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Hyperhomocysteinaemia as a risk factor for venous thrombosis: an update of the current evidence

Martin den Heijer1

  • 1Department of Endocrinology (531), University Medical Center Nijmegen, Nijmegen, The Netherlands. m.denheijer@endo.umcn.nl

Clinical Chemistry and Laboratory Medicine
|December 6, 2003
PubMed

Insights

Moderate hyperhomocysteinemia, often linked to the MTHFR gene mutation, is increasingly recognized as a significant risk factor for venous thrombosis. Current evidence supports its causal role, with further trial results anticipated.

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Thrombosis Research

Background:

  • Classical homocystinuria is linked to arterial and venous vascular diseases.
  • Emerging evidence suggests moderate hyperhomocysteinemia is a risk factor for venous thrombosis.
  • The methylenetetrahydrofolate reductase (MTHFR) gene 677C>T mutation is a key cause of mild hyperhomocysteinemia.

Purpose of the Study:

  • To discuss the current evidence linking hyperhomocysteinemia to venous thrombosis.
  • To evaluate the role of MTHFR gene mutations in hyperhomocysteinemia and thrombosis risk.

Main Methods:

  • Review of published studies, including prospective research and meta-analyses.
  • Application of Mendelian randomization principles to assess causality.
  • Discussion of ongoing homocysteine-lowering clinical trials.

Main Results:

  • Meta-analyses indicate an elevated venous thrombosis risk in individuals with the MTHFR TT-genotype.
  • The association supports hyperhomocysteinemia as a causal risk factor for venous thrombosis.

Conclusions:

  • Hyperhomocysteinemia, particularly associated with the MTHFR 677C>T mutation, is a significant risk factor for venous thrombosis.
  • Further evidence from homocysteine-lowering trials is expected to solidify this causal link.

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