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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Wygrecka, M; Birnhuber, A; Seeliger, B; Michalick, L; Pak, O; Schultz, AS; Schramm, F; Zacharias, M; Gorkiewicz, G; David, S; Welte, T; Schmidt, JJ; Weissmann, N; Schermuly, RT; Barreto, G; Schaefer, L; Markart, P; Brack, MC; Hippenstiel, S; Kurth, F; Sander, LE; Witzenrath, M; Kuebler, WM; Kwapiszewska, G; Preissner, KT.
Altered fibrin clot structure and dysregulated fibrinolysis contribute to thrombosis risk in severe COVID-19.
Blood Adv. 2022; 6(3):1074-1087 Doi: 10.1182/bloodadvances.2021004816 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Co-Autor*innen der Med Uni Graz
Birnhuber Anna
Gorkiewicz Gregor
Kwapiszewska-Marsh Grazyna
Zacharias Martin
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Abstract:
The high incidence of thrombotic events suggests a possible role of the contact system pathway in COVID-19 pathology. In this study, we determined the altered levels of factor XII (FXII) and its activation products in critically ill patients with COVID-19 in comparison with patients with severe acute respiratory distress syndrome related to the influenza virus (acute respiratory distress syndrome [ARDS]-influenza). Compatible with those data, we found rapid consumption of FXII in COVID-19 but not in ARDS-influenza plasma. Interestingly, the lag phase in fibrin formation, triggered by the FXII activator kaolin, was not prolonged in COVID-19, as opposed to that in ARDS-influenza. Confocal and electron microscopy showed that increased FXII activation rate, in conjunction with elevated fibrinogen levels, triggered formation of fibrinolysis-resistant, compact clots with thin fibers and small pores in COVID-19. Accordingly, clot lysis was markedly impaired in COVID-19 as opposed to that in ARDS-influenza. Dysregulated fibrinolytic system, as evidenced by elevated levels of thrombin-activatable fibrinolysis inhibitor, tissue-plasminogen activator, and plasminogen activator inhibitor-1 in COVID-19 potentiated this effect. Analysis of lung tissue sections revealed widespread extra- and intravascular compact fibrin deposits in patients with COVID-19. A compact fibrin network structure and dysregulated fibrinolysis may collectively contribute to a high incidence of thrombotic events in COVID-19.
Find related publications in this database (using NLM MeSH Indexing)
COVID-19 - administration & dosage
Fibrin - administration & dosage
Fibrinolysis - administration & dosage
Humans - administration & dosage
SARS-CoV-2 - administration & dosage
Thrombosis - etiology

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