Riboflavin status in acute ischaemic stroke.

BACKGROUND: There is experimental evidence that riboflavin (vitamin B2) supplementation reduces oxidative damage and cerebral oedema following acute stroke. OBJECTIVE: To measure riboflavin levels in acute stroke before and after supplementation with this vitamin. DESIGN: Ninety-six acute ischaemic stroke patients had their riboflavin status measured at baseline and then randomly assigned to receive 5 mg of oral riboflavin and other B-group vitamins within 12 h of the stroke onset and then daily or no B-vitamins for 14 days. Non-fasting venous blood was obtained at baseline, days 7 and 14 post-randomization for measurement of riboflavin status using erythrocyte glutathione reductase activity coefficient (EGRAC). EGRAC is a measure of riboflavin tissue saturation. This assay has the advantage of being extremely stable and sensitive. EGRAC values are inversely proportional to riboflavin status, so that values greater than 1.3 indicate biochemical deficiency. RESULTS: Fifty-one per cent of patients studied were riboflavin deficient at baseline. Fourteen days of riboflavin supplementation significantly improved the measure of B2 status compared with the control group. Seven out of 37 patients in the supplement group (19%) were riboflavin deficient compared with 22 out of 39 patients (56%) in the control group at the end of the treatment period (P=0.035 for the differences in cumulative changes between groups over 2 weeks). CONCLUSIONS: A high proportion of acute stroke patients were biochemically deficient of riboflavin immediately post-infarct. Supplementation with 5 mg of riboflavin for 2 weeks significantly improved riboflavin status; however, the clinical significance of these findings is not yet known.

Antioxidant supplementation enhances antioxidant capacity and mitigates oxidative damage following acute ischaemic stroke.

OBJECTIVE: To test whether supplementary antioxidants immediately following acute ischaemic stroke will enhance antioxidant capacity and mitigate oxidative damage. DESIGN: A randomised controlled trial. SETTING: A university teaching hospital. SUBJECTS: A total of 48 acute ischaemic stroke patients within 12 h of symptom onset. INTERVENTION: Daily oral 800 IU (727 mg) of alpha-tocopherol and 500 mg of vitamin C (n = 24), or no treatment (n = 24) for 14 days. Treatment group and controls were matched for stroke subtype and age. MAIN OUTCOME MEASURES: alpha-Tocopherol, ascorbic acid, total antioxidant capacity (TAOC), plasma malondialdehyde (MDA) and C-reactive protein (CRP) before treatment, at day 7 and day 14 following recruitment. RESULTS: In all, 14 days of vitamin supplementation significantly improved plasma alpha-tocopherol and ascorbic concentrations in the treatment group compared with the decrease seen in the control group (P < 0.005 for difference in cumulative changes). TAOC increased significantly in the treatment group compared with controls (P < 0.003). There was a significant reduction in plasma MDA concentration in the treatment group, in contrast to the increase seen in the control group (P < 0.002). After adjusting for clinical complications CRP concentrations within 90 days postinfarct were significantly lower in the treatment group compared with controls. CONCLUSION: Supplementation with antioxidant vitamins within 12 h of onset of acute ischaemic stroke increased antioxidant capacity, reduced lipid peroxidation products and may have an anti-inflammatory effect. SPONSORSHIP: Sheffield Teaching Hospital NHS Trust.