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Homocysteine, an intermediate of methionine metabolism, has been found to be an independent risk factor for thromboembolism [1]. Various mechanisms have been proposed to explain possible homocysteine-induced thrombogenicity, including endothelial damage, enhanced lipid peroxidation, impaired activity of the anticoagulant protein C system and increased expression of tissue factor [1–5]. Relevance of these findings in vivo remains controversial. Much less is known on the effects of homocysteine on platelet function [6]. In patients with homocystinuria, homocysteine might increase thromboxane A2 production [7] and stimulate platelet aggregation [8], though the effect of homocysteine on platelet survival is less evident [6]. Oxidative stress might lead to homocysteine oxidation, enhanced platelet activation and increased prothrombotic potential in hyperhomocysteinemia [9]. Methionine loading test is recognized as a method to induce a transient acute hyperhomocysteinemia and helps to identify individuals with abnormal methionine metabolism [10,11]. It remains to be determined whether in mild hyperhomocysteinemia platelet-mediated prothrombotic effects might be of importance. The aim of the study was to evaluate potential alterations in thrombin formation in platelet-rich plasma after oral methionine loading in healthy subjects. 2. Materials and methods |
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