What is the role of venom and toxins in the pathophysiology of factor XIII (FXIII) deficiency?

Updated: Aug 01, 2019
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Perumal Thiagarajan, MD  more...
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Answer

Venoms and toxins can affect clot stability. Excessive bleeding resulting from envenomation can affect the functions of FXIII in different ways. Acuthrombin A, one of two proteases in the venom of Agkistrodon acutus (five-pace snake), activates FXIII. [52] Ancrod, obtained from the venom of Agkistrodon species, causes defibrination, thereby removing the substrate for FXIII.

A severe systemic bleeding disorder may develop several hours after initial contact with 2 types of caterpillars in the Saturniidae family (from Brazil and Venezuela). Intracranial and intracerebral bleeding and renal failure may follow. In this case, FXIII reduction results from generalized disseminated intravascular coagulation (DIC) induced by several activities directed against the hemostatic mechanism, including a FXIII proteolytic-urokinase–like activity. [53] Tridegin, a peptide inhibitor of FXIII present in the saliva of an Amazon leech (Haementeria ghilianii) accelerates fibrinolysis by inhibiting FXIIIa; tridegin is under investigation as a potential new antithrombotic agent. Destabilase, an enzyme present in the leech, hydrolyzes g-g fibrin cross-links and breaks down blood clots. [54]


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