The coagulopathy, endotheliopathy, and vasculitis of COVID-19
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Inflammation Research
REVIEW
The coagulopathy, endotheliopathy, and vasculitis of COVID‑19 Toshiaki Iba1 · Jean Marie Connors2 · Jerrold H. Levy3 Received: 27 June 2020 / Revised: 2 September 2020 / Accepted: 4 September 2020 © Springer Nature Switzerland AG 2020
Abstract Background COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy. Methods The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19. Results The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed. Conclusion The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease. Keywords COVID-19 · Thromboembolism · Coagulopathy · Endotheliopathy · Vasculitis
Introduction
Responsible Editor: John Di Battista. * Toshiaki Iba [email protected] Jean Marie Connors [email protected] Jerrold H. Levy [email protected] 1
Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, 2‑1‑1 Hongo Bunkyo‑ku, Tokyo 113‑8421, Japan
2
Hematology Division Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
3
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA
Ongoing reports have described the hypercoagulability and thrombotic tendency in COVID-19 [1]. The high incidence of deep vein thrombosis and pulmonary embolism has focused on the critical role of routine antithrombotic prophylaxis for COVID-19 management, especially in critically ill patients and
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