Decreased protein C activity, lower ADAMTS13 antigen and free protein S levels accompanied by unchanged thrombin generation potential in hospitalized COVID-19 patients

Wójcik, Krzysztof; Bazan-Socha, Stanisława; Celejewska-Wójcik, Natalia; Górka, Karolina; Lichołai, Sabina; Polok, Kamil; Stachura, Tomasz; Zaręba, Lech; Dziedzic, Radosław; Gradzikiewicz, Ada; Sanak, Marek; Musiał, Jacek; Sładek, Krzysztof; Iwaniec, Teresa

doi:10.1016/j.thromres.2023.01.016

Cited by 12 publications

(8 citation statements)

References 41 publications

(49 reference statements)

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“…We believe that increased concentrations of potent fibrinolysis inhibitors (α2AP and PAI-1) outweighed increased levels of tPA and shifted the balance towards hypofibrinolysis. [23,24] Finally, increased vWF:Ag, PAI-1and particularly high vWF:Ag/ADAMTS-13 ratio suggest significant endothelial dysfunction and significant deviations in the ADAMTS13-von Willebrand factor axis [15,[25][26][27]. Presented results corroborate previous reports in terms of observed abnormalities and confirm their association with severity of COVID-19.…”

Section: Discussionsupporting

confidence: 89%

The temporal changes of hemostatic activity in hospitalized patients with COVID-19: a prospective observational study

Polok¹,

Iwaniec²,

Stachura³

et al. 2023

Polish Archives of Internal Medicine

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This prospective observational study including 245 patients hospitalized due to COVID-19 confirms that the degree of hypercoagulability, hypofibrinolysis and endothelial dysfunction is associated with the requirement for more advanced respiratory support. These abnormalities are significantly attenuated within 28 days since the admission but inter-group differences persist in the most severely ill patients. This may suggest that endotheliopathy may play more important role in pathogenesis of COVID-19 than abnormalities in coagulation and fibrinolysis. There is not sufficient evidence to support statement that presence of antiphospholipid antibodies is related to severity of COVID-19. Analysis of temporal changes suggests an upward trend in their prevalence and concentration in a 28-day follow-up.

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Section: Discussionsupporting

confidence: 89%

The temporal changes of hemostatic activity in hospitalized patients with COVID-19: a prospective observational study

Polok¹,

Iwaniec²,

Stachura³

et al. 2023

Polish Archives of Internal Medicine

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“…Furthermore, SARS-CoV-2 activates the complement system, enhances platelet activation, and induces the release of procoagulant factors, while the intrinsic anticoagulant activity becomes suppressed [ 10 , 11 , 12 ]. Wójcik and colleagues reported that COVID-19 patients may have significantly lower protein C activity, decreased free protein S levels, and ADAMTS13 antigens, but increased von Willebrand Factor (vWF) and a higher prevalence of antiphospholipid antibodies, while their thrombin generation potential was similar to controls [ 13 ]. Contribution of these dysregulated pathways drive CAC and may lead to immunothrombosis and multiple organ dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Thromboelastometry-Guided Individualized Fibrinolytic Treatment for COVID-19-Associated Severe Coagulopathy Complicated by Portal Vein Thrombosis: A Case Report

Forgács,

Bokrétás,

Monori

et al. 2023

Biomedicines

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COVID-19-associated coagulopathy (CAC), mainly characterized by hypercoagulability leading to micro- and macrovascular thrombotic events due to the fibrinolysis shutdown phenomenon, is a life-threatening complication of severe SARS-CoV-2 infection. However, optimal criteria to assess patients with the highest risk for progression of severe CAC are still unclear. Bedside point-of-care viscoelastic testing (VET) appears to be a promising tool to recognize CAC, to support the appropriate therapeutic decisions, and to monitor the efficacy of the treatment. The ClotPro VET has the potential to reveal fibrinolysis resistance indicated by a clot lysis time (LT) > 300 s on the TPA-test. We present a case of severe SARS-CoV-2 infection complicated by CAC-resulting portal vein thrombosis (PVT) and subsequent liver failure despite therapeutic anticoagulation. Since fibrinolysis shutdown (LT > 755 s) caused PVT, we performed a targeted systemic fibrinolytic therapy. We monitored the efficacy of the treatment with repeated TPA assays every three hours, while the dose of recombinant plasminogen activator (rtPA) was adjusted until fibrinolysis shutdown completely resolved and portal vein patency was confirmed by an ultrasound examination. Our case report highlights the importance of VET-guided personalized therapeutic approach during the care of severely ill COVID-19 patients, in order to appropriately treat CAC.

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“…Chronic endothelial inflammation is associated with increased levels of procoagulant factors including factor VIII, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (vWF), thrombomodulin, ICAM-1, VCAM-1, P-selectin, and D-dimer [ 91 ]. Moreover, in COVID-19 patients, an acquired natural anticoagulant deficiency has been described.…”

Section: Endothelial Dysfunction In Covid-19 With Associated Metaboli...mentioning

confidence: 99%

“…Moreover, in COVID-19 patients, an acquired natural anticoagulant deficiency has been described. This condition consists of the decrease in protein C activity and free protein S and in a higher prevalence anticardiolipin IgM antibodies levels [ 91 ].…”

Section: Endothelial Dysfunction In Covid-19 With Associated Metaboli...mentioning

confidence: 99%

New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications

Gallo,

Savoia

2024

IJMS

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The endothelium is a monocellular layer covering the inner surface of blood vessels. It maintains vascular homeostasis regulating vascular tone and permeability and exerts anti-inflammatory, antioxidant, anti-proliferative, and anti-thrombotic functions. When the endothelium is exposed to detrimental stimuli including hyperglycemia, hyperlipidemia, and neurohormonal imbalance, different biological pathways are activated leading to oxidative stress, endothelial dysfunction, increased secretion of adipokines, cytokines, endothelin-1, and fibroblast growth factor, and reduced nitric oxide production, leading eventually to a loss of integrity. Endothelial dysfunction has emerged as a hallmark of dysmetabolic vascular impairment and contributes to detrimental effects on cardiac metabolism and diastolic dysfunction, and to the development of cardiovascular diseases including heart failure. Different biomarkers of endothelial dysfunction have been proposed to predict cardiovascular diseases in order to identify microvascular and macrovascular damage and the development of atherosclerosis, particularly in metabolic disorders. Endothelial dysfunction also plays an important role in the development of severe COVID-19 and cardiovascular complications in dysmetabolic patients after SARS-CoV-2 infection. In this review, we will discuss the biological mechanisms involved in endothelial dysregulation in the context of cardiometabolic diseases as well as the available and promising biomarkers of endothelial dysfunction in clinical practice.

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Decreased protein C activity, lower ADAMTS13 antigen and free protein S levels accompanied by unchanged thrombin generation potential in hospitalized COVID-19 patients

Cited by 12 publications

References 41 publications

The temporal changes of hemostatic activity in hospitalized patients with COVID-19: a prospective observational study

The temporal changes of hemostatic activity in hospitalized patients with COVID-19: a prospective observational study

Thromboelastometry-Guided Individualized Fibrinolytic Treatment for COVID-19-Associated Severe Coagulopathy Complicated by Portal Vein Thrombosis: A Case Report

New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications

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