Increased plasma von Willebrand factor in the systemic inflammatory response syndrome is derived from generalized endothelial cell activation

Abstract

We postulate that the increased plasma levels of vWf and the decreased staining in the peripheral dermal plexus represent the generalized activation and degranulation of endothelium in vascular beds remote from the original inflammatory focus.

Active von Willebrand factor predicts 28-day mortality in patients with systemic inflammatory response syndrome

“…As observed previously, 7 total VWF levels were increased fivefold in the entire patient cohort. However, in contrast to aVWF, total VWF failed to predict mortality.…”

“…5 Regarded as a gold marker of endothelial activation, 6 VWF levels were reported to be 11 times higher in patients with SIRS compared with controls and were postulated to reflect generalized endothelial activation. 7 High VWF levels were also found in patients with severe sepsis or septic shock when compared with healthy controls, where it was suggested that VWF might predict survival. 8 Nevertheless, the prognostic value of VWF in SIRS and sepsis patients remains controversial.…”

Biomarkers of endothelial dysfunction: can they help us deciphering systemic inflammation and sepsis?

“…However, these data demonstrated moderate sensitivity (87%) and specificity (77%) (Rubin et al 1990;Sadler 1998). McGill et al (1998) also demonstrated that vWF might be useful to serve as prognostic marker, predicting survival with a positive predictive value by 80%. Sensitivity was 80% and specificity was 87% (McGill et al 1998).…”

“…McGill et al (1998) also demonstrated that vWF might be useful to serve as prognostic marker, predicting survival with a positive predictive value by 80%. Sensitivity was 80% and specificity was 87% (McGill et al 1998). However, Moss et al (1996) could not verify these findings.…”

Increased levels of soluble adhesion molecules, E-selectin and P-selectin, in patients with infective endocarditis and embolic events

“…The inter-relationships between endothelial damage, alterations in platelet activation and the occurrence of embolic events have not been previously investigated in a large patient population with definite infective endocarditis. In previous reports, it was stated that infections, especially severe bacterial infections, change the prostacycline-thromboxane ratio in the direction of thrombosis and induce the production of cytokines, interleukin-1 and the tumour necrosis factor, which may lead to the activation of endothelial cells and increase blood coagulation and platelet aggregation [17,18] . Soluble forms of P-selectin have been shown to be secreted from activated platelets and endothelial cells [11,12,19] .…”