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Neurology:常规的血液测试或可预测中风发作风险

来源:生物谷 2016-03-04 11:37

2016年3月4日/生物谷BIOON/--一项关于缺血性中风(ischemic stroke,也译作缺血性卒中)的新发现可能允许医生们利用常见的血液测试和病人的基因特征来预测他们第二次中风发作风险。

研究人员已发现高水平的C反应蛋白(C-Reactive Protein, CRP)---血液中发现的一种酶---与复发的缺血性中风风险增加存在关联。CRP是由于肝脏对炎症作出反应而产生的,而且人们已经通过检测它来测量病人患上冠状动脉疾病的风险。这项新的研究提示着对缺血性中风病人而言,它可能也是一种有用的工具。

美国弗吉尼亚大学医学院研究员Stephen Williams博士说,“对已经历中风发作的病人而言,死亡的最大风险是中风再次发作。因此,非常重要的事情就是能够寻找中风再次发作风险最高的那些人。”

缺血性中风风险

缺血性中风是由于流向大脑中的血液受阻而产生的,大约占了85%的中风病例;剩下的中风病例是出血性中风(hemorrhagic stroke),是由于血管破裂后血液流进大脑中而产生的。

为了更好地理解缺血性中风,Williams和他的同事们着手确定我们的基因如何影响我们血液中诸如CRP之类的生物标志物的水平。他们不仅发现上升的CRP水平提示着增加的中风风险,而且他们还鉴定出促进这种风险提高的基因变异:他们在2100名参与维他命介入中风预防临床试验(Vitamin Intervention for Stroke Prevention Trial, VISP)的人当中,检测到CRP基因单核苷酸多态性(SNP)与血液中的CRP水平存在关联,其中最为关联的CRP SNP就是rs2592902;他们还鉴定出AKR1D1基因座位上的一个SNP:rs2589998也与CRP水平存在关联;而且他们还鉴定出之前已被发现的FGB基因和LEPR基因上的SNP与血液中的纤维蛋白原(fibrinogen)水平存在关联。最后,他们发现在这些VISP参与者中,CRP相关性SNP和CRP水平与缺血性中风和复发性中风显著相关联;纤维蛋白原水平而不是纤维蛋白原相关性SNP也与复发性中风存在关联。相关研究结果近期发表在Neurology期刊上,论文标题为“Shared genetic susceptibility of vascular-related biomarkers with ischemic and recurrent stroke”。

Williams说道,他们发现这些影响CRP水平的基因变异会增加复发性中风发作风险,而且这种相同的遗传易感性不仅与增加的CRP水平相关联,而且也与增加的中风风险相关联。

Williams畅想着有那么一天:医生们可能根据病人的CRP水平和基因特征确定病人的第二次中风发作的整体风险。不过,即便仅仅是CRP水平也可能是一种有用的评估初次中风发作后复发性中风发作风险的工具。Williams说,“测量一个人的CRP水平非常简单。只需采集一下血液即可。你不必做一些诸如活组织检测之类的事情,这是因为病人可能不愿意做。不过,当与基因信息结合在一起时,我们可能有更大的能力鉴定出有更大风险的病人。”(生物谷 Bioon.com)

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Shared genetic susceptibility of vascular-related biomarkers with ischemic and recurrent stroke

doi:10.1212/WNL.0000000000002319

MStephen R. Williams, PhD, Fang-Chi Hsu, PhD, Keith L. Keene, PhD, Wei-Min Chen, PhD, Sarah Nelson, MPH, Andrew M. Southerland, MD, MSc, Ebony B. Madden, MSGC, PhD, Bruce Coull, MD, Stephanie M. Gogarten, PhD, Karen L. Furie, MD, Godfrey Dzhivhuho, Joe L. Rowles, Prachi Mehndiratta, MD, Rainer Malik, PhD, Josée Dupuis, PhD, Honghuang Lin, PhD, Sudha Seshadri, MD, Stephen S. Rich, PhD, Michèle M. Sale, PhD* and Bradford B. Worrall

Objective: To investigate the genetic contributors to cerebrovascular disease and variation in biomarkers of ischemic stroke.

Methods: The Vitamin Intervention for Stroke Prevention Trial (VISP) was a randomized, controlled clinical trial of B vitamin supplementation to prevent recurrent stroke, myocardial infarction, or death. VISP collected baseline measures of C-reactive protein (CRP), fibrinogen, creatinine, prothrombin fragments F1+2, thrombin-antithrombin complex, and thrombomodulin prior to treatment initiation. Genome-wide association scans were conducted for these traits and follow-up replication analyses were performed.

Results: We detected an association between CRP single nucleotide polymorphisms (SNPs) and circulating CRP levels (most associated SNP, rs2592902, p = 1.14 × 10−9) in 2,100 VISP participants. We discovered a novel association for CRP level in the AKR1D1 locus (rs2589998, p = 7.3 × 10−8, approaching genome-wide significance) that also is an expression quantitative trait locus for CRP gene expression. We replicated previously identified associations of fibrinogen with SNPs in the FGB and LEPR loci. CRP-associated SNPs and CRP levels were significantly associated with risk of ischemic stroke and recurrent stroke in VISP as well as specific stroke subtypes in METASTROKE. Fibrinogen levels but not fibrinogen-associated SNPs were also found to be associated with recurrent stroke in VISP.

Conclusions: Our data identify a genetic contribution to inflammatory and hemostatic biomarkers in a stroke population. Additionally, our results suggest shared genetic contributions to circulating CRP levels measured poststroke and risk for incident and recurrent ischemic stroke. These data broaden our understanding of genetic contributors to biomarker variation and ischemic stroke risk, which should be useful in clinical risk evaluation.

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