?FIBRINOGEN G-455-A GENE POLYMORPHISM: IS IT A FACTOR FOR ASPIRIN PLATELET INSENSIVITY IN PATIENTS WITH POLYCYTHEMIA VERA?
(Abstract release date: 05/19/16)
EHA Library. Cacciola R. 06/09/16; 134926; PB2026
Prof. Rossella Cacciola
Contributions
Contributions
Abstract
Abstract: PB2026
Type: Publication Only
Background
Polycythemia vera (PV) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. According to PVSG, the antithrombotic therapy includes low dose ASA. However, there are insensivity ASA PV patients. It is debated if inherited thrombophilia increases the polycythemic platelet activation and, hence, the ASA platelet insensivity.
Aims
Therefore, we evaluated βFibrinogen G-455-A gene polymorphism, as thrombophilic molecular mutation associated with increased platelet aggregation, platelet count, hematocrit (HCT), β-thromboglobulin (β-TG) and platelet factor 4 (PF4) as markers of platelet activation, fibrinogen (Fg), Platelet functional activity (PFA) as indicator of ASA platelet sensitivity and clot formation time (CFT), as indicator of aspirinated platelets contribution to clot firmness. We studied 40 patients (28 men, 12 women; mean age 64 years, range 35_85 years) with PV according to WHO criteria. Fifty subjects served as controls.
Methods
The mean duration of disease was 9 years. All patients were on phlebotomy and ASA (100 mg once day). The βFibrinogen G-455-A genotype was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets and HCT were measured by automated analyzer. βTG and PF4 were determined by ELISA. PFA and CFT were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
All patients had heterozygous βFibrinogen G-455-A. The mean platelet and mean HCT value were 428±180 x109/L and 47±3%. All patients had normal Fg (244±47mg/dl), high β-TG and PF4 (133±47 IU/ml vs 20±11 IU(ml and 45±21 IU/ml vs 6±2 IU7ml, respectively) (p<.0001 and p<.001, respectively), prolonged C/EPI closure time (CT, units: s, n.v. 84-160 s) (252±48 s) and normal CFT (CFT, units: s, n.v. 30-110 s) ( 50±7 s).
Conclusion
These findings suggest that βFibrinogen G-455-A gene polymorphism is not associated with ASA platelet insensitivity in patients with polycythemia vera.
Session topic: E-poster
Type: Publication Only
Background
Polycythemia vera (PV) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. According to PVSG, the antithrombotic therapy includes low dose ASA. However, there are insensivity ASA PV patients. It is debated if inherited thrombophilia increases the polycythemic platelet activation and, hence, the ASA platelet insensivity.
Aims
Therefore, we evaluated βFibrinogen G-455-A gene polymorphism, as thrombophilic molecular mutation associated with increased platelet aggregation, platelet count, hematocrit (HCT), β-thromboglobulin (β-TG) and platelet factor 4 (PF4) as markers of platelet activation, fibrinogen (Fg), Platelet functional activity (PFA) as indicator of ASA platelet sensitivity and clot formation time (CFT), as indicator of aspirinated platelets contribution to clot firmness. We studied 40 patients (28 men, 12 women; mean age 64 years, range 35_85 years) with PV according to WHO criteria. Fifty subjects served as controls.
Methods
The mean duration of disease was 9 years. All patients were on phlebotomy and ASA (100 mg once day). The βFibrinogen G-455-A genotype was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets and HCT were measured by automated analyzer. βTG and PF4 were determined by ELISA. PFA and CFT were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
All patients had heterozygous βFibrinogen G-455-A. The mean platelet and mean HCT value were 428±180 x109/L and 47±3%. All patients had normal Fg (244±47mg/dl), high β-TG and PF4 (133±47 IU/ml vs 20±11 IU(ml and 45±21 IU/ml vs 6±2 IU7ml, respectively) (p<.0001 and p<.001, respectively), prolonged C/EPI closure time (CT, units: s, n.v. 84-160 s) (252±48 s) and normal CFT (CFT, units: s, n.v. 30-110 s) ( 50±7 s).
Conclusion
These findings suggest that βFibrinogen G-455-A gene polymorphism is not associated with ASA platelet insensitivity in patients with polycythemia vera.
Session topic: E-poster
Abstract: PB2026
Type: Publication Only
Background
Polycythemia vera (PV) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. According to PVSG, the antithrombotic therapy includes low dose ASA. However, there are insensivity ASA PV patients. It is debated if inherited thrombophilia increases the polycythemic platelet activation and, hence, the ASA platelet insensivity.
Aims
Therefore, we evaluated βFibrinogen G-455-A gene polymorphism, as thrombophilic molecular mutation associated with increased platelet aggregation, platelet count, hematocrit (HCT), β-thromboglobulin (β-TG) and platelet factor 4 (PF4) as markers of platelet activation, fibrinogen (Fg), Platelet functional activity (PFA) as indicator of ASA platelet sensitivity and clot formation time (CFT), as indicator of aspirinated platelets contribution to clot firmness. We studied 40 patients (28 men, 12 women; mean age 64 years, range 35_85 years) with PV according to WHO criteria. Fifty subjects served as controls.
Methods
The mean duration of disease was 9 years. All patients were on phlebotomy and ASA (100 mg once day). The βFibrinogen G-455-A genotype was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets and HCT were measured by automated analyzer. βTG and PF4 were determined by ELISA. PFA and CFT were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
All patients had heterozygous βFibrinogen G-455-A. The mean platelet and mean HCT value were 428±180 x109/L and 47±3%. All patients had normal Fg (244±47mg/dl), high β-TG and PF4 (133±47 IU/ml vs 20±11 IU(ml and 45±21 IU/ml vs 6±2 IU7ml, respectively) (p<.0001 and p<.001, respectively), prolonged C/EPI closure time (CT, units: s, n.v. 84-160 s) (252±48 s) and normal CFT (CFT, units: s, n.v. 30-110 s) ( 50±7 s).
Conclusion
These findings suggest that βFibrinogen G-455-A gene polymorphism is not associated with ASA platelet insensitivity in patients with polycythemia vera.
Session topic: E-poster
Type: Publication Only
Background
Polycythemia vera (PV) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. According to PVSG, the antithrombotic therapy includes low dose ASA. However, there are insensivity ASA PV patients. It is debated if inherited thrombophilia increases the polycythemic platelet activation and, hence, the ASA platelet insensivity.
Aims
Therefore, we evaluated βFibrinogen G-455-A gene polymorphism, as thrombophilic molecular mutation associated with increased platelet aggregation, platelet count, hematocrit (HCT), β-thromboglobulin (β-TG) and platelet factor 4 (PF4) as markers of platelet activation, fibrinogen (Fg), Platelet functional activity (PFA) as indicator of ASA platelet sensitivity and clot formation time (CFT), as indicator of aspirinated platelets contribution to clot firmness. We studied 40 patients (28 men, 12 women; mean age 64 years, range 35_85 years) with PV according to WHO criteria. Fifty subjects served as controls.
Methods
The mean duration of disease was 9 years. All patients were on phlebotomy and ASA (100 mg once day). The βFibrinogen G-455-A genotype was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets and HCT were measured by automated analyzer. βTG and PF4 were determined by ELISA. PFA and CFT were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
All patients had heterozygous βFibrinogen G-455-A. The mean platelet and mean HCT value were 428±180 x109/L and 47±3%. All patients had normal Fg (244±47mg/dl), high β-TG and PF4 (133±47 IU/ml vs 20±11 IU(ml and 45±21 IU/ml vs 6±2 IU7ml, respectively) (p<.0001 and p<.001, respectively), prolonged C/EPI closure time (CT, units: s, n.v. 84-160 s) (252±48 s) and normal CFT (CFT, units: s, n.v. 30-110 s) ( 50±7 s).
Conclusion
These findings suggest that βFibrinogen G-455-A gene polymorphism is not associated with ASA platelet insensitivity in patients with polycythemia vera.
Session topic: E-poster
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