Significance of Apolipoprotein E in Subarachnoid Hemorrhage: Neuronal Injury, Repair, and Therapeutic Perspectives–A Review

Lanterna, Luigi Andrea; Biroli, Francesco

doi:10.1016/j.jstrokecerebrovasdis.2008.09.006

Cited by 16 publications

(13 citation statements)

References 87 publications

(110 reference statements)

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“…Eleven patients who had intracranial hemorrhage, seven patients who had brain trauma and sixteen patients admitted to intensive care more than 24 h after SAH onset were excluded, leaving 120 patients for analysis. The demographic and clinical characteristics of the study patients are shown in Table 1 [6][7][8][9]. During the period of monitoring, a significant number of patients (n = 112, 93.3 %) developed ICP elevation.…”

Section: Clinical Datamentioning

confidence: 99%

“…The overall mortality of it ranges from 33 to 45 % [1][2][3]. The principal causes of death and severe disability are the direct effect of the initial hemorrhage, re-hemorrhage, and cerebral infarction secondary to vasospasm [1,[4][5][6][7]. Furthermore, elevated intracranial pressure (ICP) occurs frequently in patients with SAH and affect adversely patient outcome [8,9].…”

Section: Introductionmentioning

confidence: 99%

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Clinical observation of the time course of raised intracranial pressure after subarachnoid hemorrhage

Wang

Jin

et al. 2015

Neurol Sci

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The time course of intracranial pressure (ICP) after subarachnoid hemorrhage (SAH) is not well known. This retrospective study was conducted to investigate the occurrence and the dynamic variation of raised ICP post-SAH. ICP was prospectively studied in 120 patients with SAH who were admitted to neurocritical care within 24 h of hemorrhage. Patients underwent continuous ICP monitoring for at least 7 days, unless they died. Clinical status on admission, radiographic tests, treatment details and neurological outcome on discharge were analyzed in relation to ICP. The highest daily mean ICP and the day when ICP reduced to normal levels were assessed. Of the 120 patients studied, 112 (93.3 %) encountered ICP elevation whilst in hospital. The daily mean ICP was higher in Hunt and Hess grades IV-V patients than grades I-III patients (P = 0.01). The elevated ICP remained at a higher level for the initial 3 days (grades I-III patients) or 4 days (grades IV-V patients), after which the pressure decreased towards normal levels. The in-patient mortality was significantly increased in the high ICP variability group (P = 0.001), which was divided by the cutoff point using receiver operating characteristic curve analysis. Raised ICP mainly occurs within 8 days post-SAH, especially the initial 3-4 days. Those highlight the need for earlier management of ICP after SAH.

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Section: Clinical Datamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical observation of the time course of raised intracranial pressure after subarachnoid hemorrhage

Wang

Jin

et al. 2015

Neurol Sci

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“…As an essential apolipoprotein with three major isoforms in the human CNS, each isoform is coded by the allelic forms of the APOE gene ε2, ε3, and ε4 alleles, and apoE has been identified to take part in SAH (Alfieri et al, 2008;Gallek et al, 2009;Lanterna and Biroli, 2009). Although still being debated, the effects of apoE4 have been observed in different clinical settings associated with the poor outcome in SAH patients (Gallek et al, 2009;Juvela et al, 2009;Lanterna and Biroli, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Although still being debated, the effects of apoE4 have been observed in different clinical settings associated with the poor outcome in SAH patients (Gallek et al, 2009;Juvela et al, 2009;Lanterna and Biroli, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…As one of the important apolipoproteins in the CNS, apolipoprotein E (apoE protein, APOE gene) has been proven to be associated with SAH (Lanterna and Biroli, 2009), and the effect of the APOE polymorphism on the SAH patients' prognosis (Dunn et al, 2001). However, APOE polymorphism did not completely explain the rebleeding after SAH (Yin et al, 2012), and the subsequent researches, which are concerned on the polymorphism of APOE promoter, showed that it may regulate the expression of apoE (Li et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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The APOE promoter polymorphism is associated with rebleeding after spontaneous SAH in a Chinese population

Chen

Huang

Ruan

et al. 2015

Gene

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The Role of Apolipoprotein E in the Pathological Events Following Subarachnoid Hemorrhage: A Review

Guo

Sun

Zhang

2011

Early Brain Injury or Cerebral Vasospasm

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Subarachnoid hemorrhage (SAH) strikes individuals with devastating neurological results. Traditional viewpoints do not explain all the differences that are usually found in clinical practice. The role of genetic predisposition in SAH has recently been investigated. Particular attention has been paid to the apolipoprotein E (apoE) genotype. APOE genotype is a major prognostic factor in patient outcome after spontaneous aneurysmal SAH. In patients with SAH, the expression of the apoE ε4 allele is associated with a higher risk of negative outcome and delayed ischemia. Evidence from experimental and clinical studies confirms that apoE plays an important role in the pathological events after SAH. This article reviews related research and surveys the links between the pathological events of SAH and apoE.

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Significance of Apolipoprotein E in Subarachnoid Hemorrhage: Neuronal Injury, Repair, and Therapeutic Perspectives–A Review

Cited by 16 publications

References 87 publications

Clinical observation of the time course of raised intracranial pressure after subarachnoid hemorrhage

Clinical observation of the time course of raised intracranial pressure after subarachnoid hemorrhage

The APOE promoter polymorphism is associated with rebleeding after spontaneous SAH in a Chinese population

The Role of Apolipoprotein E in the Pathological Events Following Subarachnoid Hemorrhage: A Review

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