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Hepatogastroenterology. 2010 Mar-Apr;57(98):316-20.

ADAMTS13 activity decreases after hepatectomy, reflecting a postoperative liver dysfunction.

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Department of Surgery, Nara Medical University, Kashihara, Nara, Japan.



The precise mechanism and prophylactic strategy of deteriorated hepatic function after liver surgery have not been fully understood. The substrate of ADAMTS13, unusually large von Willebrand factor multimers, is produced in vascular endothelial cells at liver injury, leading to platelet aggregation. The decrease of plasma ADAMTS13 activity may involve not only the formation of platelet thrombi in the liver, but also subsequent progression of liver dysfunction through a microcirculatory disturbance. This study evaluated changes of plasma ADAMTS13 activity and its clinical relevance in patients with hepatectomy.


Plasma ADAMTS13 activity and its related parameters were sequentially determined after hepatectomy in 70 patients.


ADAMTS13 activity significantly decreased preoperative 67.0 +/- 30.6 to 48.1 +/- 24.6% after hepatectomy (p < 0.0001). Pringle's maneuver for longer than 45 minutes (p = 0.0007) and major hepatectomy (p = 0.0002) were significantly associated with the decrease of ADAMTS13 activity to less than 40%. The decreased ADAMTS13 activity reflected postoperative thrombocytopenia (p = 0.0028) and hyperbilirubinemia (p < 0.05).


Plasma ADAMTS13 activity significantly decreased after hepatectomy due to ischemic injury together with liver mass reduction, reflecting a postoperative liver dysfunction. Monitoring of ADAMTS13 activity may be useful to prevent further development of the liver failure after hepatectomy.

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