&lt;p&gt;D-Dimer, Fibrinogen, and IL-6 in COVID-19 Patients with Suspected Venous Thromboembolism: A Narrative Review&lt;/p&gt;

Eljilany, Islam; Elzouki, Abdel‐Naser

doi:10.2147/vhrm.s280962

Cited by 115 publications

(120 citation statements)

References 38 publications

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“…To date, a wide spectrum of stimuli has been recognized as inducers of NET formation (Table 1). Direct exposure to microbial pathogens, both Gram-positive bacteria (Staphylococcus aureus, Staphylococcus suis, Streptococcus pyogenes, Streptococcus pneumoniae) [8][9][10] and Gram-negative bacteria (Escherichia coli, Salmonella enterica, Shigella flexneri, Pseudomonas aeruginosa), exposure to hyphae or yeast (Candida albicans), and exposure to protozoan parasites (Leishmania amazonensis or Trypanosoma cruzi) are able to induce NET generation [25][26][27]. Additionally, drugs such as statins and antibiotics can activate neutrophils to create NETs [19,28].…”

Section: Induction and Molecular Mechanisms Of Net Formationmentioning

confidence: 99%

“…It was previously reported that elevated levels of blood neutrophils are an early indicator of SARS-CoV-2 severe infection [4]. Moreover, the elevation of different coagulation parameters, such as D-dimers, prothrombin time (PT), fibrinogen, and fibrinogen degradation products (FDPs), has been observed in patients with COVID-19 [5][6][7][8][9][10]. The coagulation mechanism includes specific proteins that act as natural anticoagulants, thereby avoiding formation of clots.…”

Section: Introductionmentioning

confidence: 99%

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The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19

Iliadi

Konstantinidou

Aftzoglou

et al. 2021

IJMS

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Previous studies have shown that COVID-19 leads to thrombotic complications, which have been associated with high morbidity and mortality rates. Neutrophils are the largest population of white blood cells and play a pivotal role in innate immunity. During an infection, neutrophils migrate from circulation to the infection site, contributing to killing pathogens. This mechanism is regulated by chemokines such as IL-8. Moreover, it was shown that neutrophils play an important role in thromboinflammation. Through a diverse repertoire of mechanisms, neutrophils, apart from directly killing pathogens, are able to activate the formation of thrombi. In COVID-19 patients, neutrophil activation promotes neutrophil extracellular trap (NET) formation, platelet aggregation, and cell damage. Furthermore, neutrophils participate in the pathogenesis of endothelitis. Overall, this review summarizes recent progress in research on the pathogenesis of COVID-19, highlighting the role of the prothrombotic action of neutrophils in NET formation.

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Section: Induction and Molecular Mechanisms Of Net Formationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19

Iliadi

Konstantinidou

Aftzoglou

et al. 2021

IJMS

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“…Routine ocular fundus examination and ordering D-dimer assay in patients with COVID-19 presenting with PAMM is extremely crucial as prompt anticoagulation is mandated in these patients. 11 12 …”

Section: Descriptionmentioning

confidence: 99%

Paracentral acute middle maculopathy following SARS-CoV-2 infection: the D-dimer hypothesis

2021

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“…Another unusual feature of human COVID-19 is the widespread thrombosis of small and large vessels, contributing to morbidity and mortality [28][29][30] . It was also known that fibrinolysis was elevated in human COVID-19 due to systemic multiorgan thrombosis by SARS-CoV-2 infection [31,32]. The levels of fibrin degradation products, D-dimer and FDP, were elevated in the plasmas We next quantitated SARS-CoV-2 in the SH101 hamsters by quantitative RT-PCR after reverse transcription (RT-qPCR).…”

Section: P Roborovskii Sh101 Infected With Sars-cov-2 Progressed Similarly With Human Covid-19mentioning

confidence: 99%

Phodopus roborovskii SH101 as a systemic infection model of SARS-CoV-2

Zhai

Wang

Chung

et al. 2021

Preprint

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Severe acute respiratory syndrome CoV-2 (SARS-CoV-2) is currently causing a worldwide threat with its unusually high transmission rates and rapid evolution into diverse strains. Unlike typical respiratory viruses, SARS-CoV-2 frequently causes systemic infection by breaking the boundaries of the respiratory systems. The development of animal models recapitulating the clinical manifestations of COVID-19 is of utmost importance not only for the development of vaccines and antivirals but also for understanding the pathogenesis. However, there has not been developed an animal model for systemic infection of SARS-CoV-2 representing most aspects of the clinical manifestations of COVID-19 with systemic symptoms. Here we report that a hamster strain of Phodopus roborovskii SH101, a laboratory inbred hamster strain of P. roborovskii, displayed most symptoms of systemic infection upon SARS-CoV-2 infection as in the case of the human counterpart, unlike current COVID-19 animal models. P. roborovskii SH101 post-infection of SARS-CoV-2 represented most clinical symptoms of COVID-19 such as snuffling, dyspnea, cough, labored breathing, hunched posture, progressive weight loss, and ruffled fur, in addition to high fever following shaking chills. Histological examinations also revealed a serious right-predominated pneumonia as well as slight organ damages in the brain and liver, manifesting systemic COVID-19 cases. Considering the merit of a small animal as well as its clinical manifestations of SARS-CoV-2 infection in human, this hamster model seems to provide an ideal tool to investigate COVID-19.

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<p>D-Dimer, Fibrinogen, and IL-6 in COVID-19 Patients with Suspected Venous Thromboembolism: A Narrative Review</p>

Cited by 115 publications

References 38 publications

The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19

The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19

Paracentral acute middle maculopathy following SARS-CoV-2 infection: the D-dimer hypothesis

Phodopus roborovskii SH101 as a systemic infection model of SARS-CoV-2

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