D-二聚体及纤维蛋白原与进展性缺血性脑卒中的相关性

目的观察进展性缺血性脑卒中患者的D-二聚体(D-dimer)纤维蛋白原(Fib)动态变化,探讨其在进展性缺血性脑卒中早期诊断价值。方法急性脑梗死患者70例,分为进展性组35例和完全组35例,并选择35例门诊健康体检者做对照组,用全自动血凝仪分别测定3组的第1天、第2天、第3天、第7天、第14天D-dimer和Fib的水平。结果进展性卒中组血浆Fib水平在发病24 h、第2天、第3天、第7天均明显高于完全性卒中组和对照组(P<0.01),发病24 h内血浆Fib水平开始升高,第3天时达最高峰,第7天时下降,第14天时降至正常。进展性卒中组血浆D-dimer水平在发病24 h、第2天、第3天、第7天较完全性卒中组和对照组升高更明显(P<0.01),发病24 h开始升高,于第7天时达最高峰,第14天时迅速降至正常。结论 D-dimer和Fib水平增高与进展性脑梗死的发生相关,有助于早期预测进展性卒中的发生。     

脑出血患者急性期外周血纤溶状态及凝血功能的变化

目的 探讨脑出血(ICH)患者急性期外周血纤溶状态及凝血功能的变化.方法 检测65例ICH患者(ICH组)发病<24 h、第3 d及第7 d时外周血小板(PLT)数量、体积(MPV)、血浆纤维蛋白原(Fib)及D-二聚体(D-D)水平,并与53名正常对照者(NC组)比较.结果 与NC组比较,ICH组发病<24 h及第3 d 时PLT数量明显减少,血浆D-D 水平显著升高(均P<0.01),第7 d时均恢复至正常水平;发病后各时间点MPV明显增大(均P<0.01);发病第3 d、第7 d时血浆Fib水平显著升高(均P<0.01).结论 ICH患者急性期存在纤溶活性增高及凝血功能下降的倾向,动态观察上述指标的变化,可指导临床药物治疗.     

缺血性卒中后血浆超敏C-反应蛋白和白介素-6的早期动态变化与临床表现的关系探讨

目的 观察急性缺血性卒中患者发病后早期血浆超敏C反应蛋白（high sensitive C-reactive protein,hs-CRP）及白介素-6（interleukin-6,IL-6）水平的动态变化规律,探讨其与卒中患者临床表现及预后的关系。方法 连续入选急性缺血性卒中患者47例,正常对照组40例,比较卒中组发病后系列时间点血浆hs-CRP和IL-6水平与正常对照组之间的差异,分析其动态变化规律;按照基线美国国立卫生研究院卒中量表（national institutes of health stroke scale,NIHSS）评分将患者分为轻型组（n=15）和重型组（n=32）,比较两组血浆hs-CRP和IL-6水平;并比较不同临床预后患者血浆hs-CRP和IL-6水平的差异。结果 卒中组发病3h时血浆hs-CRP较对照组差异无统计学意义,6 h、12 h、24 h、48 h、3 d及7 d血浆hs-CRP较对照组明显升高（均P ≤0.01）。卒中组各时间点血浆IL-6水平均高于正常对照组（均P <0.01）。重型组血浆hs-CRP水平在12 h、24 h、48 h、3 d及7 d时水平均高于轻型组（P =0.046,0.012,0.030,0.007,0.041）;重型组血浆I L-6水平在12 h、24 h、48 h、3 d及7 d时水平均高于轻型组（P =0.002,0.001,0.006,0.026,0.043）。不同预后组之间血浆hs-CRP和IL-6水平差异不明显。结论 急性缺血性卒中患者血浆hs-CRP和IL-6水平升高,且与临床严重程度有关。     

进展性脑梗死患者血浆溶血磷脂酸和酸性磷脂水平的变化及其意义

目的 探讨进展性脑梗死(PCI)患者血浆溶血磷脂酸(LPA)和酸性磷脂(AP)水平的变化及其意义.方法 93例急性脑梗死(ACI)患者,根据发病后48 h内病情变化分为PCI组(35例)和非PCI(NPCI)组(58例).检测两组发病后6 h、24 h、3 d、7 d、14 d、21 d血浆LPA和AP的水平,并与正常对照组(50人)比较.结果 与正常对照组比较,PCI组与NPCI组患者发病6 h～14 d时血浆LPA、AP水平均明显增高(均P<0.01);与NPCI组比较,PCI组患者发病6 h～14 d时血浆LPA、AP水平均明显增高(均P<0.01).结论 ACI患者血浆LPA和AP水平均增高,其中PCI患者血浆LPA、AP水平较NPCI患者更高.血浆LPA、AP水平可提示ACI患者病情进展趋势.     

高血压性脑出血患者急性期D-二聚体、纤维蛋白原及其降解产物的变化及意义

目的 观察高血压性脑出血患者急性期血象D-二聚体(D-D)、纤维蛋白原降解产物(FDP)及纤维蛋白原(Fib)的动态变化和临床意义.方法 免疫比浊法测定实验组与对照组的血浆D-D和Fib,采用乳胶凝聚法测定FDP.测定42例脑出血患者发病后1,3,7,14 d对空腹静脉血D-D、Fib和FDP的变化,同时与正常对照组34例相比较.结果 脑出血组第3,7,14天血浆FDP、D-D和Fib明显升高,与对照组比较差异有统计学意义(P＜0.01);脑出血组发病24 h内血浆FDP、D-D和Fib水平较对照组升高,但差异无统计学意义(P＞0.05);脑出血组血浆D-D于第3天、血浆FDP及Fib含量于第7天达到高峰.结论 脑出血急性期血浆D-D、FDP及Fib含量增加,这可能是脑出血后脑组织损伤引起外周血中纤溶活性增高的一种代偿反应.     

血浆脂蛋白相关磷脂酶A2水平对进展性脑梗死的预测价值

目的研究血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平对进展性脑梗死的预测价值。方法采用双抗体夹心酶联免疫吸附法检测168例急性脑梗死患者和72名正常对照者的血浆Lp-PLA2水平。ACI患者每天进行美国国立卫生研究院卒中量表(NIHSS)评分,发病第3 d NIHSS评分比发病第1 d增加≥2分者为进展性脑梗死(进展性脑梗死组),<2分者为稳定性脑梗死(稳定性脑梗死组)。结果 168例ACI患者中进展性脑梗死40例,稳定性脑梗死128例。ACI组血浆Lp-PLA2水平明显高于正常对照组(P<0.01),进展性脑梗死组明显高于正常对照组及稳定性脑梗死组(均P<0.01);稳定性脑梗死组与正常对照组的差异无统计学意义。结论进展性脑梗死患者发病后血浆Lp-PLA2水平明显升高,其可能为早期预测进展性脑梗死发生的生物学指标。     

缺血性卒中早期超氧化物歧化酶的变化特点

目的研究缺血性卒中患者血液超氧化物歧化酶在缺血性卒中不同时点的变化特点.方法对28例缺血性卒中发作不超过6h的住院病人,在发病后6h、24h、3d、7d采血,通过光谱仪法测定血浆超氧化物歧化酶及红细胞内超氧化物歧化酶的活性,对照组病人选用年龄和性别匹配的正常对照.结果缺血性卒中病人平均抗氧化酶活性低于对照组,但随着时间的延长有上升趋势.结论急性缺血性卒中后抗氧化酶水平下降可能是氧化应激增高的结果.     

缺血性卒中早期超氧化物歧化酶的变化特点

目的 研究缺血性卒中患者血液超氧化物歧化酶在缺血性卒中不同时点的变化特点。方法 对28例缺血性卒中发作不超过6h的住院病人，在发病后6h、24h、3d、7d采血，通过光谱仪法测定血浆超氧化物歧化酶及红细胞内超氧化物歧化酶的活性，对照组病人选用年龄和性别匹配的正常对照。结果 缺血性卒中病人平均抗氧化酶活性低于对照组，但随着时间的延长有上升趋势。结论 急性缺血性卒中后抗氧化酶水平下降可能是氧化应激增高的结果。     

血浆胰岛素样生长因子-1水平变化对急性缺血性脑卒中患者预后的影响

目的探讨血浆胰岛素样生长因子-1与急性缺血性脑卒中之间的关系。方法74例急性缺血性脑卒中患者,分别于发病48h内(第1次)、7d～8d(第2次)和12d～14d(第3次)采集血液标本,采用固相酶联化学荧光免疫分析方法检测血浆胰岛素样生长因子-1水平,并与对照组进行比较。脑卒中患者于发病后48h内(急诊首诊时)及发病后12d～14d进行两次神经功能缺损程度评分(CSS1和CSS2),通过两次评分的差值(CSS1-CSS2)判断预后。结果74例急性缺血性脑卒中患者第1、2次血浆胰岛素样生长因子-1检测水平明显低于正常对照组(t=3.713,2.032;P<0.05或P<0.01)。比较不同梗死面积组之间血浆胰岛素样生长因子-1水平的变化显示,大面积梗死组患者血浆胰岛素样生长因子-1水平最低,与中、小梗死面积组相应时限比较差异有统计学意义(P<0.05或P<0.01)。不同预后组之间,以病情加重组患者第1次血浆胰岛素样生长因子-1检测水平最低,与其他各组(明显改善、改善、无变化及对照组)相同时限测值相比差异有统计学意义(均P<0.01)。相关性分析显示,两次神经功能缺损程度评分差值与3次不同时限血浆胰岛素样生长因子-1水平均存在明显相关性(P<0.05或P<0.01)。结论(1)胰岛素样生长因子-1可能参与急性缺血性脑卒中的病理生理学机制,对缺血性脑卒中患者有神经保护作用,可能成为急性缺血性脑卒中的一种治疗方法。(2)血浆胰岛素样生长因子-1对判断急性缺血性脑卒中患者的临床预后有一定价值,特别是根据发病48h内其水平变化的情况能够及早判断患者预后。     

重型颅脑外伤患者血浆DNP水平的初步研究

目的研究重型颅脑损伤患者血浆树根眼镜蛇尿钠肽(DNP)水平的变化及其与低钠血症及水平衡之间的关系。方法收集实验组14例重型颅脑外伤患者(实验组)入院后第1、3及7天静脉血,同时检测血、尿电解质,血、尿渗透压,记24h出入量;收集8例健康志愿者(对照组)外周静脉血1次;采用放射免疫分析方法检测DNP浓度。结果实验组第1天、第3天的血浆DNP水平显著高于正常对照组血浆DNP水平(P<0.05),其中8例血浆DNP水平第3天较第1天出现增高并发生负水平衡,且有7例出现低钠血症。血浆DNP水平的增高与水平衡的发生呈极显著负相关(P<0.01),与低钠血症的发生显著相关(P<0.05)。结论重型颅脑外伤后,患者血浆DNP水平出现增高,并且伴随利钠利尿作用的增强。     

Hemostatic markers and platelet aggregation factors as predictive markers for type of stroke and neurological disability following cerebral infarction.

We investigated the plasma levels of D-dimer, fibrinogen, beta-thromboglobulin (BTG) and platelet factor-4 (PF-4), indices of the occurrence of platelet activation in vivo, to find out their role in pathophysiology of ischemic stroke and whether or not such a role has any effect on the disability and the prognosis of stroke patients. A total of 76 patients with AIS aged from 26 to 85 (32 men, 44 women) and 30 cases as controls with similar age (18 men, 12 women) were included in the study. The plasma levels of D-dimer, BTG and PF-4 were measured by ELISA method using a special commercial kit. The cases were allocated into two groups as non-embolic (NEI) and cardioembolic stroke (CEI). The D-dimer levels in 76% of 42 patients in NEI group (p<0.05) and 85.2% of 34 patients in CEI group (p<0.05) were outside the confidence interval (CI) defined for the control group. The levels of BTG were elevated in 81% of 42 cases with NEI (p<0.05) and in 76% of 34 cases with CEI, with reference to CI of control group. The levels of PF-4 were significantly increased in 86% of cases with NEI (p<0.05) and in 88% of cases with CEI than controls (p<0.05). It was observed that the cases with high Rankin scores had higher levels of D-dimer (p<0.005), BTG (p<0.01) and PF-4 (p<0.01) than those with lower scores. There was a correlation between hemostatic markers, platelet activation and functional disability. D-dimer levels were an important marker that determined to degree of the activation of hemostatic system, especially in CEI subtype. The platelet aggregation had an important role in pathophysiology of ischemic stroke and this condition is significant in NEI subgroup and subjects with large infarcts and high disability scores.     

Association between inflammation and hemostatic markers in atherothrombotic stroke

INTRODUCTION: It has been reported that the influence of fibrinogen on the incidence of ischemic events is related to inflammation processes and reflects an association with advance atherosclerosis. The aim of this study was to evaluate the association of thrombogenic and inflammatory profiles in patients who have suffered a stroke. MATERIALS AND METHODS: The study involved 17 patients with atherothrombotic stroke and 34 healthy subjects as control group. The patients were examined 48 h, 3 and 6 months after the stroke occurred. To determine the inflammatory and thrombogenic profiles, plasma levels of fibrinogen, total sialic acid (TSA), C-reactive protein (CRP), tissue factor (TF) and fibrin D-dimer (D-dimer) were measured. RESULTS: The study showed that at 48 h and 3 months the levels of fibrinogen, TF, D-dimer, TSA and CRP were significantly higher than control group. TF, D-dimer and TSA remains significantly elevated throughout the entire study period. TF and D-dimer decreased over time without reaching the normal values. The multiple regression analysis showed that, at 48 h, 68% of the variance of fibrinogen and 22% of the variance of TF could be explained by the influence of CRP. At 3 and 6 months, 78% of the variance of fibrinogen could be explained by the influence of TSA. CONCLUSIONS: The results suggest a relation among inflammation markers, fibrinogen and TF in the acute phase of stroke. As TF and D-dimer are still elevated at 6 months, an increased thrombogenicity for a longer period following the acute event is present.     

Anti-inflammatory and anti-thrombogenic effects of atorvastatin in acute ischemic stroke**

Atorvastatin decreases inflammation and thrombogenesis in patients with carotid artery plaque. Atorvastatin is administered to lower lipid levels, but its anti-inflammatory and anti-thrombogenic effects remain unclear. Eighty-nine patients from northeastern China with acute ischemic stroke caused by large-artery atherosclerosis were randomly divided into the study and control groups. All patients received routine treatment, including antiplatelet therapy, circulatory support, and symp-tomatic treatment. The study group (n=43) also received daily atorvastatin 20 mg/d, and the control group (n=46) received daily placebo pills containing glucose. After 4 weeks, the levels of C-reactive protein, fibrinogen, and D-dimer were significantly lower in the study group than in the control group. Decreases in the levels of C-reactive protein, fibrinogen, and D-dimer were not associated with de-creases in the levels of triacylglycerol and low-density lipoprotein cholesterol. These results suggest that atorvastatin reduces inflammation and thrombogenesis independent of its lipid-lowering effects in patients with acute ischemic stroke caused by large-artery atherosclerosis.     

进展性脑梗死患者红细胞分布宽度的动态变化及预后风险评估

目的观察进展性缺血性脑卒中(PIS)患者的红细胞分布宽度(RDW)、氧化低密度脂蛋白(ox-LDL)与超敏C反应蛋白(hs-CRP)水平的动态变化,探讨其对PIS病情严重程度及评估预后的价值。方法选择急性脑梗死患者100例,分为进展组(PIS组)50例、非进展组(非PIS组)50例,分别测定两组患者发病24h、2d、3d、7d、14d RDW、ox-LDL与hs-CRP水平及SSS评分,并随访患者3月时改良Rankin量表(m RS)评分,采用Cox比例风险回归分析进展性缺血性脑卒中预后。结果治PIS组RDW、ox-LDL与hs-CRP水平在发病24h、第2、3、7、14d明显高于非PIS组(P0.01);Pearson相关分析显示,RDW与ox-LDL、hs-CRP及SSS评分水平呈显著正相关(P0.01)。Cox回归分析显示RDW、ox-LDL、hs-CRP是患者预后不良的支持因素(P0.01)。结论 RDW联合ox-LDL与hs-CRP可提高对PIS病情严重程度的判断能力,同时有助于评估患者预后。     

Effects of fixed low-dose warfarin, aspirin-warfarin combination therapy, and dose-adjusted warfarin on thrombogenesis in chronic atrial fibrillation

BACKGROUND AND PURPOSE: Recent clinical trials have established that adjusted-dose warfarin (international normalized ratio [INR] 2.0 to 3.0) is highly effective in the reduction of ischemic stroke in patients with nonvalvular atrial fibrillation (AF). We hypothesized that the introduction of fixed low-dose warfarin alone or in combination with aspirin (300 mg) could normalize hemostatic markers, namely plasma fibrin D-dimer (an index of thrombogenesis), plasminogen activator inhibitor-1 (PAI-1, an index of fibrinolysis), fibrinogen, and von Willebrand factor (vWf, an index of endothelial dysfunction), in a manner comparable to adjusted-dose warfarin (target INR 2.0 to 3.0). METJODS: Sixty-one patients with AF (44 men, mean+/-SD age 64+/-19 years) who were not receiving any antithrombotic therapy were prospectively randomized into 1 of 3 treatment groups: warfarin (2 mg) (n=23; group 1), combination 1 mg warfarin plus 300 mg aspirin (n=21; group 2) or combination 2 mg warfarin plus 300 mg aspirin (n=17; group 3). Subjects from all 3 AF groups were matched for sex, age, and blood pressure. Blood samples were taken for sequential measurements for changes in plasma fibrin D-dimer, PAI-1, fibrinogen, and vWf before and at 2 and 8 weeks after randomization (phase 1). All patients were subsequently offered adjusted-dose warfarin therapy (phase 2), and an additional blood sample was taken 6 weeks later. RESULTS: When pretreatment results were compared with those from 60 age- and sex-matched healthy control subjects in sinus rhythm, there were significant elevations in levels of fibrinogen (P=0.025), vWf (P<0.0001), and fibrin D-dimer (P<0.0001) in patients with AF compared with control subjects. There were no significant changes in the levels of various indices measured after 2 and 8 weeks of therapy in all 3 groups, except for an increase in PAI-1 level (P=0.024) in group 3. After 6 weeks of therapy with dose-adjusted warfarin (INR 2.0 to 3.0), there was a significant decrease in plasma fibrinogen (P=0.023) and fibrin D-dimer (P=0.0067) levels. There were no significant changes in the levels of PAI-1 (P=0.198) or vWf (P=0.33). CONCLUSIONS: The present results confirmed that high levels of vWf, fibrinogen, and fibrin D-dimer levels were present in patients with AF compared with control subjects. Moreover, the introduction of 300 mg aspirin plus low-dose warfarin (1 mg/d), low-dose warfarin alone (2 mg/d), or 300 mg aspirin plus low-dose warfarin (2 mg/d) did not significantly reduce any of the hemostatic markers studied (except PAI-1 levels), whereas conventional full-dose warfarin (INR 2.0 to 3.0) significantly reduced levels of fibrin D-dimer and fibrinogen. These results are in keeping with the disappointing ineffectiveness of low-intensity warfarin therapy, aspirin-warfarin combination, and ultralow-dose warfarin therapy in the recent prematurely terminated clinical trials and the established benefits of conventional adjusted-dose anticoagulation therapy.     

Hemostatic markers in ischemic stroke of undetermined etiology

To evaluate the role of the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis. Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects. Fibrinopeptide-A and thrombin-antithrombin III complex levels were not elevated significantly, whereas the D-dimer level was markedly raised in acute (p<0.001) and chronic (p<0.05) phases of ischemic stroke in comparison with the control group. Prolonged elevation of D-dimer concentration suggests that hemostatic abnormalities have a primary role in the pathogenesis of ischemic stroke. The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.     

Risk factors for progressive ischemic stroke——A retrospective analysis

BACKGROUND: Progressive ischemic stroke has higher fatality rate and disability rate than common cerebral infarction, thus it is very significant to investigate the early predicting factors related to the occurrence of progressive ischemic stroke, the potential pathological mechanism and the risk factors of early intervention for preventing the occurrence of progressive ischemic stroke and ameliorating its outcome. OBJECTIVE: To analyze the possible related risk factors in patients with progressive ishcemic stroke, so as to provide reference for the prevention and treatment of progressive ishcemic stroke. DESIGN: A retrospective analysis. SETTING: Department of Neurology, General Hospital of Beijing Coal Mining Group. PARTICIPANTS: Totally 280 patients with progressive ischemic stroke were selected from the Department of Neurology, General Hospital of Beijing Coal Mining Group from March 2002 to June 2006, including 192 males and 88 females, with a mean age of (62±7) years old. They were all accorded with the diagnostic standards for cerebral infarction set by the Fourth National Academic Meeting for Cerebrovascular Disease in 1995, and confired by CT or MRI, admitted within 24 hours after attack, and the neurological defect progressed gradually or aggravated in gradients within 72 hours after attack, and the aggravation of neurological defect was defined as the neurological deficit score decreased by more than 2 points. Meanwhile, 200 inpatients with non-progressive ischemic stroke (135 males and 65 females) were selected as the control group. METHODS: After admission, a univariate analysis of variance was conducted using the factors of blood pressure, history of diabetes mellitus, fever, leukocytosis, levels of blood lipids, fibrinogen, blood glucose and plasma homocysteine, cerebral arterial stenosis, and CT symptoms of early infarction, and the significant factors were involved in the multivariate non-conditional Logistic regression analysis. MAIN OUTCOME MEASURES: Results of the univariate analysis of variance of the factors related to progressive ischemic stroke; Results of the multivariate regression analysis. RESULTS: All the 480 patients were involved in the analysis of results. ① Results of the univariate analysis variance: There were significantly more patients with fever, leukocytosis, history of diabetes mellitus, cerebral arterial stenosis and CT symptoms of early infarction in the progressive ischemic stroke group than in the control group (P < 0.01); The levels of blood glucose and fibrinogen in the progressive ischemic stroke group were significantly higher than those in the control group, while the level of blood pressure was significantly lower than that in the control group (P < 0.05–0.01). ② Results of the multivariate Logistic regression analysis: The independent predicting factors for progressive ischemic stroke were history of diabetes mellitus, fever, leukocytosis, cerebral arterial stenosis, CT symptoms of early infarction, blood glucose and blood pressure (OR =2.61, 2.96, 3.79, 1.03, 3.57, 2.68, 95% CI 0.92–3.59, P < 0.05–0.01). CONCLUSION: History of diabetes mellitus, fever, leukocytosis, levels of blood pressure, blood glucose, cerebral arterial stenosis and CT symptoms of early infarction are the risk factors for progress ischemic stroke     

Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation

We studied whether hemostatic abnormalities contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation. Hemostatic function was studied in four age-matched groups: 20 patients with nonvalvular atrial fibrillation and a previous ischemic stroke, 20 patients with nonvalvular atrial fibrillation without a previous stroke, 20 stroke patients with sinus rhythm, and 40 healthy controls. Both groups with nonvalvular atrial fibrillation had significantly higher concentrations of von Willebrand factor, factor VIII:C, fibrinogen, D-dimer (a fibrinolytic product), beta-thromboglobulin, and platelet factor 4; a significantly higher fibrinogen/antithrombin ratio; and significantly higher spontaneous amidolytic activity than the healthy controls. Prekallikrein levels were significantly lower in both groups with nonvalvular atrial fibrillation. Stroke patients with sinus rhythm had normal hemostatic function, normal concentrations of platelet-related factors, and a slightly increased concentration of fibrinopeptide A compared with the healthy controls. Both groups with nonvalvular atrial fibrillation differed from the stroke patients with sinus rhythm as they did from the healthy controls. No difference in hemostatic function was seen between the nonvalvular atrial fibrillation patients with and without a previous ischemic stroke. Thus, alterations in hemostatic function may contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation.     

前列腺癌相关脑梗死的发病特点

目的 探讨前列腺癌相关脑梗死的发病特点。方法 收集2003年1月-2015年12月在广西医科大学第一附属院住院治疗的前列腺癌合并脑梗死患者的临床表现、实验室及器械检查等资料。结果 本研究共筛查前列腺癌患者2 584例,其中符合前列腺癌合并脑梗死的患者共有34例(1.31%),平均年龄(61.60±6.28)岁。入选的患者中无脑卒中危险因素21例(61.76%)。血液学检查发现D-二聚体水平升高22例(64.71%),总前列腺特异性抗原(Total prostate specific antigen,T-PSA)水平异常升高(>100 ng/mL )19例(55.88%),头颅MRI显示脑内单一梗死灶8例(23.52%),出现累及多个动脉供血区的2个或2个以上梗死灶26例(76.47%),脑梗死发生30 d多数患者预后不良,其中4例(11.77%)死亡。结论 前列腺癌相关脑梗死的患者以缺少常见的脑卒中危险因素、血清D-二聚体水平升高以及T-PSA异常升高、一次发病出现累及多血管分布区的多发性梗死灶以及预后不良等为特点,其发生机制可能与患者血液的凝固性升高有关。     

Antithrombin III associated with fibrinogen predicts the risk of cerebral ischemic stroke

Background and purpose

The purpose of this study is to examine the feasibility of developing plasma predictive value biomarkers of cerebral ischemic stroke before imaging evidence is acquired.

Methods

Blood samples were obtained from 198 patients who attended our neurology department as emergencies - with symptoms of vertigo, numbness, limb weakness, etc. - within 4.5 h of symptom onset, and before imaging evidence was obtained and medical treatment. After the final diagnosis was made by MRI/DWI/MRA or CTA in the following 24-72 h, the above cases were divided into two groups: stroke group and non-stroke group according to the imaging results. The levels of baseline plasma antithrombin III (AT-III), thrombin-antithrombin III (TAT), fibrinogen, D-dimer and high-sensitivity C-reactive protein (hsCRP) in the two groups were assayed.

Results

The level of the baseline AT-III in the stroke group was 118.07 ± 26.22%, which was lower than that of the non-stroke group (283.83 ± 38.39%). The levels of TAT, fibrinogen, hsCRP were 7.24 ± 2.28 μg/L, 5.49 ± 0.98 g/L, and 2.17 ± 1.07 mg/L, respectively, which were higher than those of the non-stroke group (2.53 ± 1.23 μg/L, 3.35 ± 0.50 g/L, 1.82 ± 0.67 mg/L). All the P-values were less than 0.001. The D-dimer level was 322.57 ± 60.34 μg/L, which was slightly higher than that of the non-stroke group (305.76 ± 49.52 μg/L), but the P-value was 0.667. The sensitivities of AT-III, TAT, fibrinogen, D-dimer and hsCRP for predicting ischemic stroke tendency were 97.37%, 96.05%, 3.29%, 7.89%, but the specificity was 93.62%, 82.61%, 100% and 100%, respectively, and all the P-values were less than 0.001. High levels of D-dimer and hsCRP were mainly seen in the few cases with severe large-vessel infarction.

Conclusions

Clinical manifestations of acute focal neurological deficits were associated with plasma AT-III and fibrinogen. These tests might help the risk assessment of acute cerebral ischemic stroke and/or TIA with infarction tendency in the superacute stage before positive imaging evidence is obtained.