Abstract:
:Homocysteine is a sulfhydryl-containing amino acid formed during the metabolism of methionine. Rapidly accumulating evidence links elevated homocysteine levels to thrombosis via several mechanisms such as increased tissue factor expression, attenuated anticoagulant processes, enhanced platelet reactivity, increased thrombin generation, augmented factor V activity, impaired fibrinolytic potential, and vascular injury, including endothelial dysfunction. Molecular mechanisms underlying prothrombotic actions of homocysteine are incompletely understood and involve oxidative stress, DNA hypomethylation, and proinflammatory effects. Current evidence from retrospective and prospective studies supports the concept that higher total plasma homocysteine concentration is associated with increased risk of coronary artery disease, stroke, and venous thromboembolism. Hyperhomocysteinemia is currently considered a relatively weak prothrombotic factor. It is still unclear whether administration of vitamins, that reduce homocysteine levels acting as cofactors of the enzymes involved in the methionine metabolism, may decrease the risk of arterial and/or venous thromboembolic events. Ongoing clinical trials might help clarify this issue.
journal_name
Thromb Haemostjournal_title
Thrombosis and haemostasisauthors
Undas A,Brozek J,Szczeklik Adoi
10.1160/TH05-05-0313keywords:
subject
Has Abstractpub_date
2005-11-01 00:00:00pages
907-15issue
5eissn
0340-6245issn
2567-689Xpii
05110907journal_volume
94pub_type
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journal_title:Thrombosis and haemostasis
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journal_title:Thrombosis and haemostasis
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doi:
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journal_title:Thrombosis and haemostasis
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doi:
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pub_type: 杂志文章,多中心研究,随机对照试验
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doi:
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