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Measurement of von Willebrand factor activity: relative effects of ABO blood type and race
Author(s) -
Miller C. H.,
Haff E.,
Platt S. J.,
Rawlins P.,
Drews C. D.,
Dilley A. B.,
Evatt B.
Publication year - 2003
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1046/j.1538-7836.2003.00367.x
Subject(s) - von willebrand factor , abo blood group system , medicine , population , endocrinology , analysis of variance , platelet , environmental health
Summary. Tests based on three different principles are reported to measure the activity of von Willebrand factor (VWF): ristocetin cofactor (VWF:RCo), collagen binding (VWF:CB), and the so‐called ‘activity ELISA’ (VWF:MoAb). We measured these and other diagnostic parameters in a population of 123 randomly selected female study controls, age 18–45 years. Type O subjects had significantly lower levels than non‐O subjects in each test. Race differences were seen in all tests except VWF:RCo, with Caucasians having significantly lower levels than African‐Americans. ABO differences accounted for 19% of the total variance in VWF:Ag ( P < 0.0001) and race for 7% ( P < 0.0001), for a total of 26%. Both effects were mediated through VWF:Ag and were independent. VWF:Ag level was the primary determinant of VWF function, accounting for approximately 60% of the variance in VWF:RCo and VWF:CB and 54% of the variance in factor VIII. The ratio VWF:RCo/VWF:Ag differed significantly by race within blood group. The median ratios were 0.97 for type O Caucasians vs. 0.79 for type O African‐Americans and 0.94 for non‐O Caucasians vs. 0.76 for non‐O African‐Americans. The ratio VWF:CB/VWF:Ag did not vary. This suggests racial differences in the interaction of VWF with GP1b but not with subendothelium. Alternatively, VWF:RCo may be regulated to maintain a relatively constant plasma level in the presence of excessive VWF:Ag. This heterogeneity within the normal population is partially responsible for the difficulty in defining diagnostic limits for von Willebrand disease.