scholarly journals The Association Between Vascular Inflammation and Depressive Disorder. Causality, Biomarkers and Targeted Treatment

2020 ◽  
Vol 13 (5) ◽  
pp. 92
Author(s):  
Hans O. Kalkman
Keyword(s):  
Depressive Disorder ◽  
Vascular Inflammation ◽  
High Plasma ◽  
Depression Symptoms ◽  
Reactive Protein ◽  
Symptoms Of Depression ◽  
Soluble Cell ◽  
Factor Α ◽  
Von Willebrand ◽  
Willebrand Factor

Diabetes, obesity, atherosclerosis, and myocardial infarction are frequently co-morbid with major depressive disorder. In the current review, it is argued that vascular inflammation is a factor that is common to all disorders and that an endothelial dysfunction of the blood-brain barrier could be involved in the induction of depression symptoms. Biomarkers for vascular inflammation include a high plasma level of C-reactive protein, soluble cell-adhesion molecules, von Willebrand factor, aldosterone, and proinflammatory cytokines like interleukin-6 or tumor necrosis factor α. A further possible biomarker is flow-mediated dilation of the brachial artery. Treatment of vascular inflammation is expected to prevent or to reduce symptoms of depression. Several tentative treatments for this form of depression can be envisioned: eicosapentaenoic acid (EPA), valproate, Vagus-nerve stimulation, nicotinic α7 agonists, and agonists of the cannabinoid CB2-receptor.

scholarly journals Endovascular plasty and vascular inflammation: their relationship and impact on development of restenosis of lower extremity arteries

2018 ◽  
Vol 16 (1) ◽  
pp. 51 ◽  
Author(s):  
A. A. Karpenko ◽  
G. I. Kostyuchenko ◽  
D. D. Arzamastsev
Keyword(s):  
Lower Extremity ◽  
Vascular Inflammation ◽  
Lower Extremities ◽  
High Sensitivity ◽  
Endothelial Damage ◽  
Iliac Arteries ◽  
Reactive Protein ◽  
Proinflammatory Mediators ◽  
Von Willebrand ◽  
Willebrand Factor

The baseline levels of proinflammatory mediators (high-sensitivity C-reactive protein, Interleukin-6) and markers of endothelial damage (endothelin-1, von Willebrand factor ) in the blood serum were measured in 128 patients with atherosclerosis of the lower extremities who had underwent balloon angioplasty. Hemodynamically significant restenosis in patients with lesions of the iliac arteries was observed in 34% of patients, with the postoperative loss of the lumen being equal to 58.34.29%, while in the group of patients with stenosis of the femoral and popliteal arteries it accounted for 46%, with the postoperative loss of the lumen reaching 65.25.14%. A direct correlation between the level of indicators of proinflammatory mediators, markers of endothelial damage and the degree of ischemia of the lower extremities was identified. Also determined were the predictors of restenosis formation after angioplasty of the lower extremity arteries. The level of CRP tended to exceed 10.1 mg/l, IL-6 was over 6.1 pg/ml and ET-1 was higher than 0.8 ng/ml.

Platelet Function and the Bleeding Time in Progressive Renal Failure

1988 ◽  
Vol 60 (01) ◽  
pp. 083-087 ◽  
Author(s):  
M P Gordge ◽  
R W Faint ◽  
P B Rylance ◽  
G H Neild
Keyword(s):  
Renal Failure ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Bleeding Time ◽  
C Reactive Protein ◽  
Severe Renal Failure ◽  
Reactive Protein ◽  
Thromboxane Production ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryBleeding time and platelet function tests were performed on 31 patients with progressive chronic renal failure (CRF) due to non-immunological (urological) causes, and compared with 22 healthy controls. Patients were classified as mild (plasma creatinine <300 μmol/l), moderate (300-600 μmol/l) or severe renal failure (>600 μmol/l). Bleeding time was rarely prolonged in mild and moderate CRF and mean bleeding time significantly elevated only in severe CRF (p <0.005). Haematocrit was the only index which correlated with bleeding time (r = -0.40). Platelet counts, collagen stimulated thromboxane generation, and platelet aggregation responses to ADP, collagen and ristocetin were all either normal or increased in all three CRF groups, but thromboxane production in clotting blood was reduced. Plasma fibrinogen, C reactive protein and von Willebrand factor (vWF) were elevated in proportion to CRF. We found no evidence that defects in platelet aggregation or platelet interaction with vWF prolong the bleeding time in patients with progressive CRF.

scholarly journals The Addition of C‐Reactive Protein and von Willebrand Factor to MELD‐Na Improves Prediction of Waitlist Mortality

Hepatology ◽  
2021 ◽  
Author(s):  
Patrick Starlinger ◽  
Joseph C. Ahn ◽  
Aidan Mullan ◽  
Georg P. Gyoeri ◽  
David Pereyra ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Waitlist Mortality

Combined effects of plasma von Willebrand factor and platelet measures on the risk of incident venous thromboembolism

Blood ◽  
2021 ◽  
Author(s):  
Magnus Sandvik Edvardsen ◽  
Ellen-Sofie Hansen ◽  
Kristian Hindberg ◽  
Vânia Maris Morelli ◽  
Thor Ueland ◽  
...  
Keyword(s):  
Platelet Count ◽  
Venous Thromboembolism ◽  
Von Willebrand Factor ◽  
Platelet Reactivity ◽  
High Plasma ◽  
Combined Effects ◽  
Exposure Group ◽  
Increased Risk ◽  
Von Willebrand ◽  
Willebrand Factor

Plasma von Willebrand factor (VWF) and platelet reactivity are both risk factors for venous thromboembolism (VTE), and VWF can promote hemostasis by interaction with platelets. In this study, we explored the combined effects of plasma VWF and platelet measures on the risk of incident VTE. A population-based nested case-control study with 403 cases and 816 controls was derived from the Tromsø Study. VWF, platelet count and mean platelet volume (MPV) were measured in blood samples drawn at baseline. Odds ratios (ORs) with 95% confidence intervals (CIs) for VTE were estimated across VWF tertiles, within predefined MPV (&lt;8.5, 8.5-9.5, ≥9.5 fL) and platelet count (&lt;230, 230-299, ≥300·109 L-1) strata. Here, participants with VWF levels in the highest tertile and MPV ≥9.5 fL had an OR of 1.98 (95% CI 1.17-3.36) for VTE compared with those in the lowest VWF tertile and with MPV &lt;8.5 fL in the age- and sex-adjusted model. In the joint exposure group, 48% (95% CI 15% to 96%) of VTEs were attributable to the biological interaction between VWF and MPV. Similarly, individuals with VWF in the highest tertile and platelet count ≥300·109 L-1 had an OR of 2.91 (95% CI 1.49-5.67) compared with those with VWF in the lowest tertile and platelet count &lt;230, and 39% (95% CI -2% to 97%) of VTEs in the joint exposure group were explained by the interaction. Our results suggest that both platelet reactivity and platelet count interact biologically with high plasma VWF, resulting in an increased risk of incident VTE.

scholarly journals Elevated antiviral, myeloid and endothelial inflammatory markers in severe COVID-19

2020 ◽  
Author(s):  
Ryan S Thwaites ◽  
Ashley Sanchez Sevilla Uruchurtu ◽  
Matthew Siggins ◽  
Felicity Liew ◽  
Clark D Russell ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cell Activation ◽  
Vascular Inflammation ◽  
Endothelial Cell Activation ◽  
Gm Csf ◽  
Cytokine Levels ◽  
Angiopoietin 2 ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Host Inflammatory Response

Introductory paragraphThe mechanisms that underpin COVID-19 disease severity, and determine the outcome of infection, are only beginning to be unraveled. The host inflammatory response contributes to lung injury, but circulating mediators levels fall below those in classical ‘cytokine storms’. We analyzed serial plasma samples from 619 patients hospitalized with COVID-19 recruited through the prospective multicenter ISARIC clinical characterization protocol U.K. study and 39 milder community cases not requiring hospitalization. Elevated levels of numerous mediators including angiopoietin-2, CXCL10, and GM-CSF were seen at recruitment in patients who later died. Markers of endothelial injury (angiopoietin-2 and von-Willebrand factor A2) were detected early in some patients, while inflammatory cytokines and markers of lung injury persisted for several weeks in fatal COVID-19 despite decreasing antiviral cytokine levels. Overall, markers of myeloid or endothelial cell activation were associated with severe, progressive, and fatal disease indicating a central role for innate immune activation and vascular inflammation in COVID-19.

Associations Between Diabetic Retinopathy and Plasma Levels of High-sensitive C-reactive Protein or Von Willebrand Factor in Long-term Type 1 Diabetic Patients

2012 ◽  
Vol 38 (1) ◽  
pp. 174-179 ◽  
Author(s):  
Jonas Vejvad Nørskov Laursen ◽  
Stine Skovbo Hoffmann ◽  
Anders Green ◽  
Mads Nybo ◽  
Anne Katrin Sjølie ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Diabetic Patients ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Von Willebrand ◽  
Type 1 Diabetic Patients ◽  
Willebrand Factor ◽  
Term Type

Association between beta2-glycoprotein I plasma levels and the risk of myocardial infarction in older men

Blood ◽  
2009 ◽  
Vol 114 (17) ◽  
pp. 3656-3661 ◽  
Author(s):  
Bas de Laat ◽  
Philip G. de Groot ◽  
Ronald H. W. M. Derksen ◽  
Rolf T. Urbanus ◽  
Koen Mertens ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Plasma Levels ◽  
High Plasma ◽  
In Vivo Experiments ◽  
Glycoprotein I ◽  
Adhesive Surface ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Dose Dependent

Abstract von Willebrand factor (VWF) serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2-glycoprotein I is able to inhibit platelet binding to VWF, indicating a role in the pathophysiology of arterial thrombosis. In the present study, we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. We have measured beta2-glycoprotein I and VWF antigen levels in 539 men with a first myocardial infarction and in 611 control subjects. Although we did not find a profound effect of beta2-glycoprotein I plasma levels on myocardial infarction in the overall population, we found a dose-dependent protective effect of increasing beta2-glycoprotein I plasma levels on myocardial infarction in men 60 years and older. In this age group, we found an odds ratio of 0.41 (95% confidence interval, 0.22-0.74) for high beta2-glycoprotein I levels compared with low levels. High plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of VWF. To conclude, high circulating levels of beta2-glycoprotein I appeared to be associated with a reduced risk of myocardial infarction in elderly men. In vivo experiments are needed to investigate the exact contribution of beta2-glycoprotein I on the pathophysiology of myocardial infarction.

scholarly journals von Willebrand Factor, C-Reactive Protein, and 5-Year Mortality in Diabetic and Nondiabetic Subjects

1999 ◽  
Vol 19 (12) ◽  
pp. 3071-3078 ◽  
Author(s):  
Agnes Jager ◽  
Victor W. M. van Hinsbergh ◽  
Piet J. Kostense ◽  
Jef J. Emeis ◽  
John S. Yudkin ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Factor C ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Platelet Glycoprotein Ibα Is a Counterreceptor for the Leukocyte Integrin Mac-1 (Cd11b/Cd18)

2000 ◽  
Vol 192 (2) ◽  
pp. 193-204 ◽  
Author(s):  
Daniel I. Simon ◽  
Zhiping Chen ◽  
Hui Xu ◽  
Chester Q. Li ◽  
Jing-fei Dong ◽  
...  
Keyword(s):  
Vascular Inflammation ◽  
Platelet Glycoprotein ◽  
Receptor Ligands ◽  
Monocytic Cells ◽  
A1 Domain ◽  
Von Willebrand ◽  
Flanking Regions ◽  
Inhibition Studies ◽  
Willebrand Factor ◽  
Deficient Mice

The firm adhesion and transplatelet migration of leukocytes on vascular thrombus are both dependent on the interaction of the leukocyte integrin, Mac-1, and a heretofore unknown platelet counterreceptor. Here, we identify the platelet counterreceptor as glycoprotein (GP) Ibα, a component of the GP Ib-IX-V complex, the platelet von Willebrand factor (vWf) receptor. THP-1 monocytic cells and transfected cells that express Mac-1 adhered to GP Ibα–coated wells. Inhibition studies with monoclonal antibodies or receptor ligands showed that the interaction involves the Mac-1 I domain (homologous to the vWf A1 domain), and the GP Ibα leucine-rich repeat and COOH-terminal flanking regions. The specificity of the interaction was confirmed by the finding that neutrophils from wild-type mice, but not from Mac-1–deficient mice, bound to purified GP Ibα and to adherent platelets, the latter adhesion being inhibited by pretreatment of the platelets with mocarhagin, a protease that specifically cleaves GP Ibα. Finally, immobilized GP Ibα supported the rolling and firm adhesion of THP-1 cells under conditions of flow. These observations provide a molecular target for disrupting leukocyte–platelet complexes that promote vascular inflammation in thrombosis, atherosclerosis, and angioplasty-related restenosis.

scholarly journals Endothelotropic Activity of 4-Hydroxy-3,5-Di-Tret-Butylcinnamic Acid in the Conditions of Experimental Cerebral Ischemia

2018 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Andrey Voronkov ◽  
Dmitry Pozdnyakov
Keyword(s):  
Cerebral Ischemia ◽  
Endothelial Function ◽  
Mitochondrial Function ◽  
No Synthase ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Anti Inflammatory ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Experimental Cerebral Ischemia

Introduction: The aim of the study was to evaluate the endothelioprotective activity of 4-hydroxy-3,5-di-tret-butylcinnamic acid in conditions of experimental cerebral ischemia. Materials and Methods: The brain ischemia was reproduced by the method of irreversible right-sided thermocoagulation of the middle cerebral artery. As comparative drugs, mexidol (30 mg/kg) and sulodexide (30 U/kg) were used. The vasodilating function of the vascular endothelium was assessed by the change in the rate of cerebral blood flow when the synthesis of nitric oxide was modified. Antithrombotic function was assessed by changes in the concentration of thromboxane A2, fibrinogen, von Willebrand factor activity and platelet aggregation activity. Serum concentration of C-reactive protein served as a marker of the state of anti-inflammatory endothelial function. To determine the potential mechanism of endothelioprotective activity of 4-4-hydroxy-3,5-di-tret-butylcinnamic acid, the anti-radical activity of this compound toward superoxide and nitrosy-radicals was assessed; and the effect of the compound on the mitochondrial function was studied, by evaluating the functional activity of mitochondrial ATP synthetase and cytochrome-c-oxidase by ELISA. Results and Discussion: In the course of the study, a positive effect of 4-hydroxy-3,5-di-tret-butylcinnamic acid on the state of endothelial function in cerebral ischemia was established, which was expressed in the preservation of vasodilating (restoring the vascular reaction to acetylcholine, nitro-L-arginine methyl ether, L-arginine), antithrombotic (a decrease in the concentration of thromboxane A2, fibrinogen and von Willebrand factor activity by 241.9% (p &lt;0.05), 73.5% (p &lt;0.05), 20.4% (p &lt;0.05), respectively, a decrease in the degree of aggregation and platelet aggregation rate by 56.7 % (p &lt;0.05) and 52.8% (p &lt;0.05), respectively, and anti-inflammatory vascular endothelial function (99.1% C-reactive protein reduction (p &lt;0.05)). The 4-hydroxy-3,5-di-tret-butylcinnamic acid compound in vitro tests suppressed generation of superoxide (IC50 = 1.99 mg/ml) and nitrosyl radical (IC50 = 1.92 mg/ml), eliminated NO-synthase uncoupling, and restored the mitochondrial function (increase in mitochondrial ATP synthase and cytochrome-c-oxidase activity by 23.5% (p &lt;0.05) and 110.8% (p &lt;0.05), respectively). Conclusion: The study demonstrated the presence of endotheliotropic activity of 4-hydroxy-3,5-di-tret-butylcinnamic acid, which is expressed in the preservation of vasodilating, antithrombotic and anti-inflammatory functions of the vascular endothelium in conditions of cerebral ischemia. At the same time, the anti-radical properties of this compound, as well as the direct effect on the functional activity of the NO-synthase system and the improvement of the mitochondrial function, may underlie the endotheliotropic effects of 4-hydroxy-3,5-di-tret-butylcinnamic acid.

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