C反应蛋白与缺血性卒中

C反应蛋白（CRP）是一种急相蛋白，是机体潜在炎症的征兆，在机体天然免疫过程中发挥着重要作用。近年来的研究表明炎症与缺血性卒中有关。文章就CRP与缺血性卒中发病和预后之间的关系做了综述。     

急性后循环缺血性脑卒中患者血清淀粉样蛋白A和C反应蛋白浓度变化

目的观察急性缺血性脑卒中患者发病早期血清淀粉样蛋白A(SAA)、C反应蛋白(CRP)浓度变化。方法对88例前循环缺血性脑卒中患者、87例后循环缺血性脑卒中患者和88例健康对照者进行研究,采用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含量在前循环缺血性脑卒中组、后循环缺血性卒中组和对照组之间差异有统计学意义(P均0.05),SAA与CRP显著呈正相关。结论后循环缺血性卒中患者SAA、CRP水平较高,炎症反应较强。     

青年脑梗死患者C-反应蛋白的测定及其临床意义

脑梗死又称缺血性脑卒中，约占全部脑卒中的80％，是严重影响人类生存及生活质量的疾病之一。近年来，脑梗死发病有年轻化趋势，青年脑梗死的发病率逐年增高。国内报道青年卒中占全部卒中的13，4％。其病因除与老年患者有共同之处外，还有其自身特点。C-反应蛋白（C—reactive protein，CRP）是一种急相蛋白，是机体可能存在炎症的征兆。关于CRP与青年脑梗死之间的关系，国内外报道较少。本文通过测定青年脑梗死患者和正常人血浆CRP水平来探讨两者之间可能存在的关系，为临床青年脑梗死提供相关基础资料，现报道如下。     

C-反应蛋白与脑梗死

C-反应蛋白(CRP)是最敏感的急相蛋白指标.越来越多的证据表明,作为脑梗死的主要病因,动脉粥样硬化是一种慢性炎症过程.目前的研究发现,CRP水平及基因多态性与动脉粥样硬化和脑梗死有关.与冠心病相比,超敏CRP与缺血性卒中的关联性更为紧密.文章就CRP的生物学特征、影响CRP水平的因素、CRP水平和基因多态性与脑梗死的相关性的研究进展做了综述.     

C-反应蛋白与缺血性卒中

C-反应蛋白(CliP)是一种炎性标志物,其主要通过凝血纤溶、炎症和补体系统等发挥作用。已有大量研究证实CRP与缺血性卒中的风险性相关,并且在急性缺血性卒中后的循环中有高水平的表达。它的水平增高是不稳定性动脉粥样硬化疾病发生的危险信号,也预示着脑梗死患者的预后不良。降低ClIP水平有望可减少缺血性卒中的复发,改善其预后。     

不同年龄急性脑梗死患者血清超敏C反应蛋白检测的临床意义

超敏C反应蛋白（hs-CRP）是急性相蛋白，在感染、炎症或组织损伤时浓度迅速升高，它参与动脉粥样硬化（AS）及脑梗死的形成。hs—CRP浓度升高是缺血性卒中复发或死亡的危险因素，降低hs-CRP水平可减少缺血性卒中复发，改善预后.hs—CRP作为一种新的脑梗死的危险标志，通过检测其血浆基础水平可预测脑梗死的发生，但hs—CRP与患者年龄的关系目前尚未见有报道。本研究通过检测不同年龄及不同体积脑梗死患者血清hs—CRP水平，探讨脑梗死患者血清hs-CRP水平与年龄及梗死体积的关系。     

炎症标记物可预测卒中风险

据报道，检测炎症标记物可确定缺血性卒中高危患者。脂蛋白相关性磷脂酶A2（lipoprotein-associated phospholipase A2，Lp-PLA2）是一种由巨噬细胞分泌的促炎性酶。美国休斯顿贝勒大学医学院动脉粥样硬化和脂蛋白研究部的Ballantyne等对Lp—PLA2和C反应蛋白（C-reactive protein，CRP）水平与传统危险因素进行了评价以探讨其与缺血性卒中的关系。     

C-反应蛋白为伴心血管疾病患者罹发缺血性卒中的预测指标之一

业已证实，c-反应蛋白（CRP）为罹发心血管疾病的重要预测指标之一，但迄今关于其与高危患者继发缺血性卒中风险间关系尚罕有前瞻调查研究，本文意就CRP与先前伴有心血管疾病患者继发缺血性卒中风险间关系进行了大样本调查分析。     

C反应蛋白与脑出血

C反应蛋白(C-reactive protein,CRP)是一种对炎性反应非常敏感的急相反应蛋白.许多研究证实,CRP与缺血性卒中和动脉粥样硬化密切相关,但其与脑出血相关性的研究较少.文章就CRP与脑出血的关系进行了综述.     

C反应蛋白与缺血性卒中

近年研究发现,C反应蛋白除了作为炎性标记物外,其血浆基础水平还可预测缺血性卒中的发生,其浓度升高是缺血性卒中复发或死亡的危险因素。C反应蛋白主要通过凝血纤溶、炎症和补体系统等发挥作用,降低C反应蛋白水平有可能减少缺血性卒中的复发,改善预后。     

Association between blood pressure and C-reactive protein levels in acute ischemic stroke

Among patients with acute stroke, high blood pressure (BP) and higher levels of circulating C-reactive protein (CRP) at the entry are often associated with poor outcome, although the reason is unclear. If the link between BP and stroke outcome is indeed mediated by inflammatory response, one would expect to see positive associations between BP and CRP. In a prospective observational stroke data bank involving 535 first-ever ischemic stroke patients, we studied the association between BP and baseline concentrations of CRP within 24 hours after stroke onset. The association between BP components and the odds of having an elevated CRP level (> or =1.5 mg/dL) was assessed by logistic regression analysis. An increase in systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), or pulse pressure (PP) was significantly associated with an increase in the odds of having an elevated CRP level, independent of other associated study factors. For each 10 mm Hg increase in SBP, DBP, MAP, or PP, the odds of having a high CRP level increased by 72% (P<0.0001), 10% (P<0.0001), 21% (P<0.0001), and 10% (P<0.0001), respectively. When the same model was rerun, adjusting for all considered BP components, only SBP significantly increased the odds of an elevated CRP level by 77% (P<0.0001). Increased SBP was significantly associated with elevated levels of circulating CRP in ischemic stroke patients. These findings support a possible role of acute hypertension after stroke as an inflammatory stimulus contributing to ischemic brain inflammation.     

C反应蛋白基因-717A/G多态性与老年缺血性脑卒中的相关分析

目的探讨C反应蛋白(CRP)基因-717A/G多态性与老年缺血性脑卒中的关系。方法选择年龄≥60岁的缺血性脑卒中患者196例为脑卒中组,同期健康体检者197例为对照组,PCR-RFLP方法检测CRP基因型,并测血清高敏CRP(hs-CRP),logistic回归分析CRP与缺血性脑卒中的关系。结果脑卒中组hs-CRP显著高于对照组(p<0.01),两组CRP基因-717A/G多态性分布无统计学差异(P>0.05)。脑卒中组AA基因型患者hs-CRP浓度显著高于AG+GG基因型[2.30(0.95～3.45)mg/L vs 1.05(0.61～2.12)mg/L,P<0.01],但时照组不同基因型hs-CRP浓度无统计学差异。hs-CRP是老年缺血性脑卒中发生的独立危险因素。结论血清hs-CRP浓度升高与老年脑卒中相关。CRP基因-717A/G多态性与老年缺血性脑卒中无相关性,但与血清hs-CRP浓度有关。     

Depressive symptoms, inflammation, and ischemic stroke in older adults: a prospective analysis in the cardiovascular health study

OBJECTIVES: To investigate the mediator role of inflammation in any relationship between depressive symptoms and ischemic stroke.
DESIGN: Longitudinal prospective study.
SETTING: Review of medical records, death certificates, and the Medicare healthcare utilization database for hospitalizations.
PARTICIPANTS: Total of 5,525 elderly men and women aged 65 and older who were prospectively followed from 1989 to 2000 as participants in the Cardiovascular Health Study.
MEASUREMENTS: Depression symptom scores, inflammatory markers.
RESULTS: Greater depressive symptoms were associated with risk of ischemic stroke (unadjusted hazard ratio (HR)=1.32, 95% confidence interval (CI)=1.09–1.59; HR=1.26, 95% CI=1.03–1.54, adjusted for traditional risk factors). When a term for inflammation (C-reactive protein (CRP)) was introduced in the model, the HRs were not appreciably altered (unadjusted HR=1.31, 95% CI=1.08–1.58; adjusted HR=1.25, 95% CI=1.02–1.53), indicating that CRP at baseline was not a mediator in this relationship. In analyses stratified according to CRP levels, a J-shaped relationship between depressive symptoms and stroke was evident in the unadjusted analyses; in the fully adjusted model, only CRP in the highest tertile was associated with a higher risk for stroke in the presence of higher depressive symptoms scores.
CONCLUSION: The analyses from this prospective study provide evidence of a positive association between depressive symptoms and risk of incident stroke. Inflammation, as measured according to CRP at baseline, did not appear to mediate the relationship between depressive symptoms and stroke.     

C-reactive protein in atherosclerosis: A causal factor?

Atherosclerosis is considered a to be multifactorial disease driven by inflammatory reactions. The process of inflammation also contributes to the pathogenesis of acute atherothrombotic events. C-reactive protein (CRP) is an acute phase protein and its concentration in serum reflects the inflammatory condition of the patient. Levels of CRP are consistently associated with cardiovascular disease (CVD) and predict myocardial infarctions and stroke. Since CRP is present in the atherosclerotic lesion, it may actively contribute to the progression and/or instability of the atherosclerotic plaque. The role of CRP in inflammation and its causality in atherosclerosis are the subject of many investigations but are not yet fully elucidated. This review focuses on recently identified mechanisms by which CRP may modulate and evolve the process of atherosclerosis. We discuss the function of CRP and review the most recent evidence for an independent role of CRP in the development of atherosclerosis. Many studies suggest such a role, but a number of the described effects may be the result of contamination of the CRP preparations.     

C-reactive protein (CRP) in cerebro-vascular events.

BACKGROUND AND PURPOSE: C-reactive protein (CRP) is a useful prognostic factor in coronary heart disease. It has not been previously studied in acute cerebro-vascular events, which was the topic of the present study. METHODS: Patients admitted to the hospital for an acute cerebro-vascular event were prospectively investigated. C-reactive protein was determined nephelometrically. Infection or inflammation were excluded clinically and with an erythrocyte sedimentation rate <30 mm/h. Computed tomography or nuclear magnetic resonance imaging of the brain was performed. RESULTS: According to initial brain imaging and the clinical course the 138 patients were divided into five groups: 20 with transient ischemic attack, 20 with reversible neurological deficit lasting less than 2 weeks, 61 with completed stroke and restitution, 16 with stroke without restitution and 21 with cerebral hemorrhage. Median CRP values (range) were 3.2 (2.4-13.5), 3.3 (2.4-39.4), 4.2 (2.4-73. 4), 3.4 (3.2-44.0) and 3.5 (2.4-104.0 mg/l), respectively with no significant differences between groups in a non-parametric test (Kruskal-Wallis). Risk factors for vascular disease in general and stroke in particular had no visible influence on CRP levels. No relationship was found between time interval since onset of symptoms and CRP measurement, suggesting that an acute cerebro-vascular event has little influence on CRP values. CONCLUSION: CRP is not a useful marker to predict the outcome of an acute cerebro-vascular event on hospital admission. This is in contrast to acute coronary events.     

脑梗死患者血清C-反应蛋白水平变化及临床意义

目的观察脑梗死患者不同时期血清C-反应蛋白(CRP)的变化及病情的严重性和预后的关系,探讨脑梗死患者不同时期血清CRP水平的临床意义。方法对病程在2周以内的90例脑梗死患者在入院时及1周后进行血清CRP水平的测定,应用美国国立卫生研究院卒中量表及Barthel指数记分对入选患者在入院时及3个月后的神经功能缺损程度进行评分。结果入院时的CRP水平低于入院1周后的CRP水平,但其差异无显著意义。前者与患病当时及病后3个月神经功能缺损的严重程度显著相关,且这种相关性存在着量化的关系,而后者则无此相关。结论根据脑梗死患者病后2周内的CRP水平可以对病情的严重性及预后进行量化的判定。     

进展性缺血性脑卒中患者血清IL-6和C-反应蛋白水平的变化及临床意义

目的探讨白细胞介素6(IL-6)、C-反应蛋白(CRP)在进展性缺血性脑卒中发病中的作用。方法分别采用双抗体夹心酶联免疫法和透射比浊法测定80例急性脑梗死患者不同时期血清IL-6、CRP水平变化,并根据临床神经功能缺损程度量表(NDS)评分判断是否发展为进展性脑卒中。另选40名健康体检者作为对照组。结果 80例急性脑梗死患者中有27例(33.75%)于7d内发展为进展性脑卒中,其发病后第1、3、7、14天外周血IL-6、CRP水平明显高于无进展的脑梗死患者(P0.05),第14天与正常对照组比较差异无统计学意义(P0.05)。发病当天IL-6、CRP水平与人院时体温、血白细胞数、血浆纤维蛋白原呈正相关(相关系数r=0.87、0.66、0.51,P均0.01),IL-6、CRP是进展性脑卒中危险因素。结论急性脑梗死患者血清IL-6、CRP增高与进展性缺血性脑卒中密切相关,可能在进展性缺血性脑卒中的发病过程中具有重要作用,监测血清IL-6、CRP水平对于监测疾病活动情况及严重程度等具有重要意义。     

补体系统激活与急性缺血性脑血管疾病

目的　了解补体系统在人类急性缺血性脑血管疾病中的激活情况及其作用。方法　分别于脑卒中后4h、12h、2 4h、4 8h、72h、7d、14d、30d抽血,检测新发脑卒中病人血液中补体C3 的表达情况及C反应蛋白(CRP)的表达情况。相同的血液标本从对照组获得。结果　对照组和病例组CRP的表达在早期不存在显著性差异(P >0 . 0 5 ) ,CRP于卒中后2 4h显著增加,至4 8h仍增加明显,72h逐渐降低,至7d仍保持较高水平,30d基本恢复正常。C3 的浓度在卒中早期也不存在显著性差异(P >0 . 0 5 ) ,从72h开始显著增加,7d达高峰,14d已有降低,以后逐渐恢复正常。结论　急性缺血性脑血管疾病早期存在短暂的补体激活。     

Carotid plaque, stroke pathogenesis, and CRP: Treatment of ischemic stroke

Opinion statement  Inflammation is receiving increased attention as a cause of atherosclerosis and stroke. Several inflammatory biomarkers, and particularly high-sensitivity C-reactive protein (hsCRP), have been identified as likely predictors of the risk of a future stroke. In clinical settings, it has been consistently observed that higher concentrations of CRP are associated with larger brain infarcts, stroke severity, neurologic disability, and future vascular events. However, there is still controversy over the degree of risk conferred by elevated CRP concentrations. Some studies reported that the predictive value of CRP is moderate compared with classical risk factors and is only weakly related to cardiovascular damage after adjustment for traditional cardiovascular risk factors. CRP like many other hemostatic factors is an acute-phase protein and, therefore, it is not always clear whether its association with cerebrovascular disease reflects its contribution to atherothrombosis, its acute-phase condition, or both. Furthermore, the value of single measurements of CRP in patients with concurrent infection or other inflammatory conditions has not been established and reported data should be interpreted cautiously. Several drugs, especially hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), have been demonstrated to reduce hsCRP levels independently of their effects on plasma cholesterol. Recently, emerging therapies have been aimed at the control of blood pressure and inflammation in stroke patients. Whether a reduction of hsCRP levels could be beneficial to stroke patients remains to be clarified, and it is also unclear whether other drugs may be useful to lower hsCRP levels. More studies are needed before hsCRP becomes a routine part of the evaluation of stroke patients. This should also prompt the search for new agents directly blocking CRP actions.