miércoles, 6 de octubre de 2010

B Vitamin Treatment Does Not Prevent Recurrent Stroke or TIA

Andrew JosephsonM.D., Department of Neurology, University of California San Francisco, San Francisco, USAElevated levels of plasma total homocysteine are an important risk factor for vascular events.
Treatment of elevated homocysteine with B vitamins is effective in reducing plasma levels, but trials examining the role of B vitamins in primary prevention of actual vascular events have been largely disappointing. Patients who experience a stroke or transient ischemic attack (TIA) are at high risk for recurrence, and a recent trial (VITATOPS Trial Study Group, 2010) examined whether B vitamin supplementation in these patients would mitigate this risk.The authors report the results of a large, randomized, double-blind, placebo-controlled trial of patients with recent (in the last 7 months) stroke or TIA that took place at 123 medical centers in 20 countries. Both hemorrhagic and ischemic stroke subtypes were included. Patients were randomized to treatment with either placebo or a single daily pill of B vitamins containing 2 mg folic acid, 25 mg B6, and 0.5 mg B12. The primary outcome examined was the composite endpoint of nonfatal stroke, nonfatal myocardial infarction (MI), or vascular death.Over a 10-year period, a total of 4089 patients were assigned to treatment with B vitamins and 4075 assigned to placebo. Baseline characteristics were similar between the two ethnically diverse groups, which consisted of 42% of patients who were white, 24% east or southeast Asian, and 26% south Asian. The median follow-up was 3.4 years, although 702 patients (9%) were lost to follow-up. After the first year, 10-11% of each group had discontinued their study medication; this number rose to 27-28% by the end of the trial.The composite primary endpoint was reached by 616 patients (15%) in the treatment group and 678 patients (17%) in the placebo group [relative risk (RR), 0.91; 95% confidence interval (CI), 0.82–1.00; p = .05]. Adjustments for follow-up duration and baseline variables yielded no substantial differences in this result. Despite this nonsignificant difference in events, treatment with B vitamins did indeed lower total homocysteine by a mean of 1.09 (standard deviation, 5.5) μmol/L. There were no significant differences in adverse events in the two groups.The authors added their data to other previously published randomized trials of homocysteine lowering and concluded that a meta-analysis does not suggest that B vitamins reduce the composite risk of stroke, MI, or vascular death (RR, 0.99; 95% CI, 0.94–1.03; p = .49). When examining stroke or MI individually, no significant reductions with B vitamins could be found.This trial failed to show a significant benefit of B vitamin supplementation after stroke.
This result follows a long list of trials that all seem to show effective lowering of homocysteine without any significant improvement in outcomes. One of the advantages of this particular trial is that many of the patients were enrolled in countries with little folic acid fortification of the food supply, thereby increasing the chances that supplementation would be of benefit. While there are an additional three ongoing randomized trials to be published in the coming years, for now there is simply no evidence that B vitamin supplementation should be used by clinicians for secondary prevention of vascular events.-
Josephson SA. B Vitamin Treatment Does Not Prevent Recurrent Stroke or TIA. Harrison’s Online, September 9, 2010. http://www.accessmedicine.com
Related to Chapter 364 Cerebrovascular Diseases, in Harrison’s Principles of Internal Medicine, 17th edition, Anthony S. Fauci, Eugene Braunwald, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo, J. Larry Jameson, and Joseph Loscalzo, Eds. McGraw-Hill, New York, 2008.
ReferenceVITATOPS Trial Study Group. B vitamins in patients with recent transient ischaemic attack or stroke in the VITAmins TO Prevent Stroke (VITATOPS) trial: A randomised, double-blind, parallel, placebo-controlled trial. Lancet Neurol 2010;9:855. [PubMed Abstract]

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