Cerebral Endothelial Injury in Elderly Patients With Severe Head Injury Measured by Serum Thrombomodulin and von Willebrand Factor

The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

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Vascular endothelial injury in mediterranean spotted fever assessed by circulating endothelial cells, plasma thrombomodulin and von willebrand factor measurements

Thrombosis Research ◽

10.1016/0049-3848(92)90738-v ◽

1992 ◽

Vol 65 ◽

pp. S213

Author(s):

F. George ◽

P. Brouqui ◽

M.C. Boffa ◽

M. Drancourt ◽

D. Raoult ◽

...

Keyword(s):

Endothelial Cells ◽

Von Willebrand Factor ◽

Spotted Fever ◽

Endothelial Injury ◽

Circulating Endothelial Cells ◽

Mediterranean Spotted Fever ◽

Vascular Endothelial ◽

Von Willebrand ◽

Willebrand Factor

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Demonstration of Rickettsia conorii-induced endothelial injury in vivo by measuring circulating endothelial cells, thrombomodulin, and von Willebrand factor in patients with Mediterranean spotted fever [see comments]

Blood ◽

10.1182/blood.v82.7.2109.2109 ◽

1993 ◽

Vol 82 (7) ◽

pp. 2109-2116 ◽

Cited By ~ 113

Author(s):

F George ◽

P Brouqui ◽

MC Boffa ◽

M Mutin ◽

M Drancourt ◽

...

Keyword(s):

Von Willebrand Factor ◽

Spotted Fever ◽

Clinical Manifestations ◽

Endothelial Injury ◽

Enzyme Linked Immunosorbent Assay ◽

Rickettsia Conorii ◽

Mediterranean Spotted Fever ◽

Von Willebrand ◽

Willebrand Factor

Abstract The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

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Correlation between Oxidized Low Density Lipoproteins and von Willebrand Factor in Chronic Renal Failure

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650639 ◽

1996 ◽

Vol 76 (05) ◽

pp. 663-669 ◽

Cited By ~ 122

Author(s):

Paul Holvoet ◽

Jan Donck ◽

Michèle Landeloos ◽

Els Brouwers ◽

Kristel Luijtens ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Von Willebrand Factor ◽

Wide Spectrum ◽

Endothelial Injury ◽

Maintenance Hemodialysis ◽

Apo B ◽

The Individual ◽

Von Willebrand ◽

Willebrand Factor

SummaryAn ELISA specific for a wide spectrum of oxidized apo B-100 in OxLDL was developed and applied to blood samples from 27 control subjects, 20 mild chronic renal failure (MCRF) patients, 21 severe chronic renal failure patients on conservative treatment (SCRF) and 56 severe chronic renal failure patients on maintenance hemodialysis (HEMO). Mean levels of OxLDL were 0.59 mg/dl in controls (95% Cl, 0.52-0.66 mg/dl), and were 2.7-fold (p <0.01), 3.1-fold (p <0.001) and 5.4-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Levels of von Willebrand factor, a marker of endothelial injury, were 100 percent in controls (95% Cl, 90-110 percent), and were 1.5-fold (p = NS), 1.6-fold (p <0.01) and 2.1-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Multiple regression analysis revealed that the extent of renal failure (F = 14; p = 0.0004) accounted for a significant fraction of the variation in OxLDL levels, also after exclusion of patients with evidence of ischemic atherosclerotic disease (F = 21; p = 0.0001). After adjustment for the extent of renal failure, hemodialysis (F = 5.6; p = 0.021) and LDL cholesterol levels (F = 7.1, p = 0.0095) contributed significantly to the variation in OxLDL levels. Whereas the extent of renal failure contributed only marginally to the individual variations in vWF levels (F = 4.1; p = 0.048), these levels correlated significantly with plasma levels of OxLDL (F=26; p=0.0001). In conclusion, atherogenic OxLDL increase progressively during the development of renal failure suggesting that the oxidation of LDL may be associated with endothelial injury and atherogenesis in these patients.

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Contribution of the von Willebrand Factor/ADAMTS13 Imbalance to COVID-19 Coagulopathy

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00204.2021 ◽

2021 ◽

Author(s):

Ryan Seth ◽

Thomas A. J. McKinnon ◽

X. Frank Zhang

Keyword(s):

Von Willebrand Factor ◽

Therapeutic Strategies ◽

Endothelial Injury ◽

System A ◽

High Incidence ◽

Prior Literature ◽

A Disintegrin And Metalloproteinase ◽

Von Willebrand ◽

Willebrand Factor

The 2019 coronavirus disease (COVID-19) is the disease caused by SARS-CoV-2 infection. While this infection has been shown to affect the respiratory system, a high incidence of thrombotic events has been observed in severe cases of COVID-19 and in a significant portion of COVID-19 non-survivors. While prior literature has reported on both the coagulopathy and hypercoagulability of COVID-19, the specifics of coagulation have not been fully investigated. Observations of microthrombosis in COVID-19 patients have brought attention to potential inflammatory endothelial injury. Von Willebrand factor (VWF) and its protease, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), play an important homeostatic role in responding to endothelial injury. This report provides an overview of the literature investigating the role the VWF/ADAMTS13 axis may have in COVID-19 thrombotic events and suggests potential therapeutic strategies to prevent the progression of coagulopathy in COVID-19 patients.

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