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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5520. This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Marcucci, R. Articles by Abbate, R. Search for Related Content PubMed Articles by Marcucci, R. Articles by Abbate, R. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CORRESPONDENCE Vitamin supplementation in the secondary prevention of venous thromboembolism: about the VITRO study To the editor: We read with great interest and expectation the article by den Heijer et al1 on a randomized, placebo-controlled double-blind trial in the secondary prevention of venous thromboembolism. We point out some issues to be clarified by the authors, and a general comment. (1) The authors do not give any information on the prevalence of thrombophilic polymorphisms, such as factor V Leiden and prothrombin G20 210A, which are expected to be highly prevalent in these patients with no major acquired risk factors. (2) Were patients with venous thromboembolism on hormonal therapy equally distributed? The risk of recurrence in these patients is, in fact, different from those with ‘true’ idiopathic venous thrombosis. (3) In den Heijer,1(Table 1) the range of geometric mean baseline homocysteine (Hcy) levels in the hyperhomocysteinemic group is reported to be 6.3 to 84.8 in the multivitamin group and 7.4 to 108.3 in the placebo group. Does this mean that patients with Hcy levels below the cut-off of hyperHcy were considered as hyperhomocysteinemic? On the other hand, the range of geometric mean baseline Hcy levels in the normohomocysteinemic group treated with multivitamins is reported to be 4.0 to 23.0. Does this mean that patients with Hcy levels above the reported cut-off were considered as normohomocysteinemic? (4) What was the renal function of patients enrolled? Also documented by Spence et al,2 patients with significant renal impairment do not respond to vitamin therapy, in particular to vitamin B12. A limitation of the trial, as of other published trials (eg, VISP3), is the level of Hcy chosen to diagnose and treat hyperHcy. Indeed, the 75th percentile of Hcy distribution in controls identifies a quite low level of Hcy in the population of the Netherlands of 12.6 µM/L, which is even lower in the population enrolled in Milan (10.6 µM/L) and Wien. Lowering Hcy concentrations has been shown to have a significant effect on reducing the cardiovascular disease risk in patients with homocystinuria.4,5 However, because of this cut off level, we would probably miss, once again, the opportunity to know if the lowering of intermediate Hcy levels rather than levels of 8 to 12 µM/L may be useful for reducing the recurrence rate. The debate continues, and we still look forward to an adequately-sized study addressing patients not homocystinuric but with intermediate hyperHcy. Authorship Correspondence: R. Marcucci, Department of Heart and Vessels, Azienda Ospedaliero–Universitaria Careggi, University of Florence, Florence, Italy; e-mail: r.marcucci{at}DAC.UNIFI.IT. Conflict-of-interest disclosure: The authors declare no competing financial interests. Rossella Marcucci, Francesco Sofi, Anna Maria Gori, Gian Franco Gensini, and Rosanna Abbate References den Heijer M, Willems HPJ, Blom HJ, et al. Homocysteine lowering by B vitamins and the secondary prevention of deep vein thrombosis and pulmonary embolism: a randomized, placebo-controlled, double blind trial. Blood 2007; 109:139–144.[Abstract/Free Full Text] Spence DJ, Bang H, Chambless LE, Stampfer MJ. Vitamin intervention for stroke prevention trial. An efficacy analysis. Stroke 2005; 36:2404–2409.[Abstract/Free Full Text] Toole JF, Malinow MR, Chambless LE, et al. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA 2004; 291:565–575.[Abstract/Free Full Text] Kluijtmans IAJ, Boers GHD, Kraus JP, van de Heuvel LP, Cruysberg JR, Trijbels FJ. The molecular basis of cystathionine neta synthase deficiency in Dutch patients with homocystinuria: effect of CBS genotype on biochemical and clinical phenotype and on response to treatment. Ann J Hum Genet 1999; 65:59–67.[CrossRef] Yap S and Naughten E. Homocysteinemia due to cystathionine beta synthase deficiency in Ireland: 25 years experience of a newborn screened and treated population with reference to a clinical outcome and biochemical control. J Inherit Metab Dis 1998; 21:738–747.[CrossRef][Medline] [Order article via Infotrieve] CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Marcucci, R. Articles by Abbate, R. Search for Related Content PubMed Articles by Marcucci, R. Articles by Abbate, R. Social Bookmarking                   What's this?

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