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机构地区:[1]山东省淄博市临淄区人民医院神经内科,2554001 [2]青岛大学医学院附属医院神经内科
出 处:《临床内科杂志》2014年第4期259-261,共3页Journal of Clinical Internal Medicine
摘 要:目的 探讨大动脉粥样硬化型脑梗死患者颈动脉粥样硬化性斑块与血清淀粉样蛋白A(SAA)、C反应蛋白(CRP)水平的关系.方法 对88例大动脉粥样硬化型脑梗死患者(A组)、62例无症状颈动脉硬化患者(B组)和30例健康对照者(C组)进行研究,使用64排CT检测颈动脉斑块的形态、性质特征,酶联免疫吸附试验测定SAA含量,免疫散射比浊法检测CRP含量.结果 SAA、CRP含量在A、B和C组之间比较差异有统计学意义(P均<0.05),A组患者颈动脉斑块以软斑块(51.5%)为主,B组以钙化斑块(40.8%)为主,差异有统计学意义(P<0.05).Spenman分析显示,SAA与CRP呈正相关.结论 SAA、CRP参与炎症反应是影响颈动脉粥样斑块稳定性的重要原因,在大动脉粥样硬化型脑梗死发病机制中发挥作用.Objective To study the relationship between serum amyloid A protein(SAA) and Creactive protein(CRP) and destabilization of carotid plaque with large-artery atherosclerosis cerebral infarction.Methods Total 88 patients with large-artery atherosclerosis cerebral infarction (group A),62with asymptomatic carotid atherosclerosis(group B) and 30 normal controls(group C) were investigated.The character of carotid atherosclerotic plaque was detected by 64 slices computed tomography(CT).The serum levels of SAA were measured by ELISA.The serum levels of CRP were measured by immunonephelometric assay.Results There were significant differences among levels of Serum SAA,CRP levels in the group A,group B and group C (average P < 0.05).The distribution of plaque' s type was significant different between group A and group B,of which,the incidences of fatty plaque were 51.5% in the group A,calcified plaque were 40.8% in the group B(P < 0.05).Spearman correlation analysis showed SAA had the strongest correlation with CRP (P < 0.05).Conclusoin These results suggest that SAA and CRP participate in carotid plaque destabilization and piay a key role in the pathogenesis of large-artery atherosclerosis cerebral infarction.
关 键 词:大动脉粥样硬化型脑梗死 颈动脉粥样硬化斑块 血清淀粉样蛋白 C反应蛋白
分 类 号:R541.4[医药卫生—心血管疾病]
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