Subscribe to RSS
Download PDF
DOI: 10.1055/a-1760-0445
The Burden of Hypercoagulability in COVID-19
Abstract
The novel coronavirus disease 2019 (COVID-19) infection has widespread impact on multiple organ systems, including damage to endothelial cells. Various studies have found evidence for direct mechanisms by which interaction between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and endothelial cells lead to extensive damage to the latter, and indirect mechanisms, such as excessively elevated cytokines, can also result in the same outcome. Damage to the endothelium results in release of thrombotic factors and inhibition of fibrinolysis. This confers a significant hypercoagulability burden on patients infected or recovering from COVID-19 infection. In this case report, the authors report the case of a gentleman presenting with extensive deep vein thrombosis and pulmonary embolism, in the context of recent COVID-19 infection. The postulated mechanisms and management are discussed.
Publication History
Received: 01 January 2022
Accepted: 20 January 2022
Accepted Manuscript online:
03 February 2022
Article published online:
29 April 2022
© 2022. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/).
Georg Thieme Verlag KG
Rüdigerstraße 14, 70469 Stuttgart, Germany
-
References
- 1
Kichloo A,
Dettloff K,
Aljadah M.
et al.
COVID-19 and hypercoagulability: a review. Clin Appl Thromb Hemost 2020; 26: 1076029620962853
MissingFormLabel
- 2 Nahum J, Morichau-Beauchant T, Daviaud F. et al. Venous thrombosis among critically ill patients with coronavirus disease 2019 (COVID-19). JAMA Netw Open 2020; 3 (05) e2010478
- 3 Middeldorp S, Coppens M, van Haaps TF. et al. Incidence of venous thromboembolism in hospitalized patients with COVID-19. J Thromb Haemost 2020; 18 (08) 1995-2002
- 4 Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost 2020; 18 (04) 844-847
- 5 Han H, Yang L, Liu R. et al. Prominent changes in blood coagulation of patients with SARS-CoV-2 infection. Clin Chem Lab Med 2020; 58 (07) 1116-1120
- 6 Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ. HLH Across Speciality Collaboration, UK. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet 2020; 395 (10229): 1033-1034
- 7 Sawdey MS, Loskutoff DJ. Regulation of murine type 1 plasminogen activator inhibitor gene expression in vivo. Tissue specificity and induction by lipopolysaccharide, tumor necrosis factor-alpha, and transforming growth factor-beta. J Clin Invest 1991; 88 (04) 1346-1353
- 8 Jose RJ, Manuel A. COVID-19 cytokine storm: the interplay between inflammation and coagulation. Lancet Respir Med 2020; 8 (06) e46-e47
- 9 Varga Z, Flammer AJ, Steiger P. et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet 2020; 395 (10234): 1417-1418
- 10 Leisman DE, Deutschman CS, Legrand M. Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation. Intensive Care Med 2020; 46 (06) 1105-1108
- 11 Xu P, Zhou Q, Xu J. Mechanism of thrombocytopenia in COVID-19 patients. Ann Hematol 2020; 99 (06) 1205-1208
- 12 Chen N, Zhou M, Dong X. et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395 (10223): 507-513
- 13 Hottz ED, Bozza FA, Bozza PT. Platelets in immune response to virus and immunopathology of viral infections. Front Med (Lausanne) 2018; 5: 121
- 14 Cameron SJ, Mix DS, Ture SK. et al. Hypoxia and ischemia promote a maladaptive platelet phenotype. Arterioscler Thromb Vasc Biol 2018; 38 (07) 1594-1606
- 15 Frangou E, Chrysanthopoulou A, Mitsios A. et al. REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A). Ann Rheum Dis 2019; 78 (02) 238-248
- 16 Pugh CW, Ratcliffe PJ. New horizons in hypoxia signaling pathways. Exp Cell Res 2017; 356 (02) 116-121
- 17 Zuo Y, Yalavarthi S, Shi H. et al. Neutrophil extracellular traps in COVID-19. JCI Insight 2020; 5 (11) 138999
- 18 Zhang S, Zhang J, Wang C. et al. COVID–19 and ischemic stroke: mechanisms of hypercoagulability (review). Int J Mol Med 2021; 47 (03) 21
- 19 Riedl M, Fakhouri F, Le Quintrec M. et al. Spectrum of complement-mediated thrombotic microangiopathies: pathogenetic insights identifying novel treatment approaches. Semin Thromb Hemost 2014; 40 (04) 444-464
- 20 Cugno M, Meroni PL, Gualtierotti R. et al. Complement activation in patients with COVID-19: a novel therapeutic target. J Allergy Clin Immunol 2020; 146 (01) 215-217