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Abstract Background: Neonatal sepsis is a global burden, being a leading cause of neonatal morbidity and mortality worldwide. Platelet glycoprotein VI impacts sepsis at multiple stages of the inflammatory response. The expression of the GPVI receptor is genetically determined, thus influencing the coagulation processes. We focused in our study on the role of platelet glycoprotein VI genetic polymorphism T13254C (rs1613662) in neonatal sepsis in relation to other risk factors, laboratory tests, sepsis progression, and outcome. Methods: We studied 50 neonates with early-onset sepsis. We detected platelet glycoprotein VI T13254C polymorphism by using TaqMan allelic discrimination method by the real-time polymerase chain reaction technique. Results: Our results showed that GPVI mutant polymorphic group was associated with higher D-dimer levels (P=0.032). Also, septic neonates with mutant homozygous type showed poor survival (P=0.047). However, GPVI mutant polymorphic types weren’t significantly related to other demographic, laboratory data, and different scoring systems; Sepsis Induced Coagulopathy score (SIC), International Society on Thrombosis and Hemostasis score (ISTH), and Score for Neonatal Acute Physiology (SNAP II). Conclusion: We found a relation between platelet glycoprotein VI T13254C polymorphism and D-dimer levels, hence suggesting a relation with neonatal sepsis associated coagulopathy which might further affect patients’ outcome |