超敏C反应蛋白与脑梗死病情演变的关系被引量：12

The relationship between high-sensitivity C-reactive protein and the progress of cerebral infarct

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摘要目的探讨早期超敏C反应蛋白(hs-CRP)含量与脑梗死病情进展的关系。方法对经头颅CT或磁共振成像(MRI)证实的急性缺血性脑梗死患者于发病24h内与7d采用化学发光免疫法测定hs-CRP,采用加拿大卒中量表对发病后48h病情发展变化进行评定,根据评分结果分为进展性与非进展性脑梗死两组。结果进展性脑梗死患者血清hs-CRP水平明显高于非进展性患者(P<0.01),发病后24h的血清hs-CRP水平高于7d的水平(P<0.01)。结论hs-CRP与脑梗死所致神经功能损害程度密切相关,早期检测可以为脑梗死的病情变化提供有用的信息。 Objective To study the relationship between high sensitive C-reactive protein （hs-CRP） and the progress of cerebral infarct. Methods The levels of hs-CRP were measured in 24 hours and seven days after using chemiluminescence immunoassay in the patients of acute isehemie stroke who were diagnosed hy CT or MRI. The disease progress were valued by Canadian neurologieal seale in 48 hours after eerebral isehemie stroke.The patients were divided into progressing group and no-progressing group. Result The serum levels of hs-CRP in the progressing group were significantly higher than that in the no-progressing group （P〈0.01）. The serum levels of hs-CRP in 24 hours were significantly higher than that after 7 days（P〈0.01 ）. Conclusion The level of hs-CRP is closely associated with the degree of the neurological damage caused by isehemie stroke. It can provide useful information for cerebral infarct.

作者黄宗青叶志中刘素英李爱东刘洪涛张志张小燕史少凤谭琦

机构地区广东医学院附属福田人民医院神经科广东医学院深圳风湿病研究所中山大学东华医院神经科

出处《中国药物与临床》 CAS 2006年第7期488-489,共2页 Chinese Remedies & Clinics

基金广东省医学科学技术研究基金资助项目(A2001798)

关键词脑梗死超敏C反应蛋白炎症进展性 Cerebral infarct High sensitive C-reactive protein Inflammation Progress

分类号 R743.33 [医药卫生—神经病学与精神病学]

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参考文献5

1孙国兵,赵薛旭,李作汉.脑缺血后炎症及其治疗对策[J].国外医学（脑血管疾病分册）,2005,13(3):194-198. 被引量：31
2Bassuk SS,Rifai N,RidKer PM.High-sensitivity C-reactive protein.Curr Prubl Cardiol,2004,29:439-493.
3Bartosik-Psujek H,Belniak E,Stelmasiak Z.Markers of inflammation in cerehral ischemia.Neurul Sci,2003,24:279-280.
4费丽萍,王少黎,朱永莲.C反应蛋白对老年冠心病患者高危事件的预测价值[J].中国药物与临床,2005,5(1):66-66. 被引量：4
5曹红,孙长凯,赵杰,许晶,陶定波,唐树良,汪秋艳,侯宇,刘新胜,黄爱莉.血清C反应蛋白水平与脑梗死病情及预后的关系[J].临床神经病学杂志,2005,18(6):422-424. 被引量：50

二级参考文献46

1彭华,郭洪志.急性脑梗死及其并发多脏器功能障碍综合征患者血清C反应蛋白水平的变化[J].临床神经病学杂志,2004,17(5):330-332. 被引量：58
2Schaller B, Graf R. Cerebral ischemia and reperfusion: the pathophysi-ologic concept as a basis for clinical therapy. J Cereb Blood Flow Metab, 2004, 24:351 -371.
3Clemens JA, Smalstig EB, Rash KS, et al. Global cerebral ischemia activates nuclear factor-κB prior to evidence of DNA fragmentation.Brain Res Mol Brain Res, 1997, 48:187 - 196.
4Stephenson D, Yin T, Smalstig EB, et al. Transcription factor nuclear factor-κB is activated in neurons after focal cerebral ischemia. J Cereb Blood Flow Metab, 2000, 20:592 -603.
5Yu Z, Zhou D, Bruce-Keller AJ, et al. Lack of the p50 subunit of κuclear factor-κB increases the vulnerability of hippocampal neurons to excitotoxic injury. J Neurosci, 1999, 19:8856 -8865.
6Botchkina GI, Geimonen E, Bilof ML, et al. Loss of NF-κB activity during cerebral ischemia and TNF cytotoxicity. Mol Med, 1999, 5:372 -381.
7Mattson MP, Culmsee C, Yu Z, et al. Roles of nuclear factor κB in neuronal survival and plasticity. J Neurochem, 2000, 74:443 -456.
8Sharp FR, Lu A, Tang Y, et al. Multiple molecular penumbras after focal cerebral ischemia. J Cereb Blood Flow Metab, 2000, 20:1011 - 1032.
9Nawashiro H, Martin D, Hallenbeck JM. Neuroprotective effects of TNF binding protein in focal cerebral ischemia. Brain Res, 1997,778:265 -271.
10Yang GY, Gong C, Qin Z, et al. Inhibition of TNFα attenuates infarct volume and ICAM-1 expression in ischemic mouse brain. Neuroreport, 1998, 9:2131 -2134.