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【文摘发布】肿瘤坏死因子α基因与脑动脉瘤
Author： Fontanella M, Rainero I, Gallone S, Rubino E, Fenoglio P, Valfre W, Garbossa D,
Carlino C, Ducati A, Pinessi L.
Resource: Neurosurgery. 2007 Apr;60(4):668-72; discussion 672-3.
Abstract： OBJECTIVE: The pathogenesis of intracranial aneurysms is still uncertain. In
addition to atherosclerosis, immunological factors may play a role in the
disease. Recent studies have suggested that tumor necrosis factor-alpha
(TNF-alpha), one of the main proinflammatory cytokines, may play a key role in
the formation and rupture of cerebral aneurysms. The purpose of this study is to
evaluate the association of a functionally active polymorphism (-308 G<A) in the
TNF-alpha gene with the risk and the clinical features of aneurysmal
subarachnoid hemorrhage. METHODS: A total of 171 consecutive aneurysmal
subarachnoid hemorrhage patients and 144 healthy controls were involved in the
study. Computed tomographic scan findings were assessed by Fisher grade;
clinical neurological assessment was performed using the Hunt and Hess grading
system. Patients and controls were genotyped for the-308 biallelic (G<A)
polymorphism of the TNF-alpha gene. RESULTS: The TNF-alpha G allele was
significantly more frequent in patients than in controls (chi2 = 5.59; P =
0.0181) and homozygosity for the G allele, compared with remaining genotypes,
was associated with a significantly increased risk of aneurysmal subarachnoid
hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29<odds ratio<3.75).
Allelic and genotypic frequencies of the examined polymorphism were not
significantly different in disease subgroups. The different TNF-alpha genotypes
do not seem to significantly modify the main clinical features of the disease.
CONCLUSION: Our data suggests that the TNF-alpha gene or a linked locus
significantly modulates the risk for aneurysmal subarachnoid hemorrhage.
Additional studies in different populations are warranted to confirm our
findings.
PMID: 17415203 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 Title： Tumor necrosis factor-alpha gene and cerebral aneurysms.
肿瘤坏死因子α基因与脑动脉瘤 原发性蛛网膜下腔出血（ subarachnoid hemorrhage，SAH）是指脑表面血管破裂后,血液流入蛛网膜下腔而言。年发病率为5～20/10万，常见病因为颅内动脉瘤, 其次为脑血管畸形，还有高血压性动脉硬化，也可见于动脉炎、脑底异常血管网、结缔组织病、血液病、抗凝治疗并发症等。
一、诊断
（一）临床特点
蛛网膜下腔出血的临床表现主要取决于出血量、积血部位、脑脊液循环受损程度等。
1、起病形式：多在情绪激动或用力等情况下急骤发病。
2、主要症状：突发剧烈头痛，持续不能缓解或进行性加重；多伴有恶心、呕吐；可有短暂的意识障碍及烦躁、谵妄等精神症状，少数出现癫痫发作。
3、主要体征：脑膜刺激征明显，眼底可见玻璃膜下出血，少数可有局灶性神经功能缺损的征象，如轻偏瘫、失语、动眼神经麻痹等。
4、临床分级
（ 1）一般采用Hunt和Hess分级法（表1）对动脉瘤性SAH的临床状态进行分级以选择手术时机和判断预后。
表 1 Hunt和Hess分级法
分类 标 准
0级 未破裂动脉瘤
Ⅰ级 无症状或轻微头痛
Ⅱ级 中～重度头痛、脑膜刺激征、颅神经麻痹
Ⅲ级 嗜睡、意识混浊、轻度局灶神经体征
Ⅳ级 昏迷、中或重度偏瘫、有早期去脑强直或自主神经功能紊乱
Ⅴ级 深昏迷、去大脑强直、濒死状态
（ 2）根据格拉斯哥昏迷评分（Glasgow Coma Scale，GSC）和有无运动障碍制定的世界神经外科联盟（WFNS）分级（表2）也广泛应用于临床。
表 2 WFNS分级法（1988年）
分级 GCS 运动障碍
Ⅰ级 15 无
Ⅱ级 14～13 无
Ⅲ级 14～13 有局灶症状
Ⅳ级 12～7 有或无
Ⅴ级 6～3 有或无
5、发病后的主要并发症：包括再出血、脑血管痉挛、急性非交通性脑积水和正常颅压脑积水等。（1）再出血：以5～11天为高峰，81%发生在1月内。颅内动脉瘤初次出血后的24小时内再出血率最高，约为4.1%，至第14天时累计为19%。临床表现为：在经治疗病情稳定好转的情况下，突然发生剧烈头痛、恶心呕吐、意识障碍加重、原有局灶症状和体征重新出现等。（2）血管痉挛：通常发生在出血后第1～2周，表现为病情稳定后再出现神经系统定位体征和意识障碍，因脑血管痉挛所致缺血性脑梗死所引起，腰穿或头颅CT检查无再出血表现。（3）急性非交通性脑积水：指SAH后1周内发生的急性或亚急性脑室扩大所致的脑积水，机制主要为脑室内积血，临床表现主要为剧烈的头痛、呕吐、脑膜刺激征、意识障碍等，复查头颅CT可以诊断。（4）正常颅压脑积水：出现于SAH的晚期，表现为精神障碍、步态异常和尿失禁。
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作者:admin@医学,生命科学 2011-03-04 05:12
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