Abstract
S100 calcium binding protein B (S100B), a well-studied marker for neurologic injury, has been suggested as a candidate for predicting outcome after subarachnoid hemorrhage. We performed a pooled analysis summarizing the associations between S100B protein in serum and cerebrospinal fluid (CSF) with radiographic vasospasm, delayed ischemic neurologic deficit (DIND), delayed cerebral infarction, and Glasgow Outcome Scale (GOS) outcome. A literature search using PubMed, the Cochrane Library, and the EMBASE databases was performed to identify relevant studies published up to May 2015. The weighted Stouffer’s Z method was used to perform a pooled analysis of outcome measures with greater than three studies. A total of 13 studies were included in this review. Higher serum S100B level was found to be associated with cerebral infarction as diagnosed by CT (padj = 3.1 x 10−4) and worse GOS outcome (padj = 5.5 x 10−11). There was no association found between serum and CSF S100B with radiographic vasospasm or DIND. S100B is a potential prognostic marker for aSAH outcome.
Highlights
Subarachnoid hemorrhage (SAH) secondary to the rupture of an intracranial aneurysm remains a major cause of morbidity and mortality[1]
Meta-analyses have been useful tools in integrating findings from multiple studies to demonstrate genetic and molecular associations with cerebral vasospasm and SAH outcome. [13, 14] The goal of this study is to summarize the findings and perform a comprehensive review and pooled analysis that examine the associations between serum and cerebrospinal fluid (CSF) S100 calcium binding protein B (S100B) with long-term patient outcome, radiographic vasospasm, delayed ischemic neurologic deficit (DIND) and delayed cerebral infarction
Seventyseven papers were identified for full-text assessment after the removal of non-human studies (n = 31), reviews, commentaries and meta-analyses (n = 11), and those studies that were unrelated to S100B (n = 42) (Fig 1)
Summary
Subarachnoid hemorrhage (SAH) secondary to the rupture of an intracranial aneurysm remains a major cause of morbidity and mortality[1]. While aneurysmal rupture and recurrent hemorrhage contribute to a high initial mortality rate, delayed neurologic deterioration from ischemic complications continues to be a significant contributor to patient disability[2]. Cerebral vasospasm has largely accounted for a patient’s clinical deterioration and has been the major focus of clinical research. Radiographic evidence of vasospasm is observed in up to 67% of patients after aneurysmal SAH (aSAH)[3, 4]. While there is a high prevalence of radiographic vasospasm, only 20–30% of patients with vasospasm develop clinical deteriorations[3, 4, 6]. Recent trials have failed to improve outcome from the reversal of vasospasm, suggesting that the pathophysiology may be more
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