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| INVITED COMMENTS |
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| Year : 2006 | Volume
: 54
| Issue : 1 | Page : 51 |
Invited Comments
Alessandro Pezzini
Clinica Neurologica, Universitą degli Studi di Brescia, P.le Spedali Civili, 1, 25125 - Brescia, Italy
Correspondence Address:
Alessandro Pezzini
Clinica Neurologica, Universitą degli Studi di Brescia, P.le Spedali Civili, 1, 25125 - Brescia
Italy
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Pezzini A. Invited Comments. Neurol India 2006;54:51 |
Over the last decade, convincing evidence has been gathered on the relation between moderate elevation of plasma total homocysteine (tHcy) and ischemic stroke. If a causal association
really exists, then the practical implication is that the intervention of increasing folate intake at a population level could lead to a decrease in stroke risk. However, causality has yet to be established. At least theoretically, the tHcy-stroke association might be a spurious epidemiological finding and elevated tHcy could be interpreted as an epiphenomenon secondary to the vascular disease itself.[1]
Recently, evidence that tHcy may be a causal risk factor for ischemic stroke was provided by a large meta-analysis of literature, based on the principle of Mendelian randomization.[2] However, most of the studies included in this meta-analysis were from Europe or North America and focused on subjects with mean age of 40 years or older, with relatively few data from studies conducted in other continents and from younger groups.
In this issue of Neurology India, Panigrahi et al[3] report on a hospital-based, case-control study including a group of 1- to 42- year-old patients (median age: 12 years) with ischemic stroke and no history of major "traditional" cardiovascular risk factors. Among the 32 patients who were recruited over one year, these investigators found a higher prevalence of hyperhomocysteinemia in comparison to the group of 60 controls, and a trend toward a significant association between the TT677 MTHFR genotype and disease. Such findings were independent on clinical phenotype (single infarct vs recurrent infarcts). Furthermore, given the inclusion criteria, the influence of a confounding effect on the reported association seems negligible. Although the small sample size precludes extensive analysis, this study highlights the role of homocysteine as a potential risk factor for ischemic stroke at young age in this specific ethnic group.
Whether increased tHcy is as a causal risk factor for ischemic stroke remains to be proven. However, while awaiting for conclusive evidence from powered randomized trials of multi-vitamin supplementation,[4] the implication of these findings may be that measuring tHcy levels and screening of MTHFR genotypes in stroke patients of this ethnic group is warranted, since the benefits of the empirical practice of treating selected high-risk patients (such as those included in Panigrahi et al study) with folic acidbased multivitamin therapy, outweigh the potential risks.
| References | |  |
| 1. | Ueland PM, Refsum H, Beresford SA, Vollset SE. The controversy over homocysteine and cardiovascular risk. Am J Clin Nutr 2000;72:324-32.  [PUBMED] [FULLTEXT] |
| 2. | Casas PJ, Bautista LE, Smeeth L, Sharma P, Hingorani AD. Homocysteine and stroke: evidence on a causal link from Mendelian randomization. Lancet 2005;365:224-32. |
| 3. | Panigrahi I, Chatterjee T, Biswas A, Behari M, Choudhry PV, Saxena R. Role of MTHFR C677T polymorphism in ischemic stroke. Neurol India 2006;54:48- 52. |
| 4. | The VITATOPS Trial Study Group. The VITATOPS (Vitamin To Prevent Stroke) trial: rational and design of an international, large, simple, randomised trial of homocysteine-lowering multivitamin therapy in patients with recent transient ischemic attack or stroke. Cerebrovasc Dis 2002;13:120-6. |
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