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1.
目的研究血清同型半胱氨酸(Hcy)与超敏C-反应蛋白(hs-CRP)在缺血性进展性脑卒中中的作用。方法对76例缺血性进展性脑卒中和80例完全性脑卒中患者的血清同型半胱氨酸和超敏C-反应蛋白水平进行测定,比较2组血清同型半胱氨酸和超敏C-反应蛋白水平。结果缺血性进展性脑卒中患者血清同型半胱氨酸和超敏C-反应蛋白水平显著高于同时期完全性脑卒中患者。结论缺血性进展性脑卒中的发生与血清同型半胱氨酸和超敏C-反应蛋白的水平有关系,血清同型半胱氨酸和超敏C-反应蛋白可作为预测及评价缺血性进展性脑卒中的重要指标之一。  相似文献   

2.
目的探讨D-二聚体与超敏C反应蛋白(hs-CRP)在老年进展性脑梗死患者病情评估中的应用价值。方法收集2012-06—2014-06我院收治的老年脑梗死患者60例,根据临床表现分为进展组(24例)和非进展组(36例),选择同期体检健康老年人30例作为对照组,检测并比较各组的D-二聚体和hs-CRP水平。结果脑梗死组D-二聚体及hs-CRP均显著高于对照组和非进展组(P0.05)。结论血清D-二聚体与hs-CRP检测对老年进展性脑梗死的早期诊断及病情评估具有重要意义,值得推广应用。  相似文献   

3.
目的探讨血D-二聚体、纤维蛋白原、超敏C反应蛋白与脑梗死后非痴呆性血管性认知障碍的关系。方法测定50例非痴呆性血管性认知障碍患者及50例健康对照组的D-二聚体、纤维蛋白原、超敏C反应蛋白水平。采用蒙特利尔认知评估(MoCA)量表对50例非痴呆性血管性认知障碍患者及50例健康对照组进行评估。结果非痴呆性血管性认知障碍患者D-二聚体水平是(0.85±0.26)mg/L,纤维蛋白原水平是(3.10±0.85)g/L,超敏C反应蛋白水平是(11.06±4.15)mg/L。健康对照组的D-二聚体水平是(0.30±0.12)mg/L,纤维蛋白原水平是(2.30±0.31)g/L,超敏C反应蛋白水平是(3.83±0.76)mg/L。非痴呆性血管性认知障碍患者的D-二聚体、纤维蛋白原、超敏C反应蛋白均高于健康对照组,差异有统计学意义(P0.05)。相关性分析显示D-二聚体、纤维蛋白原、超敏C反应蛋白与MoCA评分呈正相关(P0.05)。结论血D-二聚体、纤维蛋白原、超敏C反应蛋白的升高可能是非痴呆性血管性认知障碍的危险因素,降低血D-二聚体、纤维蛋白原、超敏C反应蛋白水平可能可以延缓非痴呆性血管性认知障碍进展为血管性痴呆。  相似文献   

4.
目的探讨同型半胱氨酸、高敏C反应蛋白及D-二聚体在急性脑梗死患者中的变化及意义。方法选择急性脑梗死180例为脑梗死组,以梗死灶大小为依据,分为大面积亚组、中面积亚组以及小面积亚组。以临床神经功能缺损严重程度为依据分为重度亚组、中度亚组以及轻度亚组;选择180例同期体检健康者为健康对照组;监测及对比2组血清同型半胱氨酸、高敏C反应蛋白及D-二聚体的水平。结果与健康对照组比较,脑梗死组患者血清同型半胱氨酸、高敏C反应蛋白及D-二聚体水平均明显升高,差异有统计学意义(P0.05);大面积亚组患者血清的含量大于中面积亚组,中面积亚组的含量大于小面积亚组(P0.05)。同型半胱氨酸、高敏C反应蛋白及D-二聚体在重度亚组患者血清的含量大于中度亚组,中度亚组的含量大于轻度亚组(P0.05)。结论急性脑梗死的发生和发展与同型半胱氨酸、高敏C反应蛋白及D-二聚体具有十分密切的关系,在判断患者疾病的严重程度时对其发生、发展的检测具有十分重要意义,且在临床治疗方面具有较好的指导作用。  相似文献   

5.
目的探讨血清高敏C反应蛋白、同型半胱氨酸及颈动脉粥样硬化与进展性脑梗死发生的相关性。方法应用免疫比浊法和荧光偏振免疫分析法对80例进展性脑梗死患者、98例非进展性脑梗死患者进行血清高敏C反应蛋白、同型半胱氨酸水平测定、颈动脉彩色多普勒超声检查,并与90例健康体检者作比较。结果进展性脑梗死组血清高敏C反应蛋白、同型半胱氨酸及颈动脉IMT最高,对比非进展性脑梗死组和健康对照组,差异有统计学意义(P<0.05);且进展性脑梗死组血清高敏C反应蛋白、同型半胱氨酸与颈动脉IMT呈显著正相关(r=0.6183,r=0.5862,P<0.01)。结论血清高敏C反应蛋白、同型半胱氨酸水平越高,颈动脉粥样硬化越重,容易促使梗死进展加重。  相似文献   

6.
目的研究超敏C反应蛋白和D-二聚体在进展性脑梗死中的诊断价值及应用。方法将96例急性脑梗死患者分为2组,其中46例进展性脑梗死患者作为进展组,50例稳定性脑梗死患者作为稳定组,另选50例非心脑血管疾病患者作为健康对照组。进展组和稳定组患者均行西医常规治疗,与健康对照组患者血清中hs-CRP和D-D水平对比。采用美国国立卫生研究院卒中量表(NIHSS)对进展组和稳定组患者第48小时的神经功能缺损进行评分,并与患者第48小时的hs-CRP和D-D的水平进行相关性分析。比较进展组与稳定组患者入院时、入院24h、48h血清中hs-CRP和D-D水平。结果 (1)随着入院时间的延长,进展组患者hs-CRP和D-D水平逐渐升高,与同时期稳定组患者相比,差异有统计学意义(P0.05)。(2)48h的hs-CRP和D-D的水平进行相关性分析显示,进展性脑梗死患者的神经功能缺损均为卒中中型和重型,与hs-CRP和D-D的水平呈正相关。(3)经治疗,进展组和稳定组患者血清中hs-CRP和D-D水平均显著下降;治疗后进展组和稳定组hsCRP水平有显著差异,D-D水平接近,差异无统计学意义。结论进展性脑梗死患者血清中超敏C反应蛋白和D-二聚体水平较稳定性脑梗死患者和健康受检者均显著偏高,在进展性脑梗死的临床诊断及病情判断中具有重要作用。  相似文献   

7.
目的观察进展性脑梗死患者血清同型半胱氨酸(Hcy)、超敏C反应蛋白(hs-CRP)的变化并探讨其临床意义。方法根据临床特征,将108例急性脑梗死患者分为进展组(n=52)和非进展组(n=56),分别检测其血清Hcy、hs-CRP水平。结果进展性脑梗死组患者血清Hcy、hs-CRP水平显著高于非进展组(P<0.05)。结论检测血清Hcy、hs-CRP水平对于进展性脑梗死的防治有重要意义。  相似文献   

8.
目的 探讨急性脑梗死患者血清纤维蛋白原、D-二聚体与颈动脉粥样硬化斑块的关系. 方法 选择解放军第三医院神经内科自2009年4月至2011年4月收治的120例急性脑梗死患者(脑梗死组)、同期单纯颈动脉粥样硬化而无脑梗死患者60例(颈动脉粥样硬化组)和健康体检者80例(正常对照组)作为研究对象,采用双抗体夹心法测定血清D-二聚体含量,全自动血凝仪测定纤维蛋白原含量,颈动脉彩色多普勒超声检测患者颈动脉粥样硬化斑块和颈动脉内一中膜厚度(IMT)值. 结果 脑梗死组、颈动脉粥样硬化组及正常对照组血清纤维蛋白原、D-二聚体水平及颈动脉IMT值依次降低,差异有统计学意义(P<0.05);进展性卒中患者血清纤维蛋白原、D-二聚体水平高于非进展性卒中患者,差异有统计学意义(P<0.05);随着动脉粥样硬化严重程度的升高,脑梗死患者血清纤维蛋白原及D-二聚体水平逐渐升高,差异有统计学意义(P<0.05);脑梗死患者血清纤维蛋白原、D-二聚体水平均与颈动脉粥样硬化严重程度呈正相关关系(r=0.426,P=0.006; r=0.535,P=0.001). 结论 纤维蛋白原及D-二聚体参与了急性脑梗死的发生发展,与病情进展密切相关.二者做为急时相反应物参与动脉粥样硬化的发生机制提示,相对于高凝状态,动脉粥样硬化的形成与慢性炎症反应关系更为密切.  相似文献   

9.
目的了解急性脑梗死患者体内C反应蛋白与D-二聚体的含量,研究此两种物质与患者颈部血管斑块的相关性。方法选择在我院治疗的急性脑梗死患者38例为实验组;另外选择在我院进行体检的健康人38例为对照组。观察2组体内C反应蛋白与D-二聚体指标并进行比较。结果对照组体内C反应蛋白与D-二聚体含量明显低于实验组,差异有统计学意义(P0.05)。C反应蛋白含量的相关系数γ值明显大于颈部血管斑块数量的相关系数γ值,差异有统计学意义(P0.05)。结论 C反应蛋白、D-二聚体水平与急性脑梗死患者颈部血管斑块数目之间具有相关性,为临床提供准确的诊断结果和有效的治疗方法。  相似文献   

10.
目的分析脑梗死患者血浆活化部分凝血酶时间(APFF)、纤维蛋白原(FIB)、D-二聚体、超敏C反应蛋白(hsCRP)水平及相关性。方法选择2013年80例急性脑梗死患者为观察组,根据观察组患者年龄、性别匹配选取40例正常志愿者为对照组,观察2组患者血浆APTT、FIB、D-二聚体和hs-CRP水平,分析脑梗死患者各观察指标的相关性。结果观察组患者血浆APTT较对照组明显缩短,血浆FIB、D-二聚体和hs-CRP水平较对照组明显增高,2组比较差异有统计学意义(t1=15.48,t2=2.09,t3=129.35,t4=11.08,P0.05);观察组患者血浆D-二聚体水平与hs-CRP水平呈显著正相关(r=0.533,P0.05),血浆FIB水平与D-二聚体呈显著正相关(r=0.312,P0.05)。结论脑梗死患者较正常人群血浆FIB、D-二聚体和hs-CRP水平增高,APTT缩短,FIB与D-二聚体、D-二聚体与hs-CRP水平呈正相关。  相似文献   

11.
目的 探讨急性进展性脑梗死患者颈动脉粥样硬化斑块情况及血浆D-二聚体动态变化.方法 选择急性进展性脑梗死患者102例,随机抽取同期非进展性脑梗死患者100例,以及同期健康体检者100例,分别检查血浆D-二聚体水平及颈动脉彩超,了解颈动脉内-中膜厚度及斑块硬化程度,比较3组颈动脉内-中膜厚度,观察进展组与非进展组患者颈动脉斑块检出率及血浆D-二聚体水平动态变化.结果 进展组、非进展组、健康体检组颈动脉内-中膜厚度值依次降低(P〈0.01),进展组颈动脉斑块检出率明显高于非进展组(P〈0.01),随着颈动脉斑块严重程度,D-二聚体水平有升高趋势;进展组与非进展组血浆D-二聚体水平在治疗前、治疗第7天时均有明显差异(P〈0.01),第14天时2组比较无明显差异(P>0.05).结论 D-二聚体参与了急性进展性脑梗死的发生发展,与病情进展密切相关,结合颈动脉彩超检查,更进一步预测病情,判断预后.  相似文献   

12.
目的探讨血浆D-二聚体及血清超敏C反应蛋白表达的高低与脑损伤后进展性出血性损伤(PHI)发生的关系。方法以新入院180例颅脑外伤病例为研究对象,分别检测单纯性闭合性颅脑外伤患者血浆D-二聚体浓度及血清中超敏C反应蛋白(hs-CRP)的表达情况,并与87例对照组进行比较。受试者工作特征(ROC)曲线计算血浆D-二聚体及hs-CRP浓度与PHI发生的关系。结果脑外伤患者中PHI组的D-二聚体的平均浓度为6.49±3.45mg/L,非PHI组D-二聚体的平均浓度为4.16±3.15mg/L,两组间差异有统计学意义;且D-二聚体及hs.CRP的值与脑外伤患者的预后评分成正相关。结论检测脑外伤患者血中的D-二聚体及hs—CRP的浓度表达有助于预测或早期诊断PHI的发生。  相似文献   

13.
超敏C-反应蛋白与脑梗死关系的研究   总被引:5,自引:2,他引:3  
目的 研究血清中超敏C-反应蛋白(hs-CRP)与脑梗死发生的关系.方法 采用免疫比浊法测定血清中hs-CRP浓度.结果 与健康对照组比较,脑梗死组血清中hs-CRP浓度差异有统计学意义(P<0.01).首发和复发脑梗死组急性期患者血清中hs-CRP浓度比较无显著性差异(P>0.05).重度神经功能缺损患者和中度以及轻度神经功能缺损患者血清hs-CRP 浓度比较有显著性差异(P<0.05);脑梗死患者血清hs-CRP 浓度与神经功能缺损程度呈正相关( r = 0.48, P<0.05).结论 hs-CRP可能是导致脑梗死的独立危险因素之一,血清hs-CRP检测对于脑梗死的临床诊断和病情评估具有重要意义.  相似文献   

14.
BackgroundSome researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.ObjectiveTo investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis.DesignContrast observation between two groups.SettingDepartment of Neurology, Zhenzhou Hospital, Shenyang Medical College.ParticipantsA total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent.Methods
Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric immunoassay (PENIA) were used for quantitative detection of serum high-sensitivity C-reactive protein.
Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound (Siemens Company, USA) was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria: Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 mm was regarded as normal; 0.9 mm < intima media thickness ≤ 1.2 mm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 mm and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types: steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady.Main outcome measuresThickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups.ResultsAll 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis.
Comparisons of level of high-sensitivity C-reactive protein: Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [(4.66±1.55) mg/L] than the control group [(3.49±1.24) mg/L, t =2.541, P < 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group (P > 0.05).
Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [(8.16±2.42) mg/L] than patients with normal tunica media [(4.66±1.55) mg/L, t =4.132, P < 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [(12.08±3.85) mg/L] than patients with normal tunica media (t =5.994, P < 0.01) and thickening tunica media (t =4.197, P < 0.01).
Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [(13.54±2.62) mg/L] than patients with steady carotid plaque [(8.61±3.71) mg/L, t =2.002, P < 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction.ConclusionSerum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.  相似文献   

15.
目的探讨复发—缓解型多发性硬化(RRMS)患者血清中C反应蛋白(CRP)、同型半胱氨酸(Hcy)、维生素B_(12)及叶酸水平,并探讨上述因子与RRMS发病的关系。方法选取21例急性期的RRMS患者作为RRMS组,21例同期住院的神经性头痛患者作为对照组,测定其血清中CRP、Hcy、叶酸及维生素B_(12)水平,并比较两组之间的水平差异;并比较RRMS组中不同性别、不同残疾程度组之间的血清CRP、Hcy、叶酸及维生素B_(12)水平。结果 RRMS组患者血清中CRP及Hcy水平高于对照组,而叶酸及维生素B_(12)水平低于对照组,(P0.05)。而扩展残疾状况评分量表评分(EDSS)4分的RRMS患者血清中Hcy及CRP水平高于EDSS评分≤4分的RRMS患者,(P0.05)。结论血清中高CRP、Hcy水平可能与RRMS发病及残疾程度有关。  相似文献   

16.
目的探讨神经节苷脂对急性脑梗死患者血清和肽素及N末端脑钠素原的影响。方法将82例急性脑梗死患者随便分为实验组和对照组,每组41例。2组均接受常规治疗,在此基础上,对照组给予胞二磷胆碱治疗,实验组给予神经节苷脂治疗。对比2组血清和肽素水平、N末端脑钠素原水平、同型半胱氨酸水平、超敏C反应蛋白水平及临床疗效。结果治疗后,实验组血清和肽素水平明显低于对照组(P0.01);实验组N末端脑钠素原水平显著低于对照组(P0.01);实验组同型半胱氨酸水平及超敏C反应蛋白水平均明显低于对照组(P0.05);实验组总有效率92.68%,显著高于对照组的75.61%(P0.05)。结论神经节苷脂可有效降低急性脑梗死患者的血清和肽素及N末端脑钠素原水平,改善炎症反应,具有良好的临床疗效。  相似文献   

17.
In this hospital-based cross-sectional study we investigated differences in the levels of serum atherosclerotic and fibrinolytic markers and the prevalence of metabolic syndrome (MS) among patients with four subtypes of cerebral infarctions. Blood samples were taken from 171 cerebral infarction inpatients to determine the levels of high-sensitivity C-reactive protein, serum total homocysteine, serum plasminogen activator inhibitor 1 and lipoprotein a. Subjects were also screened for MS. Atherothrombotic infarction was most prevalent, followed by lacunar and embolic infarction. The median length of hospital stay was longest for embolic infarcts. There were no statistically significant differences in serum marker concentrations. The proportion of MS varied significantly among the subtypes, and was highest among patients with embolic infarctions with the lowest high density cholesterol levels. MS was most prevalent among patients having undergone embolic events that are reported to have the worst prognoses. Further epidemiologic studies are needed to better understand the characteristics and differences in the etiology of cerebral infarction subtypes.  相似文献   

18.
目的探讨高迁移率族蛋白B1(HMGB1)及不规则趋化因子(FKN)在进展性脑梗死中的可能作用机制。方法用酶联免疫吸附试验(ELISA)法检测急性脑梗死患者不同时期血清HMGB1及FKN水平变化,根据斯堪的纳维亚脑卒中量表(scandinavian stroke scale,SSS)评分分为进展组和非进展组。根据梗死体积将180例患者分为大梗死灶组、中梗死灶组、小梗死灶组。另纳入30例健康体检者作为对照组。结果 180例急性脑梗死患者中有35例(19.44%)发展为进展性脑梗死。进展组SSS基线评分低于非进展组,差异有统计学意义(P0.05)。进展性组患者发病后1 d、7 d、14 d血清HMGB1、FKN水平高于非进展组和对照组,有统计学意义(P0.05)。梗死灶体积大则血清HMGB1、FKN水平高(P0.05)。结论血清HMGB1、FKN增加可能通过增加炎症反应促进动脉粥样硬化形成和进展,加重脑组织损伤,导致脑梗死患者病情进展。  相似文献   

19.
补体系统激活变化趋势与急性脑梗死关系的临床研究   总被引:2,自引:1,他引:1  
目的动态观察脑梗死患者发病后1月内补体C3和超敏C-反应蛋白(Hs-CRP)含量的变化趋势及其与梗死灶体积、神经功能缺损程度的相关性。方法分别在发病后12、24、48、72h、7、14d和1月,采用免疫散射比浊法测定56例脑梗死患者补体C3和Hs-CRP含量,观察并记录所有病例的病灶体积、神经功能缺损评分。同时选取46例健康受试者作为对照组。结果(1)病例组补体C3和Hs-CRP在不同测定时点浓度不同(F=163.456和97.622,P〈0.001),表现为发病12h时补体C3和Hs-CRP浓度即有所增加,此后随着发病时间的增加浓度呈上升趋势,至发病7d达峰值,随后逐渐下降,至1月时趋于正常。(2)病例组血清C3、Hs-CRP的浓度于发病后12、24、48、72h、7、14d均高于对照组(P〈0.05),1月时2组比较无明显差异(P〉0.05);(3)病例组血清补体C3、Hs-CRP水平与梗死灶体积有关系,体积越大,血清补体C3、Hs-CRP水平越高。大、中病灶组血清补体C3、Hs-CRP浓度明显高于小病灶组(P〈0.05);(4)病例组血清补体C3、Hs-CRP水平与神经功能缺损程度有关系,神经功能缺损越重,血清补体C3、Hs-CRP水平越高。重、中度神经功能缺损组血清补体C3、Hs-CRP浓度明显高于轻度缺损组(P〈0.05)。结论(1)急性缺血性脑卒中患者在急性期C3、Hs-CRP含量增高,存在补体系统激活。补体激活可能参与了急性缺血性脑卒中后脑组织的炎症过程;(2)急性缺血性脑卒中患者C3、Hs-CRP与脑梗死体积、神经功能缺损程度之间有密切关系,反映卒中时脑组织的损害程度。  相似文献   

20.
目的:动态观察急性缺血性脑血管病(脑梗死)患者发病后半月内补体C3和超敏C-反应蛋白(Hs-CRP)含量的变化及其与梗死灶体积、神经功能缺损程度的相关性。方法:分别在发病后12小时、24小时、48小时、72小时、7天、15天,采用免疫散射比浊法,测定40例脑梗死患者补体C3和Hs-CRP含量,并选取30例健康受试者作为对照。观察并记录患者的病灶体积、神经功能缺损评分。结果:脑梗死组血清C3、Hs-CRP的浓度于发病后12小时、24小时、48小时、72小时、7天均高于对照组,P<0.05;15天两组比较无明显差异,P>0.05。脑梗死组血清补体C3、Hs-CRP水平与梗死灶体积有关,体积越大,血清补体C3、Hs-CRP水平越高。大、中病灶组血清补体C3浓度、Hs-CRP浓度明显高于小病灶组,P<0.05。脑梗死组血清补体C3、Hs-CRP水平与神经功能缺损程度有关,缺损越重,血清补体C3、Hs-CRP水平越高。重、中度神经功能缺损组血清补体C3、Hs-CRP浓度明显高于轻度缺损组,P<0.05。结论:C3、Hs-CRP浓度在脑梗死发生发展中发挥重要作用,其升高与脑梗死体积和神经功能缺损程度有一定的相关性。  相似文献   

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