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Whole Blood Tissue Factor Procoagulant Activity Is Elevated in
Patients With Sickle Cell Disease
Nigel S. Key,
Arne Slungaard,
Luke Dandelet,
Stephen C. Nelson,
Christopher Moertel,
Lori A. Styles,
Frans A. Kuypers, and
Ronald
R. Bach
From the Department of Medicine, University of Minnesota Medical
School, Minneapolis, MN; Children's Health Care-Minneapolis, MN;
Children's Health Care-St Paul, MN; the Children's Hospital Oakland
Research Institute, Oakland, CA; and Research Service, Veterans'
Administration Hospital, Minneapolis, MN.
We developed a simple assay for the measurement of tissue factor
procoagulant activity (TF PCA) in whole blood samples that avoids the
need for mononuclear cell isolation. This method combines convenience
of sample collection and processing with a high degree of sensitivity
and specificity for TF. Using this method, we have determined that TF
PCA is detectable in whole blood samples from normal individuals, which
is itself a novel observation. Essentially all PCA could be shown to be
localized in the mononuclear cell fraction of blood. Compared with
controls, whole blood TF levels were significantly (P < .000001) elevated in patients with sickle cell disease (SCD),
regardless of the subtype of hemoglobinopathy (SS or SC disease). No
significant difference in TF PCA was observed between patients in pain
crisis compared with those in steady-state disease. Because TF
functions as cofactor in the proteolytic conversion of FVII to FVIIa in
vitro, it was expected that an increase in circulating TF PCA would
lead to an increased in vivo generation of FVIIa. On the contrary,
FVIIa levels were actually decreased in the plasma of patients with
SCD. Plasma TF pathway inhibitor (TFPI) antigen levels were normal in
SCD patients, suggesting that accelerated clearance of FVIIa by the
TFPI pathway was not responsible for the reduced FVIIa levels. We
propose that elevated levels of circulating TF PCA may play an
important role in triggering the activation of coagulation known to
occur in patients with SCD. Because TF is the principal cellular ligand
for FVIIa, it is possible that increased binding to TF accounts for the
diminished plasma FVIIa levels.
Blood, Vol. 91 No. 11 (June 1), 1998:
pp. 4216-4223
© 1998 by The American Society of Hematology.
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