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10.1016/j.thromres.2021.02.012

http://scihub22266oqcxt.onion/10.1016/j.thromres.2021.02.012
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suck abstract from ncbi


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pmid33662796      Thromb+Res 2021 ; 201 (ä): 100-112
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  • Recombinant ADAMTS13 reduces abnormally up-regulated von Willebrand factor in plasma from patients with severe COVID-19 #MMPMID33662796
  • Turecek PL; Peck RC; Rangarajan S; Reilly-Stitt C; Laffan MA; Kazmi R; James I; Dushianthan A; Schrenk G; Gritsch H; Ewenstein BM; Mellgard B; Erdlenbruch W; Jain N; Binder NB; Mumford AD
  • Thromb Res 2021[May]; 201 (ä): 100-112 PMID33662796show ga
  • Thrombosis affecting the pulmonary and systemic vasculature is common during severe COVID-19 and causes adverse outcomes. Although thrombosis likely results from inflammatory activation of vascular cells, the mediators of thrombosis remain unconfirmed. In a cross-sectional cohort of 36 severe COVID-19 patients, we show that markedly increased plasma von Willebrand factor (VWF) levels were accompanied by a partial reduction in the VWF regulatory protease ADAMTS13. In all patients we find this VWF/ADAMTS13 imbalance to be associated with persistence of ultra-high-molecular-weight (UHMW) VWF multimers that are highly thrombogenic in some disease settings. Incubation of plasma samples from patients with severe COVID-19 with recombinant ADAMTS13 (rADAMTS13) substantially reduced the abnormally high VWF activity, reduced overall multimer size and depleted UHMW VWF multimers in a time and concentration dependent manner. Our data implicate disruption of normal VWF/ADAMTS13 homeostasis in the pathogenesis of severe COVID-19 and indicate that this can be reversed ex vivo by correction of low plasma ADAMTS13 levels. These findings suggest a potential therapeutic role for rADAMTS13 in helping restore haemostatic balance in COVID-19 patients.
  • |*COVID-19[MESH]
  • |*Recombinant Proteins/therapeutic use[MESH]
  • |*Thrombosis[MESH]
  • |ADAMTS13 Protein[MESH]
  • |Cross-Sectional Studies[MESH]
  • |Humans[MESH]
  • |SARS-CoV-2[MESH]


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