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Year : 2022  |  Volume : 47  |  Issue : 3  |  Page : 161-166

Platelet glycoprotein VI genetic polymorphism T13254C in neonatal sepsis

1 Department of Clinical Pathology, Ain Shams University, Cairo, Egypt
2 Department of Pediatrics and Neonatology, Ain Shams University, Cairo, Egypt

Correspondence Address:
Marina Mounir William Labib
MSc of Clinical Pathology; Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ejh.ejh_74_21

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

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