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Prothrombin activation in eastern tiger snake bite.

John Desmond Parkin1, Kamal Ibrahim, Raymond John Dauer

  • 1Division of Laboratory Medicine, Austin and Repatriation Medical Centre, Melbourne, Victoria, Australia. des.parkin@armc.org.au

Pathology
|May 15, 2002
PubMed
Summary
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Eastern tiger snake envenomation triggers significant prothrombin activation, indicated by elevated F1+2 and thrombin-antithrombin (TAT) complexes. Labile clotting factors decrease due to venom

Area of Science:

  • Toxicology
  • Hematology
  • Biochemistry

Background:

  • Eastern tiger snake venom causes significant hemostatic disturbances.
  • Understanding prothrombin activation is crucial for managing envenomation.

Observation:

  • Serial plasma studies in envenomated individuals revealed marked increases in F1+2 and thrombin-antithrombin (TAT) complexes.
  • Factor V and VIII levels dropped significantly preceding declines in prothrombin and AT3.
  • Alpha2AP, plasminogen, and Protein C levels also showed marked decreases.

Findings:

  • F1+2 and TAT are sensitive biomarkers for eastern tiger snake envenomation.
  • Massive prothrombin activation may overwhelm TAT clearance mechanisms.
  • Proteolytic digestion of clotting factors contributes to labile factor depletion, especially in the absence of thrombocytopenia.

Related Experiment Videos

Implications:

  • Early detection of envenomation is possible through F1+2 and TAT monitoring.
  • The study highlights the complex coagulopathy induced by tiger snake venom.
  • Findings inform potential therapeutic strategies targeting specific hemostatic pathways.