THE DYSFUNCTION OF PLATELETS IN PAROXYSMAL NOCTURNAL HEMOGLOBINURIA
(Abstract release date: 05/19/16)
EHA Library. Fu R. 06/09/16; 134660; PB1760
Dr. Rong Fu
Contributions
Contributions
Abstract
Abstract: PB1760
Type: Publication Only
Background
Thrombosis is a dangerous complication of paroxysmal nocturnal hemoglobinuria (PNH), with a high mortality rate. However, the mechanism underlying the development of thrombosis in PNH remains unclear.
Aims
To explore the function of platelets in PNH.
Methods
Serum concentrations of the terminal complement complex (sC5b-9) were determined by ELISA and the levels of C5b-9, CD61 and CD62p on platelet membranes by flow cytometry. Clinical parameters were assessed, including D-dimer and platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid (ARA).
Results
Serum sC5b-9 concentrations were significantly lower in the PNH/PNH-AA than in the control group (p<0.01). C5b-9 deposition was significantly higher on CD59- platelets than on CD59+ platelets in PNH/PNH-AA patients and healthy controls (p<0.01 each). D-dimer concentration was significantly higher in PNH/PNH-AA patients, especially those with lactate dehydrogenase concentrations >1000 U/L, than in controls (p<0.05). CD61 (p<0.05) expression was lower on CD59+ platelets in PNH than controls and CD59− platelets in PNH. CD62p(p<0.01) expressions were lower on CD59− and CD59+ platelets (p<0.01) in PNH than controls. Platelet aggregation stimulated by the agonists ADP and ARA was lower in the PNH/PNH-AA than in the control group (p<0.05). Interestingly, CD61 expression on CD59+ platelets was higher in PNH patients than in patients with higher type II PNH clones.
Conclusion
Platelet function of platelets, especially of CD59+ platelets, was inversely inhibited in PNH/PNH-AA even in the presence of continuous hypercoagulation.
Session topic: E-poster
Keyword(s): Paroxysmal nocturnal hemoglobinuria (PNH), Platelet, Thrombosis
Type: Publication Only
Background
Thrombosis is a dangerous complication of paroxysmal nocturnal hemoglobinuria (PNH), with a high mortality rate. However, the mechanism underlying the development of thrombosis in PNH remains unclear.
Aims
To explore the function of platelets in PNH.
Methods
Serum concentrations of the terminal complement complex (sC5b-9) were determined by ELISA and the levels of C5b-9, CD61 and CD62p on platelet membranes by flow cytometry. Clinical parameters were assessed, including D-dimer and platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid (ARA).
Results
Serum sC5b-9 concentrations were significantly lower in the PNH/PNH-AA than in the control group (p<0.01). C5b-9 deposition was significantly higher on CD59- platelets than on CD59+ platelets in PNH/PNH-AA patients and healthy controls (p<0.01 each). D-dimer concentration was significantly higher in PNH/PNH-AA patients, especially those with lactate dehydrogenase concentrations >1000 U/L, than in controls (p<0.05). CD61 (p<0.05) expression was lower on CD59+ platelets in PNH than controls and CD59− platelets in PNH. CD62p(p<0.01) expressions were lower on CD59− and CD59+ platelets (p<0.01) in PNH than controls. Platelet aggregation stimulated by the agonists ADP and ARA was lower in the PNH/PNH-AA than in the control group (p<0.05). Interestingly, CD61 expression on CD59+ platelets was higher in PNH patients than in patients with higher type II PNH clones.
Conclusion
Platelet function of platelets, especially of CD59+ platelets, was inversely inhibited in PNH/PNH-AA even in the presence of continuous hypercoagulation.
Session topic: E-poster
Keyword(s): Paroxysmal nocturnal hemoglobinuria (PNH), Platelet, Thrombosis
Abstract: PB1760
Type: Publication Only
Background
Thrombosis is a dangerous complication of paroxysmal nocturnal hemoglobinuria (PNH), with a high mortality rate. However, the mechanism underlying the development of thrombosis in PNH remains unclear.
Aims
To explore the function of platelets in PNH.
Methods
Serum concentrations of the terminal complement complex (sC5b-9) were determined by ELISA and the levels of C5b-9, CD61 and CD62p on platelet membranes by flow cytometry. Clinical parameters were assessed, including D-dimer and platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid (ARA).
Results
Serum sC5b-9 concentrations were significantly lower in the PNH/PNH-AA than in the control group (p<0.01). C5b-9 deposition was significantly higher on CD59- platelets than on CD59+ platelets in PNH/PNH-AA patients and healthy controls (p<0.01 each). D-dimer concentration was significantly higher in PNH/PNH-AA patients, especially those with lactate dehydrogenase concentrations >1000 U/L, than in controls (p<0.05). CD61 (p<0.05) expression was lower on CD59+ platelets in PNH than controls and CD59− platelets in PNH. CD62p(p<0.01) expressions were lower on CD59− and CD59+ platelets (p<0.01) in PNH than controls. Platelet aggregation stimulated by the agonists ADP and ARA was lower in the PNH/PNH-AA than in the control group (p<0.05). Interestingly, CD61 expression on CD59+ platelets was higher in PNH patients than in patients with higher type II PNH clones.
Conclusion
Platelet function of platelets, especially of CD59+ platelets, was inversely inhibited in PNH/PNH-AA even in the presence of continuous hypercoagulation.
Session topic: E-poster
Keyword(s): Paroxysmal nocturnal hemoglobinuria (PNH), Platelet, Thrombosis
Type: Publication Only
Background
Thrombosis is a dangerous complication of paroxysmal nocturnal hemoglobinuria (PNH), with a high mortality rate. However, the mechanism underlying the development of thrombosis in PNH remains unclear.
Aims
To explore the function of platelets in PNH.
Methods
Serum concentrations of the terminal complement complex (sC5b-9) were determined by ELISA and the levels of C5b-9, CD61 and CD62p on platelet membranes by flow cytometry. Clinical parameters were assessed, including D-dimer and platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid (ARA).
Results
Serum sC5b-9 concentrations were significantly lower in the PNH/PNH-AA than in the control group (p<0.01). C5b-9 deposition was significantly higher on CD59- platelets than on CD59+ platelets in PNH/PNH-AA patients and healthy controls (p<0.01 each). D-dimer concentration was significantly higher in PNH/PNH-AA patients, especially those with lactate dehydrogenase concentrations >1000 U/L, than in controls (p<0.05). CD61 (p<0.05) expression was lower on CD59+ platelets in PNH than controls and CD59− platelets in PNH. CD62p(p<0.01) expressions were lower on CD59− and CD59+ platelets (p<0.01) in PNH than controls. Platelet aggregation stimulated by the agonists ADP and ARA was lower in the PNH/PNH-AA than in the control group (p<0.05). Interestingly, CD61 expression on CD59+ platelets was higher in PNH patients than in patients with higher type II PNH clones.
Conclusion
Platelet function of platelets, especially of CD59+ platelets, was inversely inhibited in PNH/PNH-AA even in the presence of continuous hypercoagulation.
Session topic: E-poster
Keyword(s): Paroxysmal nocturnal hemoglobinuria (PNH), Platelet, Thrombosis
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