Elevated Levels of Markers of Endothelial Cell Damage and Markers of Activated Coagulation in Patients with Systemic Necrotizing Vasculitis

1996 ◽  
Vol 75 (06) ◽  
pp. 892-898 ◽  
Author(s):  
Olaf Hergesell ◽  
Konard Andrassy ◽  
Peter Nawroth
Keyword(s):  
Endothelial Cell ◽  
Disease Activity ◽  
Antithrombin Iii ◽  
Cell Damage ◽  
Specific Treatment ◽  
Close Correlation ◽  
Small Vessel Vasculitis ◽  
Endothelial Cell Damage ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryActivation of coagulation and endothelial cell damage was studied in 47 patients with small vessel vasculitis [Wegener’s granulomatosis (WG) and microscopic polyangiitis (MP)] by measurement of throm-bin-antithrombin III complexes (TAT), fibrin-D-dimers (D-dimers), von Willebrand-factor (vWF) concentration and plasma thrombomodulin (TM) levels. There was a close correlation between disease activity (DA) in patients with WG or MP and markers of endothelial cell damage (correlation TM/DA r = 0.46 for WG and r = 0.43 for MP) and activated coagulation (correlation TAT/DA r = 0.58 for WG and r = 0.55 for MP).Elevation of the markers of activated haemostasis and endothelial cell damage was reversed when remission was obtained by specific treatment. The markers studied were particularly helpful in cases where measurement of antineutrophil cytoplasmatic antibodies (ANCA) did fail to assess disease activity.

Effects on Coagulation and Fibrinolysis of Desmopressin in Patients Undergoing Total Hip Replacement

1991 ◽  
Vol 66 (06) ◽  
pp. 652-656 ◽  
Author(s):  
Per Anders Flordal ◽  
Karl-Gösta Ljungström ◽  
Jan Svensson ◽  
Brenda Ekman ◽  
Gustaf Neander
Keyword(s):  
Total Hip Replacement ◽  
Hip Replacement ◽  
Bleeding Time ◽  
Antithrombin Iii ◽  
Postoperative Bleeding ◽  
Double Blind ◽  
Total Hip ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Coagulation And Fibrinolysis

SummaryTwelve patients undergoing total hip replacement, with regional anaesthesia and with dextran infusion for plasma expansion and thromboprophylaxis, were given the vasopressin analogue desmopressin (DDAVP) or placebo in a randomized, double-blind prospective study. In controls (n = 6) we found a prolongation of the bleeding time, low factor VIII (FVIII) and von Willebrand factor (vWF) and a decrease in antithrombin III to levels known to be at risk for venous thrombosis. Desmopressin shortened postoperative bleeding time, gave an early FVIII/vWF complex increase, prevented antithrombin III from falling to critically low values and appeared to activate the fibrinolytic system, both by tPA increase and PAI-1 decrease.Thus in the controls we found changes in both coagulation and fibrinolysis indicating a haemorrhagic diathesis as well as a risk for thromboembolism. Desmopressin induced factor changes that possibly reduce both risks.

Glycoprotein Ib Can Mediate Endothelial Cell Attachment to a von Willebrand Factor Substratum

1995 ◽  
Vol 73 (02) ◽  
pp. 309-317 ◽  
Author(s):  
Dorothy A Beacham ◽  
Miguel A Cruz ◽  
Robert I Handin
Keyword(s):  
Endothelial Cell ◽  
Von Willebrand Factor ◽  
Cell Attachment ◽  
Umbilical Vein ◽  
Single Amino Acid ◽  
Cell Surface Expression ◽  
Platelet Glycoprotein ◽  
Glycoprotein Ib ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryIntroduction of single amino acid substitutions into the C-terminal Arg-Gly-Asp-Ser (RGDS) site of von Willebrand Factor, referred to as RGD mutant vWF, selectively abrogated vWF binding to platelet glycoprotein IIb/IIIa (GpIIb/IIIa, αIIbβ3 and abolished human umbilical vein endothelial cell (HUVEC) spreading, but not attachment, to RGD mutant vWF (Beacham, D. A., Wise, R. J., Turci, S. M. and Handin, R. I. 1992. J. Biol. Chem. 167, 3409-3415). These results suggested that in addition to the vitronectin receptor (VNR, αvβ3), a second endothelial membrane glycoprotein can mediate HUVEC adhesion to vWF. HUVEC attachment to wild-type (WT) and RGD-mutant vWF was reduced by two proteins known to block the vWF-platelet glycoprotein Ib/IX (GpIb/IX) interaction, the monoclonal antibody AS-7 and the recombinant polypeptide, vWF-A1. The addition of cytochalasin B or DNase I to disrupt potential GPIbα-cytoskeletal interactions enhanced the immunoprecipitation of endothelial GPIbα, caused HUVEC to round up, and increased HUVEC adhesion to RGD mutant vWF. These results indicate that while the VNR is the primary adhesion receptor for vWF, endothelial GPIbα can mediate HUVEC attachment to vWF. GpIb-dependent attachment could contribute to HUVEC adhesion under conditions when cell surface expression of the VNR is downregulated, and VNR-dependent adhesion is reduced.

scholarly journals Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein

2021 ◽  
Vol 51 ◽  
pp. 151682
Author(s):  
Gerard J. Nuovo ◽  
Cynthia Magro ◽  
Toni Shaffer ◽  
Hamdy Awad ◽  
David Suster ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Mouse Model ◽  
Cell Damage ◽  
Spike Protein ◽  
Endothelial Cell Damage
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