Comparison of the coagulopathies associated with COVID‐19 and sepsis

Campbell, Robert A.; Hisada, Yohei; Denorme, Frederik; Grover, Steven P.; Bouck, Emma G; Middleton, Elizabeth; Rondina, Matthew T.; Mackman, Nigel

doi:10.1002/rth2.12525

Cited by 49 publications

(56 citation statements)

References 26 publications

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“…Although TF is recognized as one of the main actors in the inflammatory response during sepsis ( 43 ), an increase in circulating TF has never been described outside the DIC context ( 44 ). However, an increase in extracellular vesicle TF activity has been shown in COVID-19 ( 13 , 45 ) and moreover, other viral diseases including human dengue infection and HIV are characterized by an increased soluble TF release ( 46 , 47 ). Altogether, these results indicate that coagulation abnormalities of COVID-19-associated coagulopathy promote a procoagulant state.…”

Section: Discussionmentioning

confidence: 99%

Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study

et al. 2022

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Critical COVID-19, like septic shock, is related to a dysregulated systemic inflammatory reaction and is associated with a high incidence of thrombosis and microthrombosis. Improving the understanding of the underlying pathophysiology of critical COVID-19 could help in finding new therapeutic targets already explored in the treatment of septic shock. The current study prospectively compared 48 patients with septic shock and 22 patients with critical COVID-19 regarding their clinical characteristics and outcomes, as well as key plasmatic soluble biomarkers of inflammation, coagulation, endothelial activation, platelet activation, and NETosis. Forty-eight patients with matched age, gender, and co-morbidities were used as controls. Critical COVID-19 patients exhibited less organ failure but a prolonged ICU length-of-stay due to a prolonged respiratory failure. Inflammatory reaction of critical COVID-19 was distinguished by very high levels of interleukin (IL)-1β and T lymphocyte activation (including IL-7 and CD40L), whereas septic shock displays higher levels of IL-6, IL-8, and a more significant elevation of myeloid response biomarkers, including Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) and IL-1ra. Subsequent inflammation-induced coagulopathy of COVID-19 also differed from sepsis-induced coagulopathy (SIC) and was characterized by a marked increase in soluble tissue factor (TF) but less platelets, antithrombin, and fibrinogen consumption, and less fibrinolysis alteration. In conclusion, COVID-19 inflammation-induced coagulopathy substantially differs from SIC. Modulating TF release and activity should be evaluated in critical COVID-19 patients.

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Section: Discussionmentioning

confidence: 99%

Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study

et al. 2022

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“…and another study found both TF and PAI-1 activity higher in COVID-19 patients than sepsis patients. 29 Thus, TF activity and inhibition of fibrinolytic activity could contribute to COVID-19-related thrombosis.…”

Section: Pulmonaryhistopathologyof Covid-19 and Non--covid-19 Ards Patients Including Characterization Of Cd61+ Platelet Thrombimentioning

confidence: 99%

Tissue factor upregulation is associated with SARS‐CoV‐2 in the lungs of COVID‐19 patients

Subrahmanian

Salvatore

Fung

et al. 2021

Journal of Thrombosis and Haemostasis

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Background: A substantial proportion of patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop severe/critical coronavirus disease 2019 (COVID-19) characterized by acute respiratory distress syndrome (ARDS) with thrombosis. Objectives:We tested the hypothesis that SARS-CoV-2--induced upregulation of tissue factor (TF) expression may be responsible for thrombus formation in COVID-19. Methods:We compared autopsy lung tissues from 11 patients with COVID-19-associated ARDS with samples from 6 patients with ARDS from other causes (non-COVID-19 ARDS) and 11 normal control lungs.Results: Dual RNA in situ hybridization for SARS-CoV-2 and TF identified sporadic clustered SARS-CoV-2 with prominent co-localization of SARS-CoV-2 and TF RNA.TF expression was 2-fold higher in COVID-19 than in non-COVID-19 ARDS lungs (P = .017) and correlated with the intensity of SARS-CoV-2 staining (R 2 = .36, P = .04).

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“…Moreover, EV‐TF activity was significantly higher in COVID‐19 than in sepsis. 36 , 118 Guervilly et al. 36 found a higher EV‐TF activity in severe compared with nonsevere (moderate) COVID‐19 and a TF activity of more than 78.3 fM associated with thromboembolic events.…”

Section: The Contribution Of Pevs To Covid‐19mentioning

confidence: 99%

“… 117 Indeed, elevated levels of TF activity associated with EVs have been reported in COVID‐19, which may directly contribute to excessive coagulation. 36 , 70 , 118 In addition, ACE2, the primary receptor for SARS‐CoV‐2 infection in humans, is important in the regulation of the renin–angiotensin–aldosterone system and a deficiency of ACE2 is linked to enhanced risk of inflammation and thrombosis. 98 As COVID‐19 is increasingly viewed as a thromboinflammatory disease, 32 it is conceivable that platelet activation in COVID‐19 may be a consequence of the inflammation, organ damage, and pathological activation of the coagulation cascade, rather than a consequence of direct virus–platelet interaction.…”

Section: What Triggers the Release Of Pevs In Covid‐19?mentioning

confidence: 99%

“…Given the high prevalence of thrombosis in COVID‐19, 30 , 31 , 32 TF activity associated with EVs and its involvement in COVID‐19 pathology is of high interest. 36 , 70 , 118 , 130 Several studies 36 , 70 , 118 , 131 report a significant increase in TF activity associated with EVs from COVID‐19 patients when compared with healthy controls. Moreover, EV‐TF activity was significantly higher in COVID‐19 than in sepsis.…”

Section: The Contribution Of Pevs To Covid‐19mentioning

confidence: 99%

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Platelet extracellular vesicles in COVID-19: Potential markers and makers

Puhm

Flamand

Boilard

2021

Journal of Leukocyte Biology

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Platelets and platelet extracellular vesicles (pEV) are at the crossroads of coagulation and immunity. Extracellular vesicles are messengers that not only transmit signals between cells, but also provide information about the status of their cell of origin. Thus, pEVs have potential as both biomarkers of platelet activation and contributors to pathology. Coronavirus Disease‐19 (COVID‐19), caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), is a complex disease affecting multiple organs and is characterized by a high degree of inflammation and risk of thrombosis in some patients. In this review, we introduce pEVs as valuable biomarkers in disease with a special focus on their potential as predictors of and contributors to COVID‐19.

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Comparison of the coagulopathies associated with COVID‐19 and sepsis

Abstract: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Cited by 49 publications

References 26 publications

Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study

Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study

Tissue factor upregulation is associated with SARS‐CoV‐2 in the lungs of COVID‐19 patients

Platelet extracellular vesicles in COVID-19: Potential markers and makers

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