Association between fibrinogen receptor (Glycoprotein IIb) polymorphism and the risk of venous thromboembolism: a systematic review

Abstract

Background: The fibrinogen receptor is an integrin on the platelet surface and is shaped from two types of glycoprotein (GP) subunits, GPIIb and GPIIIa. Membrane glycoprotein IIb/IIIa plays an important role in platelet function. The gene encoding the glycoprotein IIIa shows a common polymorphism, PLA2 that increases the binding of the receptor to fibrinogen and enhances the platelet aggregation. The clinical impact of PLA2 polymorphism has been studied in some diseases, but the definition of its exact role on venous thromboembolism complications has been challenging. The present systematic review aimed to clarify the association of PLA2 polymorphism and venous thromboembolism. Main text: In this study, Electronic databases including PubMed, Embase, Scopus, Web of Science, and Cochrane Library were searched. All the assessed studies focused on the relationship between PLA2 polymorphism and venous thromboembolism. Five studies were eligible for systematic review. One study revealed a significant correlation between PLA2 polymorphism and venous thromboembolism. PLA2 polymorphism was associated with deep vein thrombosis in one study and pulmonary thromboembolism in another one. Conclusion: The published data supported the hypothesis that having the PLA2 polymorphism of GPIIIa may be a risk factor for venous thromboembolism, but the association cannot be concluded; it needs more clinical investigation.

Determination of the cut-off score of Human platelets membrane glycoprotein IIb/IIIa in COVID19: A novel biomarker and a therapeutic target

“…This substantiates previous findings in that under thrombin stimulation, increasing expression of the GpIIb/IIIa complex on the platelet membrane surface was observed [19]. Recent study supports our finding that vascular disorder was strongly associated with fibrinogen (a ligand of GPIIb/IIIa) and D-dimer levels in COVID-19 patients with thromboembolism [20] as well as CRP in pulmonary disease [21]. An explanation is that the proteolytic degradation of GPIIb/IIIa by plasmin produces D-dimer.…”

“…Surprisingly, one study mentioned to the benefit of GPIIb/IIIa inhibitor in the treatment of COVID-19 patients suffering from myocardial infarction [33], while another previous study detected a pulmonary haemorrhage among patients post percutaneous coronary intervention with synthetic inhibitor; Abciximab [34]. An explanation is the polymorphic variations among different populations [8,20]. Thus, COVID-19 patients who showed elevated level of GPIIb/IIIa are the only target for GPIIb/IIIa inhibitors.…”