Experimental and Clinical Medicine
Contributions
Type: Publication Only
Background
Essential thrombocythemia (ET) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. Aspirin (ASA) is the standard therapy to prevent the thrombosis. It is reported that thrombocythaemic patients have ASA insentivity. It is debated if inherited thrombophilia induces the thrombocythemic platelet activation and, hence, the ASA platelet insensitivity.
Aims
Therefore, we evaluated human platelet antigen-1 (HPA-1) gene polymorphism, as thrombophilic molecular mutation associated with platelet hyperfunction, platelet count, b-thromboglobulin (b-TG) and platelet factor 4 (PF4), as markers of platelet activation, the platelet functional activity (PFA) as indicator of ASA platelet sensitivity and the maximum clot firmness (MCF), as indicator of aspirinated platelet contribution to clot firmness. We studied 48 patients (4 men, 8 women; mean age 51 years, range 32-70) with ET according to WHO criteria.
Methods
The mean duration of disease was 11 years. All patients were on ASA 100 mg once daily. Fifty subjects served as controls. The genotype HPA-1 was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets were measured by automated analyzer. b-TG and PF4 were determined by ELISA. ASA platelet sensitivity and MCF were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
Of 48 patients, 36 were HPA-1a/1a and 12 were HPA-1a/1b. The mean platelet count was 462±240x109/L. All patients had high b-TG and PF4 (244±15 IU/ml vs 20±11 IU/ml and 162±56 IU/ml vs 6±2 IU/ml, respectively) (p<.0001 and p<.0001, respectively), prolonged C/EPI closure time (CT, unit: s, n.v. 84-160 s) (252±48 s) and normal MCF (MCF, unit: mm, n.v. 50-72 mm) (71±2 mm).
Summary
These findings suggest that HPA-1 gene polymorphism does not inhibit aspirinated platelets sensitivity in patients with ET.
Session topic: Publication Only
Type: Publication Only
Background
Essential thrombocythemia (ET) is a myeloid neoplasm characterized by platelet activation and thrombotic risk. Aspirin (ASA) is the standard therapy to prevent the thrombosis. It is reported that thrombocythaemic patients have ASA insentivity. It is debated if inherited thrombophilia induces the thrombocythemic platelet activation and, hence, the ASA platelet insensitivity.
Aims
Therefore, we evaluated human platelet antigen-1 (HPA-1) gene polymorphism, as thrombophilic molecular mutation associated with platelet hyperfunction, platelet count, b-thromboglobulin (b-TG) and platelet factor 4 (PF4), as markers of platelet activation, the platelet functional activity (PFA) as indicator of ASA platelet sensitivity and the maximum clot firmness (MCF), as indicator of aspirinated platelet contribution to clot firmness. We studied 48 patients (4 men, 8 women; mean age 51 years, range 32-70) with ET according to WHO criteria.
Methods
The mean duration of disease was 11 years. All patients were on ASA 100 mg once daily. Fifty subjects served as controls. The genotype HPA-1 was determined using a commercialized polymerase chain reaction kit with sequence-specific primers. Platelets were measured by automated analyzer. b-TG and PF4 were determined by ELISA. ASA platelet sensitivity and MCF were measured by Platelet Function Analyzer (PFA-100) and by ROTEM delta, respectively.
Results
Of 48 patients, 36 were HPA-1a/1a and 12 were HPA-1a/1b. The mean platelet count was 462±240x109/L. All patients had high b-TG and PF4 (244±15 IU/ml vs 20±11 IU/ml and 162±56 IU/ml vs 6±2 IU/ml, respectively) (p<.0001 and p<.0001, respectively), prolonged C/EPI closure time (CT, unit: s, n.v. 84-160 s) (252±48 s) and normal MCF (MCF, unit: mm, n.v. 50-72 mm) (71±2 mm).
Summary
These findings suggest that HPA-1 gene polymorphism does not inhibit aspirinated platelets sensitivity in patients with ET.
Session topic: Publication Only