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Related Experiment Videos

Thrombophilia, polymorphisms, and vascular disease.

T C Sykes1, C Fegan, D Mosquera

  • 1Academic Vascular Unit, Birmingham Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS, UK.

Molecular Pathology : MP
|February 24, 2001
PubMed
Summary

Genetic factors influence thrombosis risk, but evidence is conflicting. Only Factor V Leiden and prothrombin gene variations show clear links to venous thrombosis, often interacting with smoking. Future research needs larger, diverse studies.

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Area of Science:

  • Genetics
  • Hematology
  • Cardiovascular Medicine

Background:

  • Thrombophilia traditionally signifies rare inherited coagulation defects impacting the venous system.
  • Recent research explores genetic polymorphisms in prothrombotic genes for their role in both venous and arterial thrombosis.
  • Existing evidence stems from numerous, often small and heterogeneous, case-control studies with varied endpoints.

Purpose of the Study:

  • To investigate the impact of genetic polymorphisms in prothrombotic genes on venous and arterial thrombosis.
  • To clarify the associations between specific genetic variations and thrombotic events.
  • To understand gene-environment interactions, particularly with cardiovascular risk factors like smoking.

Main Methods:

  • Review and synthesis of case-control association studies.

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  • Analysis of data from studies with diverse endpoints including deep venous thrombosis, myocardial infarction, and stroke.
  • Examination of potential interactions between genetic polymorphisms and established cardiovascular risk factors.

    • Main Results:

    • Conflicting and inconclusive data exist for many polymorphisms.
    • Factor V Leiden and prothrombin gene polymorphisms demonstrate clear associations with venous thrombosis.
    • Interactions between polymorphisms and risk factors like smoking significantly elevate thrombotic episode risk.

    Conclusions:

    • Genetic polymorphisms, particularly Factor V Leiden and prothrombin variations, play a role in venous thrombosis.
    • Gene-environment interactions, especially with smoking, are critical in modulating thrombotic risk.
    • Future research requires larger sample sizes, standardized clinical endpoints, and consideration of race and gene-environment interactions for robust findings.