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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。
BACKGROUND: In patients with different inflammatory and autoimmune diseases, serum soluble vascular cell adhesion molecule-1 levels increase, which may be an important indicator of immunological function, but its variation in acute cerebral infarction is unclear . Objective: To observe the changes and clinical significance of serum soluble vascular cell adhesion molecule-1 in patients with cerebral infarction and to compare with those of patients with cerebral hemorrhage and normal subjects. Design: Case-control analysis. Unit: Second Military Medical University, Daping Hospital, Institute of Field Surgery, Brain Diseases. PARTICIPANTS: A total of 132 inpatients with cerebrovascular disease were selected from the Field Surgery Institute, Daping Hospital, Third Military Medical University, People’s Liberation Army from May 2002 to April 2004. Among them, 89 cases of cerebral infarction were divided into infarction group (n = 25,> 10cm3), middle infarction group (n = 31.4 ~ 10cm3), small infarction group (n = 33, Bleeding group of 43 cases. 30 healthy people as normal control group. Methods: The patients with cerebral infarction were respectively taken blood at 24h, 3,7 and 14d after onset, and the patients with cerebral hemorrhage were taken blood at 24h and 14d after onset respectively. 3 groups were taken venous blood 4mL. Serum levels of soluble vascular cell adhesion molecule 1 were measured by double antibody sandwich method in all subjects. MAIN OUTCOME MEASURES: ① The dynamic changes of serum soluble vascular cell adhesion molecule-1 in different stages of cerebral infarction were compared with those of the other two groups. ② Comparison of serum soluble vascular cell adhesion molecule-1 levels in patients with cerebral infarction of different sizes. ③ Changes of serum soluble vascular cell adhesion molecule 1 in patients with cerebral infarction complicated by infection. Results: 162 cases entered the result analysis. (1) The levels of serum soluble vascular cell adhesion molecule-1 in patients with cerebral infarction at 24 hours after onset were significantly higher than those in cerebral hemorrhage and normal controls [(1184.5 ± 68.3), (693.9 ± 41.7), (576.1 ± 39.8) μg / L, P <0.01 ]. However, the level of serum soluble vascular cell adhesion molecule 1 in patients with cerebral infarction on the 14th day was still significantly higher than that of the cerebral hemorrhage group and the normal control group (P <0.01). ② The levels of serum soluble vascular cell adhesion molecule-1 in the large infarction group were significantly higher than those in the middle infarction group and the small infarction group [(1217.4 ± 59.3), (1132.6 ± 51.9), (983.7 ± 54.2) μg / L, P <0.01 ]. ③The level of serum soluble vascular cell adhesion molecule-1 on 3, 7 and 14 days after onset of cerebral infarction was significantly higher than that on no infection (P <0.01). Conclusion: Soluble vascular cell adhesion molecule 1 participates in the process of pathological changes of cerebral infarction and can be used as a monitoring indicator of the changes of cerebral infarction. Blocking its generation and expression provides a new way to improve the prognosis of cerebral infarction.