Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complemen
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Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID‑19 Xin Wang1 · Kamal Kant Sahu2 · Jan Cerny3 Accepted: 26 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Coronavirus disease-2019 (COVID-19) is a rapidly evolving health crisis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a novel disease entity and we are in a learning phase with regards to the pathogenesis, disease manifestations, and therapeutics. In addition to the primary lung injury, many patients especially the ones with moderate to severe COVID-19 display evidence of endothelial damage, complement activation, which leads to a pro-coagulable state. While there are still missing links in our understanding, the interplay of endothelium, complement system activation, and immune response to the SARS-CoV-2 virus is a surprisingly major factor in COVID-19 pathogenesis. One could envision COVID-19 becoming a novel hematological syndrome. This review is to discuss the available literature with regards to the involvement of the complement system, and coagulation cascade and their interaction with endothelium. Keywords Coronavirus · Pandemic · COVID-19 · Immunity
Highlights • SARS-CoV2 viral infection has been associated with
a high incidence of venous thromboembolism and pulmonary embolism. • The pathophysiology and risk of thrombosis and embolism in patients with COVID-19 need elaborative research and discussion considering a higher morbidity and mortality risk. * Jan Cerny [email protected] Xin Wang [email protected] Kamal Kant Sahu [email protected] 1
Department of Medicine, UMass Memorial Health Care, University of Massachusetts Medical School, Worcester, MA, USA
2
Department of Internal Medicine, Saint Vincent Hospital, Worcester, MA 01608, USA
3
Department of Medicine ‑ Hematology, and Oncology, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, MA, USA
Introduction Currently, the World is facing an unparalleled public health challenge [1]. Since December 2019, the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has relentlessly marched around the globe. Early reports from China revealed evidence of abnormal coagulation parameters associated with COVID-19 and its correlation to a more severe clinical course [2–4]. As the pandemic continues to spread in various parts of the World, frontline clinicians have quickly recognized an unusually high incidence of thromboembolic events in COVID-19 patients, including venous and arterial thrombosis [5]. Middeldorp et al. reported cumulated venous thromboembolism (VTE) incidences of 16%, 33%, and 42% in hospitalized COVID-19 patients on days 7, 14, 21, respectively, and a significant positive correlation between VTEs and disease severity and mortality [6]. Another multicenter analysis noted a significant
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