ArticleBritish journal of anaesthesia2026
A novel role for ADAMTS13 in hyperfibrinolysis after trauma-induced shock
Article in British journal of anaesthesia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The absence of ADAMTS13 improves early outcomes in an experimental model of trauma with uncontrolled hemorrhage.The journal of trauma and acute care surgery · 2026Article
- Trauma-Induced Coagulopathy: From Endotheliopathy and Fibrinolysis Phenotypes to Viscoelastic-Guided Resuscitation.European journal of haematology · 2026Review
- Current Advances in the Physiological Roles and Disease-Associated Mechanisms of ADAMTS16.International journal of molecular sciences · 2026Review
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12 authors.
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Abstract
backgroundTrauma-induced coagulopathy with hyperfibrinolysis is associated with high mortality. The protease ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motifs 13) is cleaved after tissue injury. We analysed the underlying mechanism of ADAMTS13 proteolytic cleavage and the effect of ADAMTS13 on trauma-induced hyperfibrinolysis.
methodsThirty-nine trauma patients with shock were stratified based on ADAMTS13 conformation. Mechanisms of ADAMTS13 cleavage were explored in vitro using blood from healthy volunteers. The role of ADAMTS13 in hyperfibrinolysis was examined using rotational thromboelastometry (ROTEM) and a fibrin formation assay.
resultsADAMTS13 circulated in a truncated and hyperactive form in 23% of trauma patients in shock. Truncated ADAMTS13 was associated with a significant increase in hyperfibrinolysis (ROTEM FIBTEM maximum lysis 85 [62-100] vs 1 [0-7]%, P=0.002) and mortality (44% vs 3%, P=0.007) compared with patients with a closed ADAMTS13 conformation. In vitro, ADAMTS13 was cleaved at its distal self-regulating domains in the presence of tissue plasminogen activator and plasmin, which concentration-dependently increased ADAMTS13 activity. This activation was prevented by tranexamic acid. Hyperactivated ADAMTS13 was associated with hyperfibrinolysis by both ROTEM and fibrin formation assays compared with conditions where ADAMTS13 was inactivated.
conclusionsDuring trauma-induced shock, ADAMTS13 can circulate in a truncated and hyperactivated conformation, which is associated with hyperfibrinolysis and mortality. In vitro, tissue plasminogen activator and plasmin can truncate ADAMTS13, increasing its activity. Additionally, ADAMTS13 directly contributes to hyperfibrinolysis, and tranexamic acid can prevent ADAMTS13 degradation. INSTITUTIONAL ETHICAL REVIEW BOARD APPROVAL NUMBERS: NL58766.018.16, NL74188.018.20.
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