血清IMA、MCP-1、CD163表达水平与急性冠脉综合征患者病情严重程度的关系研究
详细信息    查看全文 | 推荐本文 |
摘要
目的研究血清IMA、MCP-1、CD163表达水平与急性冠脉综合征患者病情严重程度的关系。方法本研究的研究对象以2017年1月至2018年1月在我院诊治的100例ACS患者为观察组,同期100例非缺血性胸痛患者为对照组,分别对两组患者的血清IMA、MCP-1、CD163表达水平进行对比,对观察组患者的以上指标进行多因素相关回归分析。结果观察组患者的IMA、MCP-1、CD163水平与Gensini评分、血浆NT-proBNP水平明显高于对照组,差异具有统计学意义(P <0.05),观察组患者随着病情的加重,其血清IMA、MCP-1、CD163水平与Gensini评分、血浆NT-proBNP水平呈明显上升趋势;患者血清IMA、MCP-1、CD163这三个指标都是水平越高、Gensini评分越高,血浆NT-proBNP水平越高,呈现正相关;血清IMA、血清MCP-1、血清CD163均为ACS的独立危险因素,而血清HDL为ACS的保护因素。结论 IMA、MCP-1、CD163与NT-proBNP水平和Gensini评分均呈正相关关系,与HDL均是ACS的独立危险因素,有望成为ACS病情评估和预后预测的指标。
        Objective To study the relationship between serum levels of IMA,MCP-1 and CD163 and severity of acute coronary syndrome. Methods The subjects of this study were 100 ACS patients who were treated in our hospital from January,2017 to January,2018,and 100 non-ischemic chest pain patients during the same period as the control group. The levels of serum IMA,MCP-1 and CD163 were compared between the two groups,and the observation group were analyzed by multivariate regression analysis. Results The levels of IMA,MCP-1 and CD163 in the observation group were significantly higher than those in the control group(P < 0.05), the same as Gensini score and plasma NT-proBNP(P < 0.05). The higher the serum IMA,MCP-1 and CD163 levels,the higher the Gensini score and the plasma NT-proBNP level,showing a positive correlation. Serum IMA,MCP-1 and CD163 were all independent risk factors for ACS,while serum HDL was the protective factor for ACS. Conclusion IMA,MCP-1,CD163 were positively correlated with NT-proBNP content and Gensini score.Both IMA,MCP-1,CD163 and HDL were independent risk factors for ACS,and could be used as indicators for evaluating the disease condition and to predict the prognosis of ACS.
引文
[1]李志强,王春燕,石毅,等.慢性心力衰竭患者血红蛋白清道夫受体CD163的表达及意义[J].岭南心血管病杂志,2018,24(1):60-65.
    [2] PEREZ-SANTIAGO J,SCHRIER R D,OLIVEIRA M F D,et al.Cell-free mitochondrial DNA in CSF is associated with early viral rebound,inflammation,and severity of neurocognilive deficits in HIV infection[J]. J Neurovirol,2016,22(2):191-200.
    [3] ALVARADOVAZQUEZ P A. BERNAL L, PAIGE C A, et al.Macrophage-specific nanotechnology-driven CD 163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions[J]. Immunobiology, 2017,222(8-9):900-912.
    [4] TABATABAEI P, VISSE E, BERGSTROM P, et al. Radiotherapy induces an immediate inflammatory reaction in malignant glioma:a clinical microdialysis study[J]. J Neurooncol, 2017,131(1):83-92.
    [5]向定成.曾定尹,霍勇.冠状动脉痉挛综合征诊断与治疗中国专家共识[J].中国介人心脏病学杂志,2015,23(4):181-186.
    [6] YADAV A, BETTS M R,COLLMAN R G. Statin modulation of monocyte phenotype and function:implications for HIV-1 associated neurocognitive disorders[J]. J Neurovirol,2016,22(5):1-13.
    [7] KARABABA A,GROOS-SAHR K.ALBRECHT U,et al. Ammonia Attenuates LPS-induced upregulation of pro-inflammatory cytokine mRNA in co-cultured astrocytes and microglia[J]. Neurochem Res,2017,42(3):737-749.
    [8] MATSUTANI T,TAMURA K, KUTSUKAKE M,et al. Impact of pioglitazone on macrophage dynamics in adipose tissues of cecal ligation and puncture treated mice[J]. Biol Pharm Bull,2017,40(5):638-644.
    [9] PEREZ-SANTIAGO J,OLIVEIRA M F D, VAR S R, et al.Increased cell-free mitochondrial DNA is a marker of ongoing inflammation and better neurocognitive function in virologically suppressed HIV-infected individuals[J]. J Neurovirol, 2017,23(2):283-289.
    [10]蔡会欣,曹辉彩,张志强,等.缺血修饰清蛋白在冠心病患者经皮冠状动脉介入术前后的水平变化[J].检验医学与临床,2016,13(17):2510-2512.
    [11]曾跃红,胡景云,周勇军,等.缺血修饰白蛋白在冠状动脉综合征中肌钙蛋白阴性患者中的应用研究[J].临床医药文献电子杂志,2017,4(9):1626-1 627.
    [12]紫净,余陆娇,张子新.急性冠状动脉综合征患者缺血修饰白蛋白水平与冠状动脉病变程度的相关性研究[J].中国医科大学学报,2017,46(11):1009-1012.
    [13]马心超.血清Vaspin、Gas-6、IMA水平联合检测在冠状动脉粥样性心脏病患者病情评估中的应用价值[J].中国卫生工程学,2017(6):747-750.
    [14]吴阳,张东辉,方卫华.IMA和MMP-3与心电图ST-T改变患者冠状动脉病变的相关性研究[J].慢性病学杂志,2017(8):851-854.
    [15]李青,刘昕,林琳,等.可溶性CD163在急性冠脉综合征患者血清中的表达及意义[J].第三军医大学学报,2016,38(14):1654-1658.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700