Jiang Yong, Sun Xiaochuan, Gui Li, Xia Yuxian, Tang Wenyuan, Cao Yueqing, Gu Yingjiang
Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
J Neurotrauma. 2007 Dec;24(12):1802-10. doi: 10.1089/neu.2007.0299.
The objective of this work was to investigate the relationship between apolipoprotein E (APOE) promoters (G-219T, C-427T, A-491T) polymorphisms and the clinical deterioration in early stage of traumatic brain injury (TBI) in a cohort of Chinese patients. In this study, we used the cohort of patients which has been reported previously. A total of 110 subjects with TBI (80 males and 30 females, with mean age of 43.87 years) were admitted from December 2003 to May 2004, and demographic and clinical data were collected. The clinical deterioration of patient's condition in acute stage (<7 days after TBI) was judged by either of the following criteria: decrease of Glasgow Coma Scale (GCS) score (compared with initial admission GCS), increase in hematoma volume or delayed hematoma both detected by repeated computed tomography (CT) scanning compared to that on admission. Venous blood was collected from patients with TBI on admission to determine the APOE promoter polymorphisms. The APOE genotyping was performed by means of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). chi(2) test and logistic regression analyses were done by SPSS. In 110 Chinese patients, the distributions of APOE genotypes and alleles matched Hardy-Weinberg Law, and 19 subjects presented with deteriorated clinical condition in acute stage after hospitalization. chi(2) test showed insignificant differences in association of APOE promoter polymorphisms with clinical deterioration (p>0.05). But logistic regression analyses, after adjusting patients' age, injury severity and injury mechanism etc, showed that -491AA (OR=11.681, p=0.009, 95%, CI 1.824-74.790) and APOE epsilon4 were all risk factors, with injury severity and alcohol-drinking as other risk factors. In Chinese population, as a significant but not independent risk factor, only APOE -491AA promoter in epsilon4 carriers is apt to the clinical deterioration and may contribute to the poor outcome after TBI.
本研究旨在探讨中国患者队列中载脂蛋白E（APOE）启动子（G-219T、C-427T、A-491T）多态性与创伤性脑损伤（TBI）早期临床病情恶化之间的关系。在本研究中，我们使用了先前报道的患者队列。2003年12月至2004年5月共收治110例TBI患者（80例男性，30例女性，平均年龄43.87岁），并收集了人口统计学和临床资料。根据以下任一标准判断患者急性期（TBI后<7天）病情恶化情况：格拉斯哥昏迷量表（GCS）评分降低（与入院初始GCS评分相比）、血肿体积增加或重复计算机断层扫描（CT）检测到的延迟血肿（与入院时相比）。TBI患者入院时采集静脉血以确定APOE启动子多态性。采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）方法进行APOE基因分型。使用SPSS进行卡方检验和逻辑回归分析。110例中国患者中，APOE基因型和等位基因分布符合Hardy-Weinberg定律，19例患者住院后急性期临床病情恶化。卡方检验显示APOE启动子多态性与临床病情恶化的相关性无显著差异（p>0.05）。但在调整患者年龄、损伤严重程度和损伤机制等因素后进行的逻辑回归分析显示，-491AA（OR=11.681，p=0.009，95%CI 1.824-74.790）和APOE ε4均为危险因素，损伤严重程度和饮酒为其他危险因素。在中国人群中，作为一个显著但非独立的危险因素，只有ε4携带者中的APOE -491AA启动子易于导致临床病情恶化，可能导致TBI后预后不良。
