脑梗死患者血清可溶性血管细胞黏附分子1的变化

背景:在不同炎性和自身免疫性疾病患者中,血清内可溶性血管细胞黏附分子1水平增高,其变化可成为重要的免疫学功能检测指标,但其在急性脑梗死时的变化规律尚不清楚。目的:观察脑梗死血清可溶性血管细胞黏附分子1的变化及其临床意义,并与脑出血患者和正常人比较。设计:病例-对照分析。单位:解放军第三军医大学大坪医院野战外科研究所脑二科。对象:选择2002-05/2004-04解放军第三军医大学大坪医院野战外科研究所脑二科住院患者132例。其中脑梗死89例,根据梗死灶分为为大梗死组(n=25,>10cm3),中梗死组(n=31,4～10cm3),小梗死组(n=33,<4cm3);脑出血组43例。以30例健康人为正常对照组。方法:脑梗死患者分别在发病后分别在发病后24h、3,7和14d取血,脑出血患者分别在发病后24h和14d取血。3组均取静脉血4mL。采用双抗体夹心法测定所有受试者血清可溶性血管细胞黏附分子1水平。主要观察指标:①脑梗死不同病程中血清可溶性血管细胞黏附分子1水平的动态变化,并与其他两组比较。②不同大小梗死灶的脑梗死患者血清可溶性血管细胞黏附分子1水平比较。③脑梗死并发感染时血清可溶性血管细胞黏附分子1的变化。结果:162例进入结果分析。①脑梗死患者在发病24h血清可溶性血管细胞黏附分子1水平明显高于脑出血组和正常对照组(1184.5±68.3),(693.9±41.7),(576.1±39.8)μg/L,P<0.01]。梗死发生后24h至第7天呈上升趋势,7～14d呈下降趋势,但第14天脑梗死患者血清可溶性血管细胞黏附分子1仍明显高于脑出血组和正常对照组(P<0.01)。②大梗死灶组血清可溶性血管细胞黏附分子1水平明显高于中梗死灶组和小梗死灶组(1217.4±59.3),(1132.6±51.9),(983.7±54.2)μg/L,P<0.01]。③脑梗死后并发感染者在发病后3,7,14d血清可溶性血管细胞黏附分子1水平明显高于无感染(P<0.01)。结论:可溶性血管细胞黏附分子1参与了脑梗死的病理变化过程,可作为脑梗死时病情变化的监测指标。阻断其生成和表达为改善脑梗死的预后提供了新的思路。

Variation of soluble vascular cell adhesion molecule-1 in serum of patients with cerebral infarction

BACKGROUND: In subjects with different inflammatory and autoimmune diseases, soluble vascular cell adhesion molecule-1 (sVCAM-1) in sera increases, and its change may become an important monitoring index of immunological function, but its change rule has been unclear in acute cerebral infarction.OBJECTIVE: To observe the change of sVCAM-1 in sera of subjects with cerebral infarction and its clinical significance, and compare between the subjects with cerebral hemorrhage and normal population.DESIGN: A case controlled analysis.SETTING: Second Department of Brain, Research Institute of Surgery,Daping Hospital, Third Military Medical University of Chinese PLA.PARTICIPANTS: A total of 132 inpatients were selected from Second Department of Brain, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between May 2002 and April 2004. Among them, 89 subjects with cerebral infarction were classified into large infarction group (n=25,＞ 10 cm3), medium infarction group (n=31,4-10 cm3) and small infarction group (n=33, ＜ 4 cm3) respectively according to the size of infarct focus. There were 43 subjects in cerebral hemorrhage group, and 30 healthy persons were as normal control group.METHODS: Blood samples were isolated from subjects with cerebral infarction at hour 24, days 3, 7 and 14 after onset of the disease, while the blood samples were extracted from subjects with cerebral hemorrhage at hour24 and day 14 after the onset of the disease. 4 mL venous blood was obtained from the three groups. The serum concentration of sVCAM-1 was determined with double antibody sandwich method (DASM) in all the examinees.MAIN OUTCOME MEASURES: ①Dynamic change of the serum concentration of sVCAM-1 in the course of acute cerebral infarction, and compared with the other two groups. ②Comparison of the serum concentration of sVCAM-1 in different size of infarct focus. ③Change of the serum concentration of sVCAM-1 in acute cerebral infarction subjects complicated with infection.RESULTS: A total of 162 subjects were involved in the result analysis. ①The serum concentration of sVCAM-1 at the 24th hour after cerebral infarction was significantly higher in subjects with cerebral infarction than in subjects with cerebral hemorrhage group and normal control group (1 184.5±68.3) ,(693.9±41.7), (576.1±39.8) μg/L,P＜0.01].Serum sVCAM-1 in the cerebral infarction subjects increased from the 24th hour to the 7th day after infarction gradually, while from the 7th day to the 14th day decreased gradually. However, the serum sVCAM-1 in the cerebral infarction subjects at day 14 was still markedly higher than that in the cerebral hemorrhage group and the normal control group (P ＜ 0.01 ). ②The serum concentration of sVCAM-1 was significantly higher in the large cerebral infarction group as compared with medium and small cerebral infarction groups (1 217.4±59.3) ,(1 132.6±51.9) ,(983.7±54.2) μg/L,P ＜ 0.01]. ③The serum concentration of sVCAM-1 was significantly higher at days 3, 7and 14 in cerebral infarction subjects complicated with infection than in subjects without infection (P ＜ 0.01 ).CONCLUSION: The sVCAM-1 participates pathological change process of cerebral infarction, which can be regarded as monitoring index of cerebral infarction change. To block its production and expression can provide a new approach for improving the prognosis of cerebral infarction.