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.