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Coagulopathy in coronavirus disease 2019 (COVID-19) displays unusually. Not only do patients display impaired fibrinolysis, but also platelet aggregation, inflammation, and microthrombi. Understanding this pathology could help healthcare workers treat these symptoms, often associated with low survival levels in severe COVID-19 patients.

Study: Plasma biomarkers associated with survival and thrombosis in hospitalized COVID-19 patients. Image Credit: bangoland/ Shutterstock

A group of researchers from Columbia University has observed the mechanisms of hypercoagulability in COVID-19, finding a significant increase in fibrin-mediated clot viscosity, but no mechanism behind this observation. To further explore this phenomenon, scientists have investigated the presence of specific biomarkers in hospitalized COVID-19 patients.

A preprint version of the study is available on the medRxiv* server while the article undergoes peer review.

The study

The study included 63 patients showing positive PCR test results for COVID-19 and 43 healthy/non-infected individuals as controls. Forty-seven of the infected group had progressed to severe COVID-19, danger lipitor requiring admission to the ICU and showing symptoms such as shock, respiratory distress, and multiorgan dysfunction. Forty-six of these individuals were mechanically ventilated. The remaining patients were hospitalized, but not severe, although one did require mechanical ventilation. Blood was drawn from all individuals within five days of a PCR test and rapidly centrifuged before the plasma was separated and stored at -80C until analysis.

The analysis consisted of commercially available ELISA kits with colorimetric output, which were used to determine plasma concentrations of several potential biomarkers, including PAL-1, fibrinogen, plasminogen, tissue plasminogen activator (t-PA), platelet factor 4 (PF4), interleukin (IL), 1 receptor-like 1 (ST2) (the receptor for interleukin-33), von Willebrand factor (vWF) and tryptase. To compare the results of the control groups and infected groups, the scientists used Fisher's test, Mann-Whitney tests, or Kruskal-Wallis tests.

Most coagulation and fibrinolysis markers showed increased levels in COVID-19 patients. Fibrinogen levels were significantly higher in both COVID-19 groups compared to the control, as were t-PA levels – which were also significantly higher in ICU patients compared to non-ICU patients. Fibrinogen was also higher than normal clinical ranges. PAI-1 levels were also elevated in ICU COVID-19 patients. Plasminogen levels showed no difference between COVID-19 and control groups.

ST2 levels were higher in COVID-19 patients, as were vWF levels. PF4 levels showed no difference, and tryptase was lower in the ICU COVID-19 group than the controls. vWF tends to show higher levels as endothelial damage and platelet adhesion increases, and PF4 rises with platelet activity. The higher levels of vWF with no matching increase in PF4 indicates more endothelial damage in ICU patients – which is supported by previous studies showing abortive infection of endothelial cells by SARS-CoV-2 leads to increased inflammation.

The researchers followed this by exploring associations between some of these biomarkers and clinical outcomes. They found that higher levels of vWF were associated with thrombotic episodes, often in ICU patients, as well as lower odds of survival. t-PA and ST2 were also associated with an increased risk of death. Patients diagnosed with acute kidney injury upon admission showed higher levels of t-PA and PAI-1.


The authors highlight the value of their results in helping explain the distinctive pathophysiology of coagulopathy in severe COVID-19 patients. Increased levels of fibrinogen and D-dimer, alongside a lack of plasminogen, likely reflect the increase of fibrinogen synthesis in response to inflammation. PAI-1 inhibits the fibrinolytic system, and higher levels were seen in the infected groups. These results support previous studies' proposals of a characteristic 'fibrinolysis shutdown,' seen only in severe COVID-19 patients, partially caused by the underproduction of plasmin.

While t-PA does convert plasminogen into plasmin, high levels of t-PA were associated with non-survival. This is likely due to the association of t-PA with rare cases of bleeding in COVID-19 patients. ST2 is acted on by IL-33, which is known to play a key role in cytokine storm syndrome reported in some of the most severe COVID-19 cases. Higher concentrations of ST2 associated with increased risk of mortality likely result from this, as well as endothelial or pneumocyte inflammation and damage. These are some of the greatest risks to COVID-19 patients and indicates ST2 would make a good biomarker for use in determining prognosis.

The high level of vWF in COVID-19 patients confirms the association between inflammation and endothelial injury and could lead to an increased risk of microthrombi. Again associated with an increased risk of mortality, vWF may be part of an endothelial inflammatory response. PF4 and tryptase did not show increased levels in COVID-19 patients. PF4 is likely not involved in the pathophysiology of COVID-19. Still, the researchers do not discount the possibility that tryptase could have degraded when the samples were taken, as it has a very short half-life. These results could prove valuable for researchers investigating the path of the disease and could help healthcare workers determine prognosis in individuals, potentially allowing them to be treated before the worst symptoms present themselves.

*Important notice

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Journal reference:
  • Cabrera-Garcia, D. et al., (2021) Plasma biomarkers associated with survival and thrombosis in hospitalized COVID-19 patients. medRxiv. doi:

Posted in: Medical Science News | Medical Research News | Disease/Infection News

Tags: Acute Kidney Injury, Biomarker, Bleeding, Blood, Coronavirus, Coronavirus Disease COVID-19, Cytokine, D-dimer, Fibrinolysis, Healthcare, Inflammation, Interleukin, Kidney, Mortality, Pathology, Pathophysiology, Platelet, Receptor, Respiratory, SARS, SARS-CoV-2, Syndrome

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Written by

Sam Hancock

Sam completed his MSci in Genetics at the University of Nottingham in 2019, fuelled initially by an interest in genetic ageing. As part of his degree, he also investigated the role of rnh genes in originless replication in archaea.

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