scholarly journals Von Willebrand Factor, Soluble P-Selectin, and Target Organ Damage in Hypertension

Hypertension ◽  
2002 ◽  
Vol 40 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Charles G.C. Spencer ◽  
David Gurney ◽  
Andrew D. Blann ◽  
D. Gareth Beevers ◽  
Gregory Y.H. Lip
Keyword(s):  
Von Willebrand Factor ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor

Soluble P-selectin, Thrombocytopenia and von Willebrand Factor in HIV Infected Patients

1997 ◽  
Vol 77 (06) ◽  
pp. 1221-1222 ◽  
Author(s):  
Andrew D Blann ◽  
Martine Seigneur ◽  
Joel Constans ◽  
Jean Luc Pellegrin ◽  
Claude Conri
Keyword(s):  
Von Willebrand Factor ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor

Multi-Cellular Activation In Vivo by Endotoxin in Humans – Limited Protection by Adenosine Infusion

2000 ◽  
Vol 84 (09) ◽  
pp. 381-387 ◽  
Author(s):  
Nailin Li ◽  
Anne Soop ◽  
Alf Sollevi ◽  
Paul Hjemdahl
Keyword(s):  
Von Willebrand Factor ◽  
Thrombin Generation ◽  
Platelet Reactivity ◽  
Adenosine Infusion ◽  
Cellular Activation ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

SummaryThe influence of adenosine infusion (40 µg/kg/min for 4 h) on inflammatory and hemostatic parameters was investigated in healthy males without (n = 10) or with (n = 11) intravenous endotoxin injection (4 ng/kg). Without endotoxin, adenosine elevated circulating leukocytes and circulating platelet-leukocyte aggregates. Endotoxin activated platelets and leukocytes in vivo. Platelet activation was seen as slightly increased platelet P-selectin expression, decreased platelet counts, and elevated plasma soluble P-selectin (from 39.6 ± 3.4 to 68.9 ± 6.6 ng/ml; P <0.01). Leukocyte activation was evidenced by increased CD11b expression (from MFI of 0.54 ± 0.02 to 2.21 ± 0.17; P <0.01) and plasma elastase levels (from 25.3 ± 2.5 to 169.3 ± 22.5 ng/ml; P <0.01). Endotoxin also enhanced platelet and leukocyte responsiveness to in vitro stimulation. Endotoxin induced von Willebrand factor secretion (from 92 ± 8 units to 265 ± 19 units at 4 h; P <0.001) and enhanced thrombin generation in vivo. Endotoxin induced leukocytosis and thus increased circulating platelet-leukocyte, mainly platelet-neutrophil, aggregates. Adenosine caused slight attenuation of platelet reactivity to agonist stimulation, enhanced the endotoxin-induced leukocytosis, and detained more platelet-leukocyte aggregates in circulation, but did not attenuate endotoxin-induced neutrophil elastase secretion, von Willebrand factor secretion, or thrombin generation. Thus, endotoxemia induces multi-cellular activation in vivo. Adenosine inhibits leukocyte adhesion and extravasation, and mildly attenuates platelet responsiveness and soluble P-selectin release. Adenosine has the potential of becoming a therapeutic antiinflammatory drug, but an optimal treatment strategy needs to be developed.

scholarly journals Cost effectiveness of caplacizumab in acquired thrombotic thrombocytopenic purpura

Blood ◽  
2020 ◽  
Author(s):  
George Goshua ◽  
Pranay Sinha ◽  
Jeanne Elise Hendrickson ◽  
Christopher A Tormey ◽  
Pavan Bendapudi ◽  
...  
Keyword(s):  
Cost Effectiveness ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Von Willebrand Factor ◽  
Organ Damage ◽  
Hospital Length Of Stay ◽  
Sensitivity Analyses ◽  
Thrombocytopenic Purpura ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Relapse Rates

Acquired thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease characterized by thrombotic microangiopathy leading to end-organ damage. The standard of care (SOC) treatment is therapeutic plasma exchange (TPE) alongside immunomodulation with steroids, with increasing use of rituximab +/- other immunomodulatory agents. The addition of caplacizumab, a nanobody targeting von Willebrand factor, was shown to accelerate platelet count recovery and reduce TPE treatments and hospital length of stay in TTP patients treated in the TITAN and HERCULES trials. The addition of caplacizumab to SOC also led to increased bleeding due to transient reductions in von Willebrand factor and increased relapse rates. Using data from TITAN and HERCULES on caplacizumab, we performed the first-ever cost effectiveness analysis in TTP. Over a 5-year period, the projected incremental cost effectiveness ratio (ICER) in our Markov model was $1,482,260, significantly above the accepted 2019 US willingness-to-pay of $195,300. One-way sensitivity analyses showed the utility of the well state and the cost of caplacizumab to have the largest effects on ICER, with a reduction in caplacizumab cost demonstrating the greatest impact on lowering the ICER. In a probabilistic sensitivity analysis, SOC was favored over caplacizumab in 100% of 10,000 iterations. Our data indicate that the addition of caplacizumab to SOC in treatment of acquired TTP is not cost effective due to the high cost of the medication and its failure to improve relapse rates. The potential impact of caplacizumab on health system cost using longer-term follow-up data merits further study.

von Willebrand Factor, Soluble P-Selectin, Tissue Plasminogen Activator and Plasminogen Activator Inhibitor in Atherosclerosis

1995 ◽  
Vol 74 (02) ◽  
pp. 626-630 ◽  
Author(s):  
A D Blann ◽  
M Dobrotova ◽  
P Kubisz ◽  
C N McCollum
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor ◽  
Pai 1

SummaryTissue plasminogen activator antigen (tPA), plasminogen activator inhibitor antigen (PAI-1), soluble P-selectin and von Willebrand factor antigen (vWf) were measured by ELISA in 41 patients with peripheral vascular disease (PVD), 41 with ischaemic heart disease (IHD) and in 46 age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0002) and in patients with PVD (p = 0.0011) relative to the controls but levels did not differ between the two patients groups. Raised tPA found in both PVD (p = 0.0006) and IHD (p = 0.0061) compared to the controls also failed to differentiate the two groups of patients. Soluble P-selectin was also raised in both groups (p = 0.003 in IHD and p = 0.0102 in PVD) with no difference between the groups. There were no differences in levels of PAI-1 between the groups. In the subjects taken as a whole, there were significant Spearman’s correlations between tPA and vWf (r = 0.37, p <0.001), tPA and triglycerides (r = 0.38, p <0.001), tPA and P-selectin (r = 0.19, p = 0.032), vWf and age (r = 0.25, p = 0.005) and inversely between vWf and HDL (r = -0.25, p = 0.006). These data support the concept that increased levels of tPA may be important in atherosclerosis, and indicate that soluble P-selectin may be useful in further analysis of the role of platelets and the endothelial cell in this disease.

Repeated Exercise Induces Release of Soluble P-Selectin in Patients with Intermittent Claudication

1997 ◽  
Vol 78 (05) ◽  
pp. 1338-1342 ◽  
Author(s):  
U J Kirkpatrick ◽  
M Mossa ◽  
A D Blann ◽  
C N McCollum
Keyword(s):  
Intermittent Claudication ◽  
Von Willebrand Factor ◽  
Statistical Significance ◽  
Ischaemia Reperfusion Injury ◽  
Biochemical Effect ◽  
Control Subjects ◽  
Repeated Exercise ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryControversy exists as to whether exercise in patients with intermittent claudication causes a harmful biochemical effect associated with an ischaemia-reperfusion injury of skeletal muscle. We report on exercise-induced changes in neutrophil activation, soluble P-selectin and von Willebrand factor in 34 patients with intermittent claudication and 12 matched controls.Von Willebrand factor (vWF) showed a cyclical pattern of response to exercise in control subjects (rising from 103 ± 8 to 119 ± 7 U/dl); claudicants did not show this pattern but had higher levels of vWF throughout (p <0.03). There was no consistent pattern of response in neutrophil hydrogen peroxide production to exercise in either claudicants or control subjects. Soluble P-selectin levels increased after exercise, but this only reached statistical significance after repeated exercise in claudicants (rising from 320 ± 28 to 357 ± 28 ng/ml). This rise in soluble P-selectin after exercise may indicate progressive platelet activation which may contribute to the excess cardiovascular mortality that claudicants are prone to.

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