以急性脑梗死为首发表现的躯体恶性肿瘤34例分析

目的探讨以急性脑梗死为首发表现的躯体恶性肿瘤患者的临床特点和可能的发病机制。方法回顾性分析2007-01-01—2016-12-31第二军医大学附属长海医院和上海市杨浦区市东医院确诊的以急性脑梗死为首发表现的34例隐匿性躯体恶性肿瘤患者的临床资料。结果 34例患者中男29例,女5例,平均年龄(66.94±10.09)岁。无传统脑卒中危险因素者6例(17.65%)。所有患者以局灶性神经功能缺损为主要表现,其中3例出现昏迷。24例患者(70.59%)外周血D-二聚体水平升高。14例(41.18%)患者头颅DWI检查示急性多动脉供血区梗死灶。首次因急性脑梗死入院MRI检查发现有陈旧性无症状脑梗死者18例(52.94%)。肿瘤类型以肺癌(11例,32.35%)最多见,其次是肾癌(7例,20.59%)、结直肠癌(4例,11.76%)、胰腺癌(4例,11.76%)。诊断癌症时即有远处转移者9例(26.47%)。病程中出现脑梗死复发者5例(14.70%)。多数患者预后不良。入院后30d改良Rankin量表评分3~5分9例(26.47%),6分(死亡)6例(17.65%)。高血浆D-二聚体水平(P=0.000)与恶性肿瘤有远处转移(P=0.025)是患者30d神经功能预后差的相关危险因素。结论对于不符合单支动脉供血区的急性多发性脑梗死且D-二聚体明显升高的患者,特别是脑梗死再发者需要考虑合并隐匿性躯体恶性肿瘤的可能;高D-二聚体水平及恶性肿瘤有远处转移的患者一旦发生脑梗死,其神经功能预后更差。     

女性内生殖系统恶性肿瘤相关脑梗死的临床特点

目的探讨女性生殖系统恶性肿瘤合并脑梗死患者的临床特点及其可能的发病机制。方法分析2007年1月至2013年12月在广西医科大学第一附属医院因生殖系统恶性肿瘤住院接受治疗期间发生脑梗死的女性患者的临床资料。结果本组符合条件的患者9例,占同期1780例女性生殖系统恶性肿瘤的0.51%,年龄39~58岁,平均年龄51.56±7.20岁。肿瘤类型分别为子宫内膜癌4例、宫颈癌3例、卵巢癌2例,且所有患者肿瘤已经发生远处转移,其中血浆癌抗原125(CA-125)升高8例(88.89%),CA-199升高7例(77.78%)。脑梗死发生与肿瘤确诊后的9~42d,平均25.44±10.24d。9例患者中,6例(66.67%)患者无传统的脑卒中危险因素,6例(66.67%)外周血D-二聚体水平升高,6例(66.67%)脑内出现2个及以上分属于不同动脉供血区的病灶。脑梗死发病后90d 5例(55.56%)死亡。结论多数患者缺少传统的脑卒中危险因素,外周血D-二聚体、癌抗原水平升高,脑内出现涉及多条动脉供血区的多发性梗死灶,预后不良等可能是女性生殖系统肿瘤并发脑梗死的临床特点,并且血液高凝状态是其可能的发病机制之一。     

再发脑梗死患者血浆D-二聚体与纤维蛋白原变化的临床意义

目的探讨脑再梗死患者与初次脑梗死患者的血浆D-二聚体、纤维蛋白原的改变。方法分别对68例初次脑梗死患者及68例脑再梗死患者的血浆D-二聚体、纤维蛋白原进行测定并对不同脑再梗死体积患者血浆D-二聚体、纤维蛋白原含量进行对比。结果再次脑梗死组血浆D-二聚体、纤维蛋白原均高于初次脑梗死组(P<0.05);在再次脑梗死组大面积梗死灶患者血浆D-二聚体、纤维蛋白原含量明显高于中、小面积梗死灶者(P<0.05)。结论血浆D-二聚体、纤维蛋白原的变化与脑再梗死的发生及预后有一定的关系,是再发脑梗死事件的重要危险因素。     

前列腺癌合并急性脑梗死的临床特点及病因分析

目的 分析前列腺癌合并急性脑梗死的临床特点,探讨其相关危险因素。 方法 本研究为病例对照研究,前列腺癌合并急性脑梗死组收集2010年1月-2019年10月于首都医 科大学附属北京世纪坛医院连续就诊的前列腺癌合并急性脑梗死患者,前列腺癌无脑梗死组按年 龄匹配（1∶1）同时期泌尿外科住院被确诊为前列腺癌且未曾发生过脑梗死的患者。分析前列腺癌 合并急性脑梗死的临床特点,比较两组患者传统血管危险因素、实验室检查及肿瘤相关治疗间的差 异,采用多因素logistic回归分析前列腺癌合并急性脑梗死的影响因素。 结果 两组各纳入43例患者。前列腺癌合并急性脑梗死组年龄71～93岁,平均82.2±4.8岁;腔隙 性脑梗死（病灶＜10 mm）占74.4%（32/43）,前、后循环同时受累多发性脑梗死占23.3%（10/43)。多 因素logistic回归分析显示,高脂血症（OR 7.494,95%CI 1.371～40.971）、D-二聚体升高（OR 1.012, 95%CI 1.003～1.021）、放射性粒子植入治疗（OR 0.144,95%CI 0.037～0.557）是前列腺癌合并急性 脑梗死的独立影响因素。 结论 前列腺癌合并急性脑梗死患者年龄较大,以小病灶、多发性梗死灶常见。高脂血症和D-二聚 体升高是前列腺癌合并急性脑梗死独立危险因素,放射性粒子植入治疗是前列腺癌合并急性脑梗 死的独立保护因素。     

血浆D-二聚体水平与急性脑梗死患者预后的关系

目的探讨血浆D-二聚体水平与急性脑梗死患者预后的关系。方法采用乳胶免疫比浊法检测673例急性脑梗死患者血浆D-二聚体的含量。并于发病30 d时对患者进行改良Rankin量表评分,评定预后。对不同预后患者的结果进行比较分析。结果发病30 d时,mRS评分0~2分(预后良好组)342例;mRS评分3~6分(预后不良组)331例。预后不良组患者血浆D-二聚体水平[(386.56±31.22)μg/L]明显高于预后良好组[(379.84±33.71)μg/L](P0.01)。Logistic回归分析显示,血浆D-二聚体水平升高是急性脑梗死患者预后不良的独立危险因素(OR=2.423,95%CI:1.537~3.862,P0.05)。结论血浆D-二聚体水平升高是急性脑梗死患者预后不良的独立危险因素。     

急性脑梗死血浆D二聚体NSE的动态分析

目的分析急性脑梗死患者血浆中D-二聚体和NSE(神经元特异性的烯醇化酶)在不同时间的动态变化和临床意义。方法选取在我院治疗的急性脑梗死患者91例,分别用化学法和化学发光法检测患者入院时、发病后48h、72h、7d、14d的血浆D-二聚体和NSE水平,并检测发病72h后梗死灶的最大直径(用头颅CT)和各个时期的NIHSS评分。另外选45例经体检健康者为对照组。结果和对照组比较,脑梗死组在入院的当天血浆中D-二聚体和NSE的水平明显升高(P0.05);NSE的水平逐渐上升,于7d后有明显下降,在14d后的水平与对照组比较无显著差异(P0.05);D-二聚体水平7d前各时点逐渐显著升高,14d后显著下降,但仍显著高于对照组(P0.05);7d内NIHSS分值和梗死灶最大直径呈正相关(P0.05)。结论测量血浆中的D-二聚体和NSE的水平对急性脑梗死的早诊断、病情轻重辨别和预后评估有重要意义。     

肾病综合征合并脑梗死62例临床分析

目的 探讨肾病综合征(NS)合并脑梗死患者的临床特点及潜在发病机制。方法 收集NS合并脑梗死患者的临床表现、实验室及影像学检查,回顾性分析其临床资料。结果 收集到NS合并脑梗死患者共62例,占同期4584例NS患者的1.35%,其中男47例(75.81%),女15例(24.19%),发病年龄20～80岁,平均年龄(58.87±11.67)岁。33例(53.23%)脑梗死发生于NS发病6个月内; 35例行肾穿刺活检中31例是膜性肾病(88.57%); 32例(51.61%)血浆白蛋白水平低于20 g/L; 42例(66.74%)纤维蛋白原水平升高; 29例行D-二聚体检查中18例其水平升高(62.07%); 10例(16.13%)以脑梗死为NS的首发症状,48例(77.41%)出现非单一动脉供血区的2个及以上病灶。结论 脑梗死多发生于NS发病6个月内,NS病理类型以膜性肾病为主,多数患者血浆白蛋白水平明显降低,血浆D-二聚体、纤维蛋白原水平升高,部分患者表现为无症状脑梗死,部分患者以脑梗死为NS的首发症状,多数患者脑内出现多发性病灶,其发病机制可能与血液的高凝状态有关。     

急性脑梗死患者血浆NSE、D-二聚体的动态监测的临床研究

目的观察急性脑梗死血浆神经元特异性烯醇化酶(NSE)、D-二聚体的动态变化,评价其临床意义。方法检测62例急性脑梗死患者入院时血浆NSE和D-二聚体含量、发病后48h、72h、7d、14d的血浆NSE和D-二聚体含量。同时测量发病后72h头颅CT示梗死灶最大直径及各时期的美国国立卫生研究院卒中量表(NHSS)评分。50例健康体检者作为对照组。结果脑梗死组入院当日血浆NSE、D-二聚体的含量明显升高,较对照组差异有统计学意义;NSE含量呈逐渐升高,3d达高峰,7d后明显下降,14d后降到和对照组比较差异无统计学意义(P>0.05);D-二聚体含量的动态变化亦呈逐渐升高,7d达高峰,14d后有下降趋势,但其升高和对照组比较差异有统计学意义(P<0.05);入院时CT检查未见异常者NSE、D-二聚体也呈类似变化,早于影像学改变;7d内NSE、D-二聚体含量分别与梗死灶的最大直径、NIHSS分值呈显著正相关(r分别为0.56,0.70,0.56,P<0.05)。结论血浆NSE、D-二聚体联合测定对于急性脑梗死早期诊断、病情轻重和预后的判断具有重要的临床价值。     

鼻咽癌并发脑梗死的临床特点及发病机制

目的探讨鼻咽癌并发脑梗死的临床特点及发病机制。方法收集2012-01—2018-08在广西医科大学第一附属医院住院治疗的鼻咽癌并发脑梗死患者的临床资料,同时按照1∶2的比例收集同期住院治疗的相同年龄的单纯鼻咽癌患者为对照组。结果纳入符合条件的鼻咽癌并发脑梗死患者29例,单纯鼻咽癌患者58例。29例鼻咽癌并发脑梗死患者中21例(72.4%)头颅MRI或CT显示有累及不同动脉供血区域的2个及以上脑梗死病灶,15例(51.7%)患者无传统的脑梗死危险因素。与单纯鼻咽癌相比,鼻咽癌并发脑梗死患者的血浆D-二聚体、纤维蛋白原水平更高(P0.1),红细胞、白蛋白、血红蛋白、高密度脂蛋白更低(P0.1);Logistic回归分析显示,血浆D-二聚体、纤维蛋白原升高及白蛋白降低是鼻咽癌患者发生脑梗死的独立危险因素(OR=1.006,90%CI 1.003～1.010;OR=2.477,90%CI 1.243～4.937;OR=0.749,90%CI 0.581～0.967)。结论鼻咽癌并发脑梗死的临床特点是脑梗死病灶为多发,多数累及2个以上血管供血区域,部分患者无传统脑梗死危险因素。鼻咽癌并发脑梗死患者的血浆D-二聚体、纤维蛋白原升高可能与鼻咽癌并发脑梗死的发病机制有关。     

恶性肿瘤合并急性脑梗死的临床特点及预后分析

目的总结并分析恶性肿瘤合并脑梗死的临床及预后特点。方法收集2013年1月～2017年7月在首都医科大学附属北京世纪坛医院神经内科住院的非神经系统躯体恶性肿瘤合并急性脑梗死41例患者的临床资料,根据改良Rankin评分量表(modified Rating Scale,mRS)评价急性脑梗死后90 d功能预后,根据mRS量表是否≥3分将患者分为预后良好组(0～2分)与预后不良组(3～6分),总结两组患者病因、影像学表现、实验室指标及预后特点,分析患者预后不良的影响因素。采用SPSS 20. 0统计软件对数据进行分析,根据数据类型,两组比较采用t检验、秩和检验或精确概率检验。结果 (1) 41例患者中33例(80. 5%)具有传统脑血管病危险因素,病因分型中18例(43. 9%)为隐源性; 22例(53. 7%)病灶分布在多支血管供血区; 70. 7%为多发小病灶。病灶分布在皮质及皮质下32例(78. 5%),幕下病灶以累及小脑更常见13例(31. 7%),D-二聚体水平为0. 96(0. 22,3. 76) mg/L。(2) 41例患者住院期间死亡率9. 8%,90 d死亡率39. 0%,幸存者仍有52. 0%存在严重残疾。比较预后良好组(n=12)与预后不良组(n=29)的临床特点差异,预后不良组隐源性机制、多支血管分布区多发梗死、肿瘤4期比例更多见;入院NIHSS评分、D-二聚体水平更高,血红蛋白水平偏低,差异有统计学意义(P 0. 05)。结论恶性肿瘤合并急性脑梗死患者传统卒中危险因素常见,病因以隐源性为主,D-二聚体普遍升高,影像以多支血管分布区的多发小病灶为特点,住院期间死亡率高,90 d功能预后差。推测其发病机制与普通脑梗死患者不同,可能高凝状态同传统卒中危险因素一起影响了病情的发生和进展。     

以急性多发性脑梗死为首发表现的隐匿性躯体恶性肿瘤12例报告

目的研究以急性多发脑梗死为首发表现的隐匿性躯体恶性肿瘤患者的临床表现、实验室检查、影像学、微栓子监测检查特点,探讨其可能的发病机制。方法纳入以急性多发性脑梗死为首发表现的隐匿性躯体恶性肿瘤患者12例,收集其临床资料,分析其实验室血液学、头颅MRI、微栓子监测结果及其治疗和预后。结果所有患者均以局灶性神经功能缺损为主要表现,包括偏瘫、失语、偏身感觉障碍、构音障碍、眩晕、肢体抽搐等。头颅DWI示急性多发脑梗死,病灶播散性分布,不符合单支动脉供血区,同时累及双侧前循环或前后循环。11例行D-dimer检查者8例升高。7例行微栓子监测有5例阳性。隐匿性躯体恶性肿瘤包括:肺癌5例,胰腺癌3例,胃癌、结肠癌、子宫内膜癌、转移性低分化粘液腺癌原发肿瘤部位不明各1例;诊断时就已有远处转移者10例。病程中缺血性卒中复发者7例,急性心肌梗死4例,住院期间死亡3例,预后差。结论对于不符合单支动脉供血区的多发急性脑梗死,需要考虑可能合并隐匿性躯体恶性肿瘤,凝血功能筛查高凝状态和微栓子阳性可能是诊断提示线索。     

D-dimer and C-reactive Protein as Potential Biomarkers for Diagnosis of Trousseau's Syndrome in Patients with Cerebral Embolism

BackgroundDifferentiating stroke due to Trousseau's syndrome from other types of cerebral embolism is challenging, especially in patients with occult cancer. The current study aimed to determine predicting factors and biomarkers of stroke due to Trousseau's syndrome.MethodsThis retrospective study comprised 496 consecutive patients with acute cerebral embolism, including 19, 85, 310, and, 82 patients with stroke due to Trousseau's syndrome, artery-to-artery embolism, cardioembolic stroke, and embolic stroke with undetermined source, respectively. All patients were evaluated within 72 hours of onset. The clinical characteristics, laboratory findings, and patterns on diffusion-weighted magnetic resonance imaging (DWI) were compared among the groups.ResultsPlasma D-dimer and C-reactive protein (CRP) levels were significantly higher in the Trousseau's syndrome than in the other causes of cerebral embolism. Multivariate analyses demonstrated that female sex, multiple lesions on DWI, high D-dimer and CRP levels, and low platelet and low brain natriuretic peptide levels were independent predictors that could distinguish Trousseau's syndrome from the other causes of cerebral embolism. The cutoff values of D-dimer and CRP to identify stroke due to Trousseau's syndrome was 2.68 µg/mL fibrinogen equivalent units and .29 mg/dL, respectively.ConclusionsThe elevated D-dimer and CRP levels on admission in addition to specific clinical features may be useful for diagnosis of Trousseau's syndrome in patients with cerebral embolism.     

合并恶性肿瘤的脑梗死的临床特点及影响预后的相关因素分析

目的 分析合并恶性肿瘤的脑梗死患者的临床特征及影像学特点，探讨影响患者预后的相关因素。 方法 回顾性分析2015年10月-2020年6月于中国医科大学附属第一医院神经内科收治的合并恶性 肿瘤的脑梗死患者的临床资料，根据患者出院90 d时mRS评分将其分为预后良好组（mRS 0～2分）和 预后不良组（mRS＞2分）。采用多因素logistic回归模型分析影响合并恶性肿瘤的脑梗死患者预后的相 关因素。 结果 共纳入51例患者，平均年龄65.2±9.3岁，男性38例（74.5%）；预后良好组14例，预后不良组 37例。多发性梗死33例（64.7%），双侧半球梗死31例（60.8%）。多因素分析结果显示，高血红蛋白 水平为合并恶性肿瘤的脑梗死患者预后独立保护性因素（OR 0.925，95%CI 0.859～0.994），而高D- 二聚体水平（OR 5.124，95%CI 1.289～20.373）及双侧半球梗死（OR 11.533，95%CI 1.151～115.542） 为合并恶性肿瘤的脑梗死患者预后独立危险因素。 结论 合并恶性肿瘤的脑梗死患者影像学以多病灶、多血管支配区域受累为特点。高血红蛋白水平 为合并恶性肿瘤的脑梗死患者预后保护性因素，而高D-二聚体水平及双侧半球梗死为预后危险因素。     

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.     

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.     

D-dimer >2.785 μg/ml and multiple infarcts ≥3 vascular territories are two characteristics of identifying cancer-associated ischemic stroke patients

ABSTRACT

Background: The patterns and mechanisms underlying stroke in cancer patients differ from those of the conventional etiology. In this study, we further investigated the characteristics distinguishing cancer-associated ischemic stroke (CAIS) and the relationship of D-dimer value with CAIS.

Methods: Sixty-one acute ischemic stroke patients with cancer (cancer group) and 76 stroke patients without cancer (control group) were recruited. Cerebrovascular distribution was divided into 3 circulations and 23 vascular territories, and acute multiple brain infarcts (AMBIs) were defined as discrete MRI diffusion-weighted imaging (DWI) lesions in >1 vascular territory.

Results: Cancer patients had higher average D-dimer and fibrinogen degradation product values, and fewer stroke risk factors. The numbers of infarct-affected vascular territories, AMBIs, and AMBIs in multiple circulations were significantly higher in the cancer group. Receiver operating characteristic analysis showed that the cutoff value of D-dimer was 2.785 μg/ml; and above features were particularly evident in cancer patients whose D-dimer values were >2.785 μg/ml, while those with D-dimer values ≤2.785 μg/ml were similar to controls.

Conclusions: D-dimer >2.785 μg/ml may be an effective cutoff value and a sensitive index for identifying CAIS patients. AMBIs in ≥3 vascular territories and AMBIs in both the anterior and posterior circulations are two imaging characteristics of CAIS.     

Hemostatic markers in acute stroke

To assess the time course of thrombosis and fibrinolysis after acute stroke, we measured concentrations of fibrinopeptide A (FpA), B-beta 1-42 peptide (B-beta 1-42), B-beta 15-42 peptide (B-beta 15-42), and crosslinked D-dimer (XDP) in 31 patients at varying times following acute ischemic stroke and in 13 neurologically stable patients with chronic strokes. FpA levels were markedly elevated during the first week after stroke and declined slowly during the first month. Mean FpA levels were not significantly elevated in chronic stroke patients. Mean XDP levels were slightly elevated during the first week and increased during the next 2 weeks after stroke. B-beta 1-42 and B-beta 15-42 levels were not elevated at any time following acute stroke. Our data suggest that fibrin formation greatly exceeds endogenous fibrinolysis during the acute phase of ischemic stroke. Endogenous fibrinolysis develops slowly following stroke. Prolonged elevation of FpA concentration suggests that thrombin activity and fibrin formation continue for up to 4 weeks in some patients with ischemic stroke.     

Risk of recurrent ischemic stroke in patients with patent foramen ovale: The role of D-dimer

BackgroundParadoxical embolism under elevated thromboembolic conditions is known to be the primary mechanism of patent foramen ovale (PFO)-related stroke. We hypothesized that higher levels of D-dimer, a marker of thromboembolism, could increase the risk of stroke recurrence in patients with PFO.MethodsWe conducted a retrospective analysis of data from 1226 consecutive patients with acute ischemic cryptogenic stroke (CS) who underwent transesophageal echocardiography (TEE). D-dimer was assessed during admission. We used a multivariate Cox proportional hazards model to evaluate the association of long-term outcomes between the presence of PFO and levels of D-dimer.ResultsOf the 1226 patients, the study included 461 who underwent TEE. Among them, 242 (52.5%) had PFOs. Among PFO patients, those with a D-dimer level >1.0 mg/L had a significantly higher risk of stroke recurrence compared to those with <0.5mg/L (adjusted hazard ratio (aHR) 4.04, 95% confidence interval [CI] 1.63–10.02). A pattern of increased risk of event with increasing D-dimer levels was observed (P_trend=0.008). However, there was no significant difference in the risk of stroke recurrence at any D-dimer level compared to D-dimer level <0.5 mg/L among patients without PFO. In these patients, there was little evidence of increased risk with increasing D-dimer levels (P_trend=0.570).ConclusionsThis study demonstrated that the elevated D-dimer level increased the recurrence of stroke in CS patients with PFO, particularly showing a dose-dependent relationship between D-dimer levels and recurrence. However, no such effect was observed in patients without PFO. These findings provide valuable insights into the potential benefits of anticoagulation for strokes related to PFO.