2018
DOI: 10.1371/journal.pone.0191902
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Plasma concentration of selected biochemical markers of endothelial dysfunction in women with various severity of chronic venous insufficiency (CVI)—A pilot study

Abstract: BackgroundAlthough the endothelial dysfunction is considered to be implicated in the pathogenesis of chronic venous insufficiency (CVI) the endothelial status in patients with venous disorders is still not fully evaluated. Therefore the aim of the study was to measure the concentration of selected markers of endothelial dysfunction: von Willebrand factor (vWf), soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM) and soluble VE-cadherin (sVE-cadherin) in CVI women who constitute the most numerous gro… Show more

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Cited by 15 publications
(6 citation statements)
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“…[20][21][22][23] Other inflammation-related markers, such as interleukin-6, ICAM-1 (intercellular adhesion molecule-1), VCAM1 (vascular cell adhesion molecule-1), E-selectin, P-selectin, and VWF (von Willebrand factor) have been used as markers for EC dysfunction. [23][24][25][26] Plasma levels of these markers can be increased in response to CVD risk factor exposure, [27][28][29] and higher E-and P-selectin levels were associated with impaired acetylcholine-dependent EC vasodilation in humans, 30 indicating that they can be linked to vascular changes beyond the inflammatory response. It remains unclear whether EC dysfunction is synonymous with, or limited to, inhibited vasoreactivity or inflammation-induced activation.…”
mentioning
confidence: 99%
“…[20][21][22][23] Other inflammation-related markers, such as interleukin-6, ICAM-1 (intercellular adhesion molecule-1), VCAM1 (vascular cell adhesion molecule-1), E-selectin, P-selectin, and VWF (von Willebrand factor) have been used as markers for EC dysfunction. [23][24][25][26] Plasma levels of these markers can be increased in response to CVD risk factor exposure, [27][28][29] and higher E-and P-selectin levels were associated with impaired acetylcholine-dependent EC vasodilation in humans, 30 indicating that they can be linked to vascular changes beyond the inflammatory response. It remains unclear whether EC dysfunction is synonymous with, or limited to, inhibited vasoreactivity or inflammation-induced activation.…”
mentioning
confidence: 99%
“…Although endothelial dysfunction is considered to be implicated in the pathogenesis of CVI, the number of studies assessing the endothelial status in patients with venous disease is limited. Budzyń et al measured the concentration of selected markers of endothelial dysfunction: von Willebrand factor (vWf), soluble P selectin (sPselectin), soluble thrombomodulin (sTM) and soluble VE cadherin (sVE-cadherin) in CVI women who constitute the most numerous group of patients suffering from venous disease (19). They showed the presence of endothelial dysfunction in patients with CVI and thought that it may be associated with inflammation and enhanced oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, cellular senescence could be involved in the pathophysiology of the chronic venous disease as it is generally associated with age-related disorders. 40 Inflammation and endothelial dysfunction are relevant too 41 as for example hsCRP (high sensitive c-reactive protein), vWF (von Willebrand factor), or D-Dimer blood values seem to be higher in varicose veins. 42 Especially endothelial senescence and its relation to vascular endothelial dysfunction could play a key role.…”
Section: Limitationsmentioning
confidence: 99%