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[Homocysteine and venous thromboembolism]

C Monnerat1, D Hayoz

  • 1Division des maladies vasculaires et de l'hypertension, Département de médecine interne, Centre hospitalier et universitaire vaudois, Lausanne.

Schweizerische Medizinische Wochenschrift
|October 6, 1997
PubMed

Insights

Moderate hyperhomocysteinemia increases the risk of venous thromboembolism. Screening for high homocysteine levels is recommended for idiopathic thrombosis, with folic acid potentially beneficial for mild cases.

Area of Science:

  • Biochemistry
  • Genetics
  • Cardiovascular Medicine

Background:

  • Congenital homocysteinuria is a rare inherited disorder linked to early atherosclerosis and thrombosis.
  • Moderate hyperhomocysteinemia is a prevalent cardiovascular risk factor, associated with venous thromboembolism (VTE).
  • Mild hyperhomocysteinemia, especially with Factor V Leiden mutation, significantly elevates VTE risk.

Purpose of the Study:

  • To review the association between hyperhomocysteinemia and thrombosis.
  • To discuss the potential mechanisms of homocysteine-induced thrombosis.
  • To evaluate the role of screening and folic acid treatment.

Main Methods:

  • Review of case-control studies on hyperhomocysteinemia and venous thromboembolism.
  • Analysis of biochemical mechanisms linking homocysteine to thrombosis.
  • Evaluation of existing literature on folic acid treatment efficacy.

Main Results:

  • Moderate hyperhomocysteinemia confers a 2-3 fold increased risk of VTE.
  • Mild hyperhomocysteinemia with Factor V Leiden mutation increases VTE risk tenfold.
  • Homocysteine may promote thrombosis by inhibiting thrombomodulin and antithrombin-III binding.

Conclusions:

  • Hyperhomocysteinemia should be screened in patients with idiopathic thromboembolism.
  • Folic acid reduces homocysteine levels, and a trial may be justified for mild hyperhomocysteinemia.
  • Further studies are needed to confirm folic acid's efficacy in reducing VTE and atherosclerosis.

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