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Meta Analysis
Role of Apolipoprotein E Genotypes in Aneurysmal Subarachnoid Hemorrhage: Susceptibility, Complications, and Prognosis.
- Xin Hu, Zhiyi Xie, Xin Zan, Lu Ma, Hao Li, Chao You, and Yan Jiang.
- Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
- World Neurosurg. 2018 Oct 1; 118: e666-e676.
BackgroundAneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease. Emerging evidence has indicated that the apolipoprotein E (ApoE) genotype might be associated with the risk of aSAH as well as complications and outcomes after aSAH, although the results remain controversial.MethodsWe searched published literature on PubMed, Embase, China National Knowledge Infrastructure, and Wanfang database to identify studies involving the ApoE genotype and aSAH. A meta-analysis was performed to summarize the relationship between ApoE genotype and aSAH, including susceptibility, complications, and prognosis.ResultsEighteen studies were considered eligible for inclusion. Generally, ε4 carriers had increased risk of aSAH (odds ratio [OR] 1.23, 95% confidence interval [CI] 1.01-1.49). White patients with the ε2/ε2 genotype had a greater risk of aSAH (OR 3.38, 95% CI 1.13-10.11). The patients with aSAH carrying the ε4 allele had an increased risk of poor outcome (OR 2.21, 95% CI 1.21-4.05) compared with non-ε4 carriers, especially in Asian patients (OR 4.99, 95% CI 1.73-14.40). ApoE ε4 carriers have increased risk of delayed ischemic neurologic deficit compared with non-ε4 carriers in the overall population. No significant difference was detected regarding the effect of certain ApoE genotypes on aSAH admission severity, rebleeding, or cerebral vasospasm after aSAH.ConclusionsWe found that the ApoE genotype was significantly associated with aSAH risk, whereas its effect on certain ethnic populations differs. Patient carrying the ε4 allele might have a worse outcome, whereas current evidence was insufficient to prove the association between ApoE genotypes and post-SAH complications.Copyright © 2018 Elsevier Inc. All rights reserved.
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