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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Platelet glycoprotein Ibalpha gene polymorphism and massive or submassive pulmonary embolism
Ahmet Soylu1, Mehmet Tokaç, Tülin Cora
1Department of Cardiology, Meram Medical School of Selcuk University, S.U. Meram Tip Fakültesi Kardiyoloji AD, Konya, Turkey. asoylu44@gmail.com
Journal of Thrombosis and Thrombolysis
|February 20, 2008
Summary
The glycoprotein Ibalpha Kozak polymorphism is linked to a higher risk of massive or submassive pulmonary embolism. This genetic factor may influence the severity of pulmonary embolism, independent of other risk factors.
Area of Science:
- Genetics
- Hematology
- Cardiology
Background:
- The glycoprotein Ibalpha Kozak sequence polymorphism (-5T/C) affects platelet glycoprotein Ib-IX-V receptor density.
- Increased receptor density may influence platelet aggregation and thrombosis.
Purpose of the Study:
- To determine if the glycoprotein Ibalpha Kozak polymorphism impacts the clinical presentation of acute pulmonary embolism.
- Investigate the association between this genetic variation and the severity of pulmonary embolism.
Main Methods:
- Genotyping of 42 pulmonary embolism patients for the glycoprotein Ibalpha Kozak polymorphism.
- Utilized polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) for genotyping.
Main Results:
- Patients with massive or submassive pulmonary embolism showed a significant over-representation of the -5T/C polymorphism (OR 5.5, P=0.023).
- The association remained significant after adjusting for conventional pulmonary embolism risk factors.
Conclusions:
- The glycoprotein Ibalpha Kozak polymorphism may serve as a risk factor for developing severe pulmonary embolism.
- Clot burden appears to be a crucial factor in the clinical manifestation of pulmonary embolism associated with this polymorphism.
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