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To the Editor: In their randomized controlled trial, Dr Toole and colleagues¹ found that a high-dose formulation of pyridoxine, cobalamin, and folic acid led to moderate reduction of total homocysteine levels after nondisabling cerebral infarction, but this did not translate into any benefit in terms of clinical end points. Nonetheless, the authors also found that, across all patients, total homocysteine levels were related to risk of clinical events, and thus they concluded that serum homocysteine is a marker, rather than a cause of vascular disease.

Nevertheless, the results do not exclude the possibility that a high plasma homocysteine level may have a modest intrinsic effect on vascular disease. First, patients in the study had homocysteine levels that were only marginally elevated (mean, 13.4 µmol/L at randomization). Second, longer follow-up may be needed to detect a long-term protective effect of lowering homocysteine levels. Indeed, the authors acknowledged both limitations. Third, the . . . [Full Text of this Article]

Ciriaco Aguirre, MD, PhD
caguirre@hcru.osakidetza.net

Guillermo Ruiz-Irastorza, MD, PhD; Maria-Victoria Egurbide, MD; Agustin Martinez-Berriotxoa, MD, PhD
Service and Department of Internal Medicine
Hospital De Cruces
University of the Basque Country
Bizkaia, Spain

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