Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT00005703 |
| Other study ID # |
4310 |
| Secondary ID |
R01HL055185 |
| Status |
Completed |
| Phase |
N/A
|
| First received |
May 25, 2000 |
| Last updated |
May 12, 2016 |
| Start date |
July 1995 |
| Est. completion date |
July 1998 |
Study information
| Verified date |
March 2005 |
| Source |
National Heart, Lung, and Blood Institute (NHLBI) |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
United States: Federal Government |
| Study type |
Observational
|
Clinical Trial Summary
To assess in older children and adults with sickle cell disease (SCD) whether intrinsic
activation (relevant to the origin of pain and acute inflammation) occurs only during
vasocclusive crisis (VOC).
Description:
BACKGROUND:
Investigations into hemostatic abnormalities associated with sickle cell disease have been
numerous. The data suggested that thrombin generation and fibrin formation were increased
during steady state, with conflicting data whether further activation occurred in
vaso-occlusive crisis. Platelet activation during VOC occurred, with variable findings
during steady state. A selective, concomitant evaluation of the hemostatic pathways i.e.
intrinsic, tissue factor (TF) or extrinsic activation, fibrinolysis, and
platelet-endothelial activation had not been reported. Neither had a longitudinal evaluation
been performed in infants during the unique transition period when HbF levels fall from 70
to 80 percent to less than 10 percent.
The study was part of an initiative on "Coagulation, Platelets and Thrombosis in Sickle
Disease Pathophysiology". The Request for Applications was released in October 1994.
DESIGN NARRATIVE:
The studies used appropriate 'negative' and 'positive' control groups. Studies included
intrinsic markers [kininogen profiling, high molecular weight kininogen (HK) and low
molecular weight kininogen (LK) cleavages, western blotting of HK and LK, and
kallikrein-alpha2 macroglobulin; extrinsic markers [TF and factor V11a]; other activation
and fibrinolytic markers [prothrombin F1.2, FPA, TAT, tPA, PAI-I, D-dimer and plasma alpha2
antiplasmin]; platelet- endothelial markers [evaluation of activation dependent epitopes].
Unequivocal demonstration of contact pathway activation during VOC provided a crucial link
between VOC and its accompanying phenomenon including pain, and inflammation. Finally, the
studies provided a unique perspective on the continuum of hemostatic changes that unfolded
during the course of SCD, and those that developed as vascular insufficiencies supervened in
the adult.
The study completion date listed in this record was obtained from the "End Date" entered in
the Protocol Registration and Results System (PRS) record.
