Early elevation of serum tumor necrosis factor-α is associated with poor outcome in subarachnoid hemorrhage.
Early elevation of serum tumor necrosis factor-α is associated with poor outcome in subarachnoid hemorrhage.
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DOI：
10.2310/jim.0b013e3182686932
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发表时间：
2012-10
期刊：
影响因子：
--
通讯作者：
Ning M
中科院分区：
文献类型：
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作者：
Chou SH;Feske SK;Atherton J;Konigsberg RG;De Jager PL;Du R;Ogilvy CS;Lo EH;Ning M
蛛网膜下腔出血（SAH）与炎症相关，炎症可能导致SAH预后不良。我们假设血清肿瘤坏死因子 -α（TNFα）和白细胞介素 - 6（IL - 6）升高与SAH的血管痉挛和不良预后相关。
在52例连续的SAH患者中，我们比较了SAH后第0 - 1天、2 - 3天、4 - 5天、6 - 8天和10 - 14天的TNFα和IL - 6水平与血管痉挛以及3个月和6个月时的不良预后的关系。血管痉挛定义为血管造影显示血管管径减少>50%。不良预后定义为改良Rankin评分>2。
SAH后第2 - 3天TNFα升高与3个月时的不良预后相关（p = 0.0004）。在对Hunt - Hess分级和年龄进行调整后，TNFα随时间的总体升高（SAH后第0 - 14天）与3个月时的不良预后独立相关（p = 0.02）。无论是横断面分析还是IL - 6随时间的水平均与预后无关。TNFα和IL - 6水平均与血管痉挛无关。
在这个小队列中，SAH后第2 - 3天血清TNFα升高以及TNFα随时间的总体升高与不良预后相关，但与血管造影显示的血管痉挛无关。未来需要进一步研究以明确TNFα在SAH相关脑损伤中的作用及其作为SAH预后生物标志物的潜力。
Subarachnoid hemorrhage (SAH) is associated with inflammation which may mediate poor outcome in SAH. We hypothesize that elevated serum tumor necrosis factor-alpha (TNFα) and interleukin-6 (IL-6) are associated with vasospasm and poor outcome in SAH. In 52 consecutive SAH subjects, we compared TNFα and IL-6 levels on post-SAH days 0–1, 2–3, 4–5, 6–8, and 10–14 with respect to vasospasm and to poor outcome at 3- and 6-months. Vasospasm was defined as >50% reduction in vessel caliber on angiography. Poor outcome was defined as modified Rankin score >2. Elevated TNFα on post-SAH days 2–3 was associated with poor 3-month outcome (p=0.0004). Global elevation of TNFα over time (post-SAH days 0–14) was independently associated with poor 3-month outcome after adjusting for Hunt-and-Hess grade and age (p=0.02). Neither cross-sectional nor IL-6 levels over time were associated with outcome. Neither TNFα nor IL-6 levels were associated with vasospasm. Elevation in serum TNFα on post-SAH days 2–3 and global elevation of TNFα over time are associated with poor outcome but not with angiographic vasospasm in this small cohort. Future studies are needed to define the role of TNFα in SAH-related brain injury and its potential as a SAH outcome biomarker.