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Related Experiment Videos

[Factor XIII in man: a review].

G S Dufner1, G A Marbet

  • 1Hämostaselabor DZL, Kantonsspital Basel, Schweiz.

Hamostaseologie
|August 24, 2002
PubMed
Summary

Factor XIII (FXIIIa) stabilizes blood clots by cross-linking fibrin and other proteins. FXIII deficiency causes bleeding disorders, treatable with FXIII concentrates, and FXIII is used in fibrin glues.

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Area of Science:

  • Biochemistry
  • Hematology
  • Genetics

Context:

  • Factor XIII (FXIIIa) is a crucial enzyme in hemostasis, activated by calcium and thrombin.
  • FXIIIa's primary role is cross-linking fibrin to enhance clot stability.
  • It also cross-links other proteins like alpha(2)-plasmin-inhibitor, fibronectin, and collagen, contributing to tissue repair.

Purpose:

  • To elucidate the function of Factor XIIIa in hemostasis and tissue repair.
  • To describe the clinical manifestations and diagnosis of Factor XIII deficiency.
  • To discuss the therapeutic applications and implications of FXIII polymorphisms.

Summary:

  • Factor XIIIa cross-links fibrin and other proteins, essential for clot stability and tissue repair.
  • The Val34Leu polymorphism in FXIII is implicated in athero- and thrombogenesis.
  • FXIII deficiency, an autosomal recessive disorder, presents with bleeding tendencies, particularly from the umbilical cord, and is diagnosed via clot solubility and incorporation assays.
  • Bleeding is evident when FXIIIa activity drops below 1-2%, though severe episodes can occur at higher levels in heterozygotes.

Impact:

  • Inherited FXIII deficiency can be life-threatening and is managed with FXIII concentrates.
  • Acquired FXIII deficiency associated with diseases and surgery requires further clinical investigation.
  • Factor XIII is utilized in fibrin glues for local hemostatic applications.

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