) 8 studies (2472 cases & 2446<br />

controls)<br />

Dominant model: OR=1.12 (95% CI, 1.00-1.26); p=0.06<br />

Recessive model: OR=1.03 (95% CI, 0.88-1.20); p=0.74<br />

Homozygote model: OR=1.04 (95% CI, 0.78-1.38); p=0.80<br />

13 case-control studies (n=3300 cases & 3194 controls)<br />

TaqI polymorphism: 11 studies (3011 cases & 2810 controls)<br />

Homozygous model: OR=0.90 (95% CI, 0.78-1.04); p=0.163<br />

BsmI polymorphisms: 3 studies (247 cases & 276 controls)<br />

Codominant model: OR=0.85 (95% CI, 0.27-2.66)<br />

Allele contrast model: OR=0.91 (95%CI, 0.51-1.64); p=0.771<br />

ApaI polymorphism: 5 studies (858 cases & 1097 controls)<br />

Codominant model:<br />

OR1=0.83 (95% CI, 0.64-1.08); p=0.016<br />

OR2=1.34 (95% CI, 0.85-2.27); p=0.19<br />

OR3=1.45 (95% CI, 1.04-2.2.08); p=0.03<br />

FokI polymorphism: 7 studies (1989 cases & 1872 controls)<br />

Recessive model: OR=1.03 (95% CI, 0.86-1.24); p=0.074<br />

The VDR Apa-I, BSM-I, Fok-I <strong>and</strong><br />

Taq-I polymorphisms not associated<br />

with MS risk.<br />

No significant association between<br />

TaqI <strong>and</strong> BsmI polymorphisms <strong>and</strong><br />

multiple sclerosis risk<br />

Significant association between the<br />

AA ApaI & FF FokI polymorphisms<br />

<strong>and</strong> multiple sclerosis.<br />

231

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