Thromb Haemost 2005; 94(05): 907-915
DOI: 10.1160/TH05-05-0313
Review Article
Schattauer GmbH

Homocysteine and thrombosis: from basic science to clinical evidence

Anetta Undas
1   Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland
,
Jan Brożek
1   Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland
,
Andrzej Szczeklik
1   Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received: 06. Mai 2005

Accepted after revision: 11. August 2005

Publikationsdatum:
14. Dezember 2017 (online)

Summary

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.

 
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