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Increased Factor VIII/von Willebrand Factor Antigen and von Willebrand Factor Activity in Scleroderma and in Raynaud's Phenomenon

M. BASHAR KAHALEH, M.D.; IRENE OSBORN, M.S.; and E. CARWILE LeROY, M.D.
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Grant support: by grant AM 20571 from the National Institutes of Health and grants from the RGK Foundation and the Charlotte and Sidney Lifschultz Foundation.

▸Requests for reprints should be addressed to M. Bashar Kahaleh, M.D.; Medical University of South Carolina, 171 Ashley Avenue; Charleston, SC 29403.


Charleston, South Carolina


Ann Intern Med. 1981;94(4_Part_1):482-484. doi:10.7326/0003-4819-94-4-482
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Von Willebrand factor activity and factor VIII/von Willebrand factor (fVIII/vWf) antigen concentrations were evaluated in 17 patients with scleroderma, nine patients with Raynaud's phenomenon, and eight control volunteers. Higher circulating levels of both activities were seen: von Willebrand factor, 374% ± 40% (percent of control values) in scleroderma patients, 502% ± 104% in patients with Raynaud's phenomenon and 102% ± 6% in control subjects (p < 0. 005, scleroderma versus control); fVIII/vWf antigen, 255% ± 24% in scleroderma patients; 271% ± 46% in patients with Raynaud's phenomenon, and 99% ± 4% in control subjects (p < 0.005, scleroderma versus control). Because endothelial cells synthesize and secrete both substances, the role of endothelial injury in vitro was investigated. Wound injury induced a 344% ± 33% increase in von Willebrand factor and a 115% ± 5% increases in fVIII/vWf antigen; cold injury induced 644% ± 66% and 150% ± 10% increases, and cytotoxic endothelial injury induced 1055% ± 83% and 185% ± 20% increases. In five patients with scleroderma, cold exposure led to a further increase in both activities. The observed increase of both activities in scleroderma and Raynaud's phenomenon may reflect in-vivo endothelial injury and regeneration in these related conditions.

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