Contribution of factor VII polymorphisms to coagulopathy in patients with isolated traumatic brain injury

• Published in: Clinical neurology and neurosurgery 2021-09, Vol.208, p.106836-106836, Article 106836
• Main Authors: Fang, Jiang, Yuan, Qiang, Du, Zhuoying, Liu, Chaobo, Xu, Hao, Yang, Weijian, Chen, Long, Zhao, Jianlan, Xie, Rong, Hu, Jin, Wu, Xing
• Format: Article
• Language: English
• Subjects: Adult; Aged; Alleles; Blood Coagulation Disorders - blood; Blood Coagulation Disorders - etiology; Blood Coagulation Disorders - genetics; Brain Injuries, Traumatic - blood; Brain Injuries, Traumatic - complications; Coagulation factor VII; Coagulation factors; Coagulopathy; Coma; Deoxyribonucleic acid; DNA; Emergency medical care; Factor VII - genetics; Factor VII - metabolism; Female; Gene polymorphism; Genotype; Genotype & phenotype; Hematoma; Hemorrhage; Humans; Male; Medical imaging; Middle Aged; Patients; Plasma; Polymerase chain reaction; Polymorphism; Polymorphism, Single Nucleotide; Polymorphisms; Risk factors; Thromboplastin; Trauma; Traumatic brain injury; Young Adult
• ISSN: 0303-8467; 1872-6968
• DOI: 10.1016/j.clineuro.2021.106836

Coagulopathy is a severe complication of traumatic brain injury (TBI) and can cause secondary injuries and death. Decrease of FVII activity contributes to the coagulopathy and progressive hemorrhagic injury (PHI) in patients with isolated TBI. Some polymorphic loci of coagulation factor VII (FVII) are shown to be essential for FVII activity. However, the relationship between FVII gene polymorphisms and coagulopathy in patients with isolated TBI is still unknown. Therefore, the present study aimed to investigate the relationship between FVII gene polymorphisms and plasma FVIIa levels, and assess whether FVII polymorphisms were associated with TBI-related coagulopathy, PHI, and 6 months GOS in patients with isolated TBI. One-hundred-forty-nine patients with isolated TBI (from East of China) admitted to Huashan Hospital's Neurological Trauma Center from March 2012 to March 2016 were enrolled in this study. The Polymorphism-Polymerase Chain Reaction (PCR) method was used to analyze the five FVII polymorphism loci (-323P0/P10, R353Q, -401G/T, -402G/A, and -670A/C) of these patients. Patients' blood was collected to test the activated partial thromboplastin time, international normalized ratio, platelet, and FVIIa concentrations. Other clinical characteristics were also recorded. The minor alleles of three genotypes of -323 P0/P10, R353Q, and -401G/T each independently associated with 23.3%, 28.6%, and 27.6% lower FVIIa levels, respectively. These polymorphisms explained 21% of the total variance of FVIIa levels (adjusted R2:0.206). The genotype of -323P0/P10 was an independent risk factor for coagulopathy (OR = 2.77, p = 0.043) and PHI (OR = 3.47, p = 0.03) after adjustment for confounding factors in the logistic regression model. Polymorphisms of FVII were not independently associated with 6 months Glasgow Outcome Scale (GOS) of isolated TBI patients. -323P0/P10, R353Q, and -401 G/T genotypes were associated with FVIIa levels. -323P0/P10 genotype was independently associated with traumatic coagulopathy and PHI in isolated TBI patients. •FVII gene polymorphisms were associated with the occurrence of coagulopathy and PHI in patients with isolated TBI.•Plasma FVIIa levels in patients with TBI were significantly influenced by FVII gene polymorphisms.•The individuals harboring -323P0/P10 genotype were associated with increased risk of TBI related coagulopathy and PHI.