Methylenetetrahydrofolate Reductase Polymorphisms and Homocysteine-Lowering Effect of Vitamin Therapy in Singaporean Stroke Patients
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abstract
Background and Purpose—
Increased plasma total homocysteine (tHcy) levels are a risk factor for stroke and can be reduced with vitamin therapy. However, data on the tHcy-lowering effects of vitamins are limited largely to white populations. Thus, we aimed to determine in Singaporean patients with recent stroke: (1) the efficacy of vitamin therapy (folic acid, vitamin B
12
, and B
6
) on lowering tHcy, and (2) whether efficacy is modified by Methylenetetrahydrofolate reductase (
MTHFR
) gene polymorphism(s).
Methods—
A total of 443 eligible patients were recruited after presenting with ischemic stroke within the past 7 months. Patients were randomized to receive either placebo or vitamins. Fasting blood samples collected at baseline and at 1 year were assayed for levels of plasma tHcy. Patients were genotyped for
MTHFR C677T
and
A1298C
polymorphisms.
Results—
Mean baseline tHcy was similar in the 2 groups (placebo 13.7 μmol/L; vitamins 14.0 μmol/L;
P
=0.70). At 1 year, mean tHcy was 14.5 μmol/L in the placebo group compared with 10.7 μmol/L in the vitamin group (difference 3.8 μmol/L; 95% CI, 2.8 to 4.8 μmol/L;
P
<0.0001).
MTHFR C677T
genotype was an independent determinant of tHcy levels at baseline (
P
=0.005), but
A1298C
was not (
P=
0.08). Neither polymorphism significantly influenced the effect of vitamin therapy on tHcy at 1 year. The magnitude of the reduction in tHcy levels at 1 year with vitamin therapy was similar, irrespective of
MTHFR
genotypes.
Conclusions—
Vitamin therapy reduces mean tHcy levels by 3.8 μmol/L in the Singaporean stroke population studied.
MTHFR C677T
but not
A1298C
is independently associated with tHcy levels at baseline, and neither impacts the tHcy-lowering effect of vitamins used in this study.
