CAJ | 학술논문

背景 :S-100b, 神经元特异性烯醇化酶 (neuron-specific enolase,NSE)可以作为神经元损伤的生化标志物,但其预测缺血性神经元损伤的程度及神经功能缺损程度尚不太清楚. 目的 :探讨 S-l00b蛋白、 NSE预测神经元损伤程度及神经功能缺损程度以及血糖升高与神经元损伤之间的关系. 设计 :以诊断为依据的非随机对照研究. 地点和对象 :2002-03/2003-03洪泽县人民医院神经科住院脑梗死患者 43例,男 23例,女 20例,年龄 52～ 83岁,排除脑部其他疾病.对照组为同期本院门诊健康体检者 33例,男 19例,女 14例,年龄 48～ 80岁. 方法:应用 ELISA法测定 S-100b,NSE血清水平 ,脑 CT测量脑梗死体积(多田氏公式计算梗死体积).神经功能缺损程度用美国国立健康研究所制定的急性脑卒中评定量表 (NIHSS)评分. 主要观察指标 : ①两组患者血清 S-l00b, NSE水平.②血清 S-l00b, NSE水平与梗死体积及神经功能缺损程度的关系. 结果 :脑梗死组在病程各时点上血清 S-l00b, NSE水平与对照组相比均升高,于病后 24 h内即开始升高,分别为( 1.64± 0.41) μ g/L,( 8.54 ± 2.37) μ g/L;第 3天达高峰 [( 2.15± 0.42) μ g/L,( 11.36± 3.14) μ g/L];第 7天仍未恢复至正常水平 [( 1.74± 0.38) μ g/L,( 9.13± 2.58) μ g/L].第 3天 S-l00b与梗死体积及临床症状严重程度呈正相关 (r=0.64,0.49,P< 0.001,0.002), NSE与梗死体积呈正相关 (r=0.39,P< 0.05),而与临床症状严重程度不相关 (r=0.15,P >0.05).高血糖脑梗死组血清 S-l00b, NSE明显高于正常血糖组. 结论 :血清 S-l00b, NSE升高可以预测急性脑梗死患者神经元损伤程度及神经功能缺损程度,是预测预后的敏感生化指标,血糖升高可以加重缺血性脑损伤.
배경 :S-100b, 신경원특이성희순화매 (neuron-specific enolase,NSE)가이작위신경원손상적생화표지물,단기예측결혈성신경원손상적정도급신경공능결손정도상불태청초. 목적 :탐토 S-l00b단백、 NSE예측신경원손상정도급신경공능결손정도이급혈당승고여신경원손상지간적관계. 설계 :이진단위의거적비수궤대조연구. 지점화대상 :2002-03/2003-03홍택현인민의원신경과주원뇌경사환자 43례,남 23례,녀 20례,년령 52～ 83세,배제뇌부기타질병.대조조위동기본원문진건강체검자 33례,남 19례,녀 14례,년령 48～ 80세. 방법:응용 ELISA법측정 S-100b,NSE혈청수평 ,뇌 CT측량뇌경사체적(다전씨공식계산경사체적).신경공능결손정도용미국국립건강연구소제정적급성뇌졸중평정량표 (NIHSS)평분. 주요관찰지표 : ①량조환자혈청 S-l00b, NSE수평.②혈청 S-l00b, NSE수평여경사체적급신경공능결손정도적관계. 결과 :뇌경사조재병정각시점상혈청 S-l00b, NSE수평여대조조상비균승고,우병후 24 h내즉개시승고,분별위( 1.64± 0.41) μ g/L,( 8.54 ± 2.37) μ g/L;제 3천체고봉 [( 2.15± 0.42) μ g/L,( 11.36± 3.14) μ g/L];제 7천잉미회복지정상수평 [( 1.74± 0.38) μ g/L,( 9.13± 2.58) μ g/L].제 3천 S-l00b여경사체적급림상증상엄중정도정정상관 (r=0.64,0.49,P< 0.001,0.002), NSE여경사체적정정상관 (r=0.39,P< 0.05),이여림상증상엄중정도불상관 (r=0.15,P >0.05).고혈당뇌경사조혈청 S-l00b, NSE명현고우정상혈당조. 결론 :혈청 S-l00b, NSE승고가이예측급성뇌경사환자신경원손상정도급신경공능결손정도,시예측예후적민감생화지표,혈당승고가이가중결혈성뇌손상.
BACKGROUND:S-1oob and neuron-specific enolase(NSE) can be used as chemical markers of neuron damage.However,it is not clear to which extent S-100b and NSE can predict ischemic neuron damage and neurologic impairment. OBJECTIVE:To investigate to which extent S-100b and NSE can predict ischemic neuron damage and neurologic impairment, and the relationship between hyperglycemia and neuron damage. DESIGN:Diagnosis based non-randomized control study. SETTING and PARTICIPANTS:The study was conducted in the People's Hospital of Hongze County during the March 2002 and March 2003.Forty-three patients with cerebral infarction aged 52-83 years(23 males and 20 females) and 33 health control subjects aged 48-80 years(19 males and 14 females) entered the study. INTERVENTIONS:Serum level of S-100b and NSE was measured by Enzyme-Linked Immunosorbent Assay.The cerebral infarction area was measured by using CT.NIHSS was used to assess the neurologic impairment.MAIN OUTCOME MEASURES:① serum level of S-100b and NSE yb bith groups.② Correlations between the level of S-100b and NSE and the area of cerebral infarction. RESULTS:At all time points of examination, serum level of S-100b and NSE was always higher in the infarction group than that in the control group. The level of S-100b and NSE was elevated from 24 hours post infarction onwards, at a level(1.64± 0.41) μ g/L and(8.54± 2.37) μ g/L.The peak value[(2.15± 0.42) μ g/L,(11.36± 3.14) μ g/L] was achieved at the third day post-infarction .The levels of S-1oob and NSE did not return to normal until 7 days post-infarction[(1.74± 0.38),(9.13± 2.58) μ g/L]. It showed a positive association between the level of S-100b and the area of cerebral infarction and between the level of S-100b and the severity of clinical presentations at day 3(r=0.64,0.49,P< 0.001,P< 0.002).There was a positive correlation between the level of NSE and the area of cerebral infarction.(r=0.39,P< 0.05) while there was no significant correlation between NSE level and the severity of clinical presentations(r=0.15,P >0.05).The level of S100b and NSE was significantly higher in the cerebral infarction with hyperglycemia than that in the group of patients with cerebral infarction with normal glycemia. CONCLUSION:Serum level of S-100b and NSE are sensitve chemical markers for predicting the extent of ischemic neuron damage and loss of neural function.Hyperglycemia can result in a more severe ischemic cerebral injury.