TABLE 3.

Summary of abnormalities in hemostasis in humans with ALF

Laboratory	Primary site of synthesis	Abnormality in ALF	Potential effect on hemostasis	References
Primary hemostasis
Platelet count	Bone marrow	Decreased	Impaired	100
von Willebrand factor	Endothelium	Increased	Enhanced	138
ADAMTS-13	Liver	Decreased	Enhanceda	138
Platelet microparticles	Circulation	Increased	Enhanced	139
Secondary hemostasis
Procoagulant factors: II,V,VII,IX,X,XI,XII	Liver	Decreased	Impaired	140
Anticoagulant factors: protein C, S, AT	Liver	Decreased	Enhanced	140
Factor VIII	Endothelium	Increased	Enhanced	140
Fibrinogen	Liver	Decreased	Impaired	140
Fibrinolysis
Antiplasmin	Liver	Decreased	Impaired	141
TAFI	Liver	Decreased	Impaired	141
Plasminogen	Liver	Decreased	Enhanced	141
PAI-1	Endothelium	Increased	Enhanced	141
tPA	Endothelium	Increased	Enhanced	141

^aVery low ADAMTS has been documented in patients with ALF. However, vWF multimer size was also shown to be low, leaving the functional significance of low ADAMTS-13 as yet uncertain.

Abbreviations: ADAMTS13, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13; ALF, acute liver failure; AT, antithrombin; PAI-1, plasminogen activator inhibitor type 1; TAFI, thrombin activatable fibrinolysis inhibitor; tPA, tissue-type plasminogen activator; vWF, von Willebrand factor.