血清神经元特异性烯醇化酶与急性脑出血关系的研究被引量：21

Study of correlation between serum neuron-specific enolase and acute intracerebral hemorrhage

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摘要目的探讨血清神经元特异性烯醇化酶（NSE）与急性脑出血的关系。方法采用酶联免疫吸附法对40例急性脑出血患者血清NSE水平进行动态检测,分析其与脑出血量、神经功能缺损程度评分（NDS）、脑出血部位的关系,并与正常对照组比较。结果脑出血组患者在发病48h内血清NSE水平即明显升高,3-5d达到峰值,6-9d和10-14d时仍明显高于正常对照组（P〈0.01-0.001）;脑出血患者血清NSE水平与出血量及NDS呈正相关（r=0.421,P〈0.01;r=0.415,P〈0.01）;与脑出血部位无明显关系（P〉0.05）。结论急性脑出血患者血清NSE水平明显升高,并且与脑出血量和病情有关。 Objective To study the correlation between serum neuron-specific enolase （NSE） and acute intracerebral hemorrhage （ICH）. Methods The serum level of NSE was measured in 40 patients with acute ICH by ELISA and compared with normal control subjects. The relationship between serum NSE level and neurological deficit scores （NDS）, volume and site of hemorrhage were analyzed. Results The serum level of NSE in ICH group increased within 48 hours, peaked at 3 -5 d, obviously higher at 6 -9 d and at 10 - 14 d compared with the control group （P 〈 0.01 - 0. 001 ）. There were positive correlations between the serum NSE level and the volume of hemorrhage （r=0.421, P〈0.01） and NDS （r =0.415, P〈0.01）. Conclusions The level of NSE in serum rises in the patients with acute ICH. It is closely related to the volume of hemorrhage and the condition of disease.

作者赵明哲史万英朱荣彦闫鹤立李育臣

机构地区石家庄市中心医院神经内科河北医科大学第三医院神经内科

出处《临床神经病学杂志》 CAS 北大核心 2007年第2期134-136,共3页 Journal of Clinical Neurology

关键词急性脑出血神经元特异性烯醇化酶 acute intracerebral hemorrhage neuron-specific enolase

分类号 R743.3 [医药卫生—神经病学与精神病学]

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1Persson L,Hardemark HG,Gustafsson J,et al,S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum:makers of cell damage in human central nervous system[J].Stroke,1997,18:911.
2Schaarschmidt H,Prange HW,Reiber H.Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases[J].Stroke,1994,25:558.
3梁柯.神经元特异性烯醇酶的研究进展[J].医学综述,2000,6(5):193-195. 被引量：9
4Martens P,Raabe A,Johnsson P.Serum S-100 and neuron-specific enolase for predictor of regaining consciousness after global cerebral ischemia[J].Stroke,1998,29:2363.
5何娅,张桂莲,苏清华,冯建军.脑卒中患者血清神经元特异性烯醇化酶动态变化及其临床意义[J].临床神经病学杂志,2003,16(3):143-145. 被引量：11
6Cunningham RT,Watt M,Winder Let al.Serum neuron specific enolase as a indictor of stroke volume[J].Eur Clin Invest,2000,26:298.
7陈俊,何国厚,余绍祖,江荣翠,胡秀学,黎华.神经元特异性烯醇化酶的动态变化在急性脑梗死患者中的临床意义[J].中风与神经疾病杂志,2005,22(1):70-72. 被引量：11

二级参考文献17

1Lafon-Cazal M, Bougault I, Steinberg G, et al. Measurement of gamma enolase, a new method for selective quantification of aeurotoxicity independently from glial lysis. Brain Res, 1992,593:63.
2Hatfield RH, Mckeman RM. CSF neuron-specific enolase as a quantitative marker of neuronal damage in rat stroke model. Brain Res, 1992,577:249.
3Missler U, Wiersmann M, Friedrich C, et al. S-1O0 protein and neuronspecific enolase concentration in blood as indicators of infarction volume and prognosis in acute ischemic stroke. Stroke, 1997,28:1956.
4Schaarschmidt H, Prange HW , Reiber HO. Neuron-specific enolas concentration in blood as a prognostic parameter in cerebrovascular disease. Stroke, 1994,25:558.
5Martens P, Raabe A, Johnsson P. Serum S-100 and neuron-specific enolase for predictor of regaining consciousness after global cerebral ischemia. Stroke, 1998,29 : 2363.
6Cunningham RT, Watt M, Winder J ,et al. Serum neuron specific enolase as a intdictor of stroke volume. Eur J Clin Invest, 1996,26:298.
7Wityk RJ,Pessin MS, Kaplan RF,et al. Serial assessment of acute stroke using the NIH Stroke Scale[J]. Stroke, 1994,25(2): 362-365.
8Fano G,Biocca S,Fulle S,et al. The S-100:a protein family in search of a function[J]. Prog Neurobiol, 1995,46(1 ) : 71-82.
9Yamazaki Y, Yada K,Morii S,et al. Diagnostic significance of serum neuron-specific enolase and myelin basic protein assay in patients with acute head injury[J]. J Surg Neurol, 1995,43 : 267-271.
10Mercer DW,Virji MA, Barry GE,et al, New solid-phase enzyme immunoassay of neuron-specific enolase in serum:effect of storage ,temperature, lipemia, icterus and hemolysis [J]. Clin Chem, 1990,36:1519.