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Blood, Vol. 94 No. 1 (July 1), 1999:
pp. 179-185
von Willebrand Factor Propeptide in Vascular Disorders: A Tool to
Distinguish Between Acute and Chronic Endothelial Cell Perturbation
Jan A. van Mourik,
Ria Boertjes,
Inge A. Huisveld,
Karin Fijnvandraat,
Dasja Pajkrt,
Perry J.J. van Genderen, and
Rob Fijnheer
From the CLB, Sanquin Blood Supply
Foundation; the Department of Medical Physiology and Sports Medicine,
University of Utrecht, Utrecht; University of Amsterdam, Emma
Children's Hospital Academic Medical Center, the
Departments of Pediatrics and Experimental Internal Medicine,
Amsterdam; the Department of Hematology, University Hospital Dijkzigt,
Rotterdam; and the Department of Hematology, University Hospital
Utrecht, Utrecht, The Netherlands.
Before de novo synthesized von Willebrand factor (vWF) leaves the
endothelial cell, it undergoes endoproteolytic cleavage of its
propeptide (vW antigen II). The processed vWF and propeptide are either
released constitutively or, following activation of the endothelium,
released through the regulated pathway. In a recent study (Borchiellini
et al, Blood 88:2951, 1996), we showed that the half-life of
mature vWF and of its propeptide differ fourfold to fivefold. We
postulated that the molar ratio of the propeptide to mature vWF could
serve as a tool to assess the extent of endothelial cell activation
under physiologic and clinical conditions. To test this hypothesis, we
measured mature vWF and propeptide in patients with documented acute
and chronic vascular disease, including patients with thrombotic
thrombocytopenic purpura (TTP), acute septicemia, and diabetes
mellitus. These data were compared with experimental conditions in
healthy subjects in which perturbation of the endothelium was simulated
by physical exercise or by administration of
1-deamino-8-D-arginine vasopressin (DDAVP) or endotoxin. In
all individuals of the latter study group, both vWF and propeptide
levels were elevated during the acute phase of the experimentally
induced vascular perturbation; at later time points after stimulation,
only vWF levels remained elevated. In patients with sepsis and TTP,
both vWF and propeptide were elevated several-fold. Thus, this pattern
can readily be explained in terms of acute perturbation of the
endothelium. In contrast, in patients with diabetes mellitus propeptide
levels were only slightly elevated, whereas vWF levels were elevated
twofold to threefold. This pattern is a typical feature of chronic,
low-grade activation of the endothelium. These observations support our hypothesis that measurement of both propeptide and vWF levels allows to
discriminate between chronic and acute phases of endothelial cell
activation in vivo. Measurement of only vWF is less indicative in this respect.
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