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因子 XIIIa 启动子甲基化状态对颅内动脉瘤性蛛网膜下腔出血(aSAH)的预后意义。

Prognostic significance of factor XIIIA promoter methylation status in aneurysmal subarachnoid haemorrhage (aSAH).

机构信息

Department of Human Genetics, National Institute of Mental Health and Neuro Sciences, Bangalore/Karnataka, Karnataka, 560029, India.

Department of Biochemistry, Armed Forces Medical College, Pune, 411040, India.

出版信息

BMC Cardiovasc Disord. 2019 Jul 17;19(1):170. doi: 10.1186/s12872-019-1146-8.

DOI:10.1186/s12872-019-1146-8
PMID:31315570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6637610/
Abstract

BACKGROUND

Aneurysmal subarachnoid hemorrhage is a life- threatening condition with high rate of disability and mortality. Apolipoprotein E (APOE) and Factor XIIIA (F13A) genes are involved in the pathogenetic mechanism of aneurysmal subarachnoid haemorrhage (aSAH). We evaluated the association of promoter methylation status of APOE and F13A gene and risk of aSAH.

METHODS

For evaluating the effect of hypermethylation in the promoter region of these genes with risk of aSAH, we conducted a case -control study with 50 aSAH patients and 50 healthy control. The methylation pattern was analysed using methylation specific PCR. The risk factors associated with poor outcome after aSAH was also analysed in this study. The outcome was assessed using Glasgow outcome score (GOS) after 3 months from the initial bleed.

RESULTS

The frequency of APOE and F13A methylation pattern showed insignificant association with risk of aSAH in this study. Gender stratification analysis suggests that F13A promoter methylation status was significantly associated with the risk of aSAH in male gender. Age, aneurysm located at the anterior communicating artery and diabetes mellitus showed significant association with poor outcome after aSAH.

CONCLUSION

There was no significant association with APOE promoter methylation with the risk as well as outcome of patients after aSAH. F13A promoter methylation status was significantly associated with risk of aSAH in male gender, with no significant association with outcome after aSAH.

摘要

背景

动脉瘤性蛛网膜下腔出血是一种危及生命的疾病,其残疾率和死亡率均较高。载脂蛋白 E (APOE) 和因子 XIIIa (F13A) 基因参与了动脉瘤性蛛网膜下腔出血 (aSAH) 的发病机制。我们评估了 APOE 和 F13A 基因启动子甲基化状态与 aSAH 风险的相关性。

方法

为了评估这些基因启动子区域超甲基化与 aSAH 风险的关系,我们进行了一项病例对照研究,共纳入 50 例 aSAH 患者和 50 例健康对照。采用甲基化特异性 PCR 分析甲基化模式。本研究还分析了与 aSAH 后不良预后相关的危险因素。采用格拉斯哥结局评分(GOS)在初始出血后 3 个月评估预后。

结果

APOE 和 F13A 甲基化模式的频率与本研究中 aSAH 的风险无显著相关性。性别分层分析表明,F13A 启动子甲基化状态与男性 aSAH 风险显著相关。年龄、前交通动脉动脉瘤和糖尿病与 aSAH 后不良预后显著相关。

结论

APOE 启动子甲基化与 aSAH 患者的风险和预后无显著相关性。F13A 启动子甲基化状态与男性 aSAH 风险显著相关,与 aSAH 后预后无显著相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/6637610/f7cb04e65ec6/12872_2019_1146_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/6637610/255a77983cd3/12872_2019_1146_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/6637610/f7cb04e65ec6/12872_2019_1146_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/6637610/255a77983cd3/12872_2019_1146_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4845/6637610/f7cb04e65ec6/12872_2019_1146_Fig2_HTML.jpg

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