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- Brandon Michael Henry, Jens Vikse, Stefanie Benoit, Emmanuel J Favaloro, and Giuseppe Lippi.
- Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. Electronic address: brandon.henry@cchmc.org.
- Clin. Chim. Acta. 2020 Aug 1; 507: 167-173.
AbstractEarly clinical evidence suggests that severe cases of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are frequently characterized by hyperinflammation, imbalance of renin-angiotensin-aldosterone system, and a particular form of vasculopathy, thrombotic microangiopathy, and intravascular coagulopathy. In this paper, we present an immunothrombosis model of COVID-19. We discuss the underlying pathogenesis and the interaction between multiple systems, resulting in propagation of immunothrombosis, which through investigation in the coming weeks, may lead to both an improved understanding of COVID-19 pathophysiology and identification of innovative and efficient therapeutic targets to reverse the otherwise unfavorable clinical outcome of many of these patients.Copyright © 2020 Elsevier B.V. All rights reserved.
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