&lt;strong&gt;&lt;/strong&gt;&lt;strong&gt;COVID-19 Clot: What Is It? Why in the Lungs? Extracellular Histone, “Auto-Activation” of Prothrombin, Emperipolesis, Megakaryocytes, “Self-Association” of Von Willebrand Factor and Beyond&lt;/strong&gt;

Varatharajah, Nadarajah

doi:10.20944/preprints202007.0516.v1

Cited by 4 publications

(3 citation statements)

References 91 publications

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“…Clotting activation may occur directly due to increased expression of Factor Xa and tissue factor as well as endothelial injury with the release of large aggregates of von Willebrand factor. 117 Furthermore, ACE-2 receptors are present on platelets and this may contribute to the massive platelet aggregation characteristic of severe COVID-19 disease. 35 , 118 , 119 Platelet activation contributes to the pro-thrombotic state and increases the inflammatory response.…”

Section: Platelet Activation and Increased Circulating Serotoninmentioning

confidence: 99%

A scoping review of the pathophysiology of COVID-19

Marik

Iglesias

Varon

et al. 2021

Int J Immunopathol Pharmacol

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COVID-19 is a highly heterogeneous and complex medical disorder; indeed, severe COVID-19 is probably amongst the most complex of medical conditions known to medical science. While enormous strides have been made in understanding the molecular pathways involved in patients infected with coronaviruses an overarching and comprehensive understanding of the pathogenesis of COVID-19 is lacking. Such an understanding is essential in the formulation of effective prophylactic and treatment strategies. Based on clinical, proteomic, and genomic studies as well as autopsy data severe COVID-19 disease can be considered to be the connection of three basic pathologic processes, namely a pulmonary macrophage activation syndrome with uncontrolled inflammation, a complement-mediated endothelialitis together with a procoagulant state with a thrombotic microangiopathy. In addition, platelet activation with the release of serotonin and the activation and degranulation of mast cells contributes to the hyper-inflammatory state. Auto-antibodies have been demonstrated in a large number of hospitalized patients which adds to the end-organ damage and pro-thrombotic state. This paper provides a clinical overview of the major pathogenetic mechanism leading to severe COVID-19 disease.

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Section: Platelet Activation and Increased Circulating Serotoninmentioning

confidence: 99%

A scoping review of the pathophysiology of COVID-19

Marik

Iglesias

Varon

et al. 2021

Int J Immunopathol Pharmacol

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“…In complicated COVID-19, pulmonary artery circulation carries blood with markedly lower oxygen content which in turn upregulates and activates VWF. As lungs are the “filter” of the pulmonary circulation, therefore VWF/platelet/NETs/fibrin strings excluded from the endothelial cells of the venous system results in pulmonary embolism [ 66 ]. A cohort study among COVID-19 patients suggest increased thrombotic tendency.…”

Section: Role Of Vwf In Covid-19 Associated Thrombo-inflammatory Complicationsmentioning

confidence: 99%

Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Choudhary

Sharma

Singh

2021

Chemico-Biological Interactions

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COVID-19 is an ongoing public health emergency that has affected millions of people worldwide and is still a threat to many more. One of the pathophysiological features of COVID-19 is associated with the activation of vascular endothelial cells (ECs) leading to the disruption of vascular integrity, coagulation and inflammation. An interlink mechanism between coagulation and inflammatory pathways has been reported in COVID-19. Multiple components are involved in these pathological pathways. Out of all, Von Willebrand Factor (VWF) is one of the primary components of coagulation pathway and also a mediator of vascular inflammation that plays an important role in thrombo-inflammation that further leads to acute respiratory distress syndrome (ARDS). The thrombo-inflammatory co-morbidities such as hyper-coagulation, thrombosis, ARDS etc. have become the major cause of mortality in the patients of COVID-19 admitted to the ICU. Thus, VWF can be explored as a potential target to manage COVID-19 associated co-morbidities. Supporting this hypothesis, there are literature reports which disclose previous attempts to target VWF for the management of thrombo-inflammation in other pathological conditions. The current report summarizes emerging insights into the pathophysiology, mechanism(s), diagnosis, management and foundations for research on this less explored clinically relevant glycoprotein as coagulation biomarker in COVID-19.

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“…Clotting activation may occur directly due to increased expression of Factor Xa as well as endothelial injury with the release of large aggregates of van Willebrand factor. [77] These blood clots impair blood flow. [134,135,[137][138][139][140][141][142][143][144][145]290,291,331,332] It should be noted that the thrombotic microangiopathy appears to target predominantly the pulmonary and cerebral circulation.…”

Section: Scientific Rationale For Math+ Treatment Protocol (Pulmonary Phase)mentioning

confidence: 99%

Summary of Contact With Dr. Marik. Pulmonary Medicine and Critical Care. Eastern Virginia Medical School - Usa.

Boni¹

2021

JLPPHS

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This brief note introduces the reproduction of medical content, authored by Doctor Paul E. Marik. Dr. Marik is Professor of Medicine and Chief of Pulmonary Medicine and Critical Care at Eastern Virginia Medical School in Norfolk, Virginia (USA). Dr. Marik is an extremely qualified and experienced professional. The reprinting of the material was authorized by Dr. Marik himself on 12/02/2020. This material is relevant in the Brazilian scenario due to standardized procedures for patients infected with the coronavirus. Only 1 of the 5 files kindly provided by the author, in PDF format, was selected and reproduced as received, without any editing. Due to the pandemic's long duration, the Journal editors (who are not medical doctors) have already had the opportunity to monitor the development of the disease in more than one infected person. The type of treatment offered to patients seems to influence the course, duration, and severity of the disease. The treatments described in the materials below appear to be effective and have good results. The editors will refrain from making additional comments on the proposed methods not to influence anyone, restricting themselves to suggesting that they be discussed with the reader's trusted doctor in case of need or doubts. Complete, updated information and also translated into Portuguese are available at . We are grateful to Dr. Marik for his kindness in giving us his time in this troubled period.

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<strong></strong><strong>COVID-19 Clot: What Is It? Why in the Lungs? Extracellular Histone, “Auto-Activation” of Prothrombin, Emperipolesis, Megakaryocytes, “Self-Association” of Von Willebrand Factor and Beyond</strong>

Cited by 4 publications

References 91 publications

A scoping review of the pathophysiology of COVID-19

A scoping review of the pathophysiology of COVID-19

Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Summary of Contact With Dr. Marik. Pulmonary Medicine and Critical Care. Eastern Virginia Medical School - Usa.

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