Ignite Creation Date:
2024-05-05 @ 11:22 AM
Last Modification Date:
2024-10-26 @ 9:05 AM
Study NCT ID:
NCT00005703
Status:
COMPLETED
Last Update Posted:
2016-05-13
First Post:
2000-05-25
Brief Title:
Hemostasis in Sickle Cell Disease--Infancy to Adulthood
Sponsor:
National Heart Lung and Blood Institute NHLBI
Organization:
National Heart Lung and Blood Institute NHLBI
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2005-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief 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
Detailed 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 ie 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 F12 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
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 ie 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 F12 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
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?:
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL055185 | NIH | None | httpsreporternihgovquickSearchR01HL055185 |