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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
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Inherited Thrombophilia.

Haley M Phillippe1, Lori B Hornsby2, Sarah Treadway3

  • 1Department of Pharmacy Practice, Auburn University Harrison School of Pharmacy, Auburn, AL, USA Family Medicine-Huntsville Campus, University of Alabama School of Medicine, Huntsville, AL, USA.

Journal of Pharmacy Practice
|April 18, 2014
PubMed
Summary
This summary is machine-generated.

Thrombophilia, an imbalance favoring clot formation, includes inherited conditions like factor V Leiden and protein deficiencies. Vitamin B for homocysteine is not recommended for preventing thrombus.

Keywords:
antithrombin deficiencyfactor V Leidenhyperhomocysteinemiainherited thrombophiliaprotein C deficiencyprotein S deficiencyprothrombin mutationthrombophilia

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Area of Science:

  • Hematology
  • Genetics

Background:

  • Thrombophilia disrupts normal hemostasis, promoting thrombus formation.
  • Inherited thrombophilias encompass factor V Leiden (FVL), prothrombin G20210A mutation, deficiencies in natural anticoagulants (antithrombin [AT], protein C, protein S), hyperhomocysteinemia, and elevated clotting factors (VIII, XI).
  • While FVL and prothrombin mutations are prevalent, natural anticoagulant deficiencies are rare.

Purpose of the Study:

  • To review the landscape of inherited thrombophilias.
  • To discuss the varying risks associated with different thrombophilias.
  • To clarify treatment implications for thrombophilia in nonpregnant patients.

Main Methods:

  • Literature review of inherited thrombophilias and their clinical impact.
  • Analysis of risk stratification based on thrombophilia type and inheritance pattern.
  • Evaluation of current treatment recommendations for acute events and preventative strategies.

Main Results:

  • The risk of thrombosis varies, with homozygous FVL, homozygous prothrombin mutation, or antithrombin deficiency conferring the highest risk.
  • In nonpregnant individuals, existing thrombophilia does not alter the management of an acute thrombotic event.
  • Vitamin B supplementation to lower homocysteine levels has not demonstrated efficacy in preventing thrombosis and is not advised.

Conclusions:

  • Understanding inherited thrombophilias is crucial for risk assessment.
  • Current treatment protocols for acute events remain consistent regardless of thrombophilia status in nonpregnant patients.
  • Evidence does not support vitamin B supplementation for thrombotic event prevention.