短暂性脑缺血发作患者血浆溶血磷脂酸含量变化及氯吡格雷对其影响

目的观察短暂性脑缺血发作(TIA)患者血浆溶血磷脂酸(LPA)含量变化及氯吡格雷对其影响。方法选TIA患者143例为TIA组,于症状出现后24h内测血浆LPA含量,选健康体检者120例为对照组。在143例TIA患者中选取近1个月未服用抗血小板药物的116例TIA患者随机分为氯吡格雷组(75mg/d)和阿司匹林组(75mg/d),每组58例。检测患者服药1个月后的血浆LPA含量,并记录1个月内缺血发作次数。结果TIA组和健康对照组血浆LPA含量分别为(5.97±1.22)μmol/L、(2.79±1.24)μmol/L(P<0.001)。服药1个月后,氯吡格雷组和阿司匹林组血浆LPA含量分别为(3.17±0.87)μmol/L、(3.51±0.92)μmol/L(P<0.05)。两组缺血发作次数分别为(2.07±1.02)μmol/L、(3.36±1.14)μmol/L(P<0.01)。结论TIA患者血浆中LPA含量明显增高。氯吡格雷能明显降低TIA患者血浆LPA含量并减少缺血发作次数。     

氯吡格雷对短暂性脑缺血发作患者血浆溶血磷脂酸含量的影响

目的:探讨短暂性脑缺血发作(TIA)患者血浆溶血磷脂酸(LPA)含量的变化和氯吡格雷和(或)阿司匹林对LPA的影响。方法:检测128例TIA患者和110例年龄相匹配的健康对照者血浆LPA含量。近1个月未服用抗血小板药的93例TIA患者随机分为阿司匹林(100mg/d)组、氯吡格雷(75mg/d)组和氯吡格雷(75mg/d)+阿司匹林(100mg/d)组,每组31例。检测患者基线服药1个月后的血浆LPA含量,并记录1个月内的缺血发作次数。结果:TIA组和健康对照组血浆LPA的含量分别为(3.36±0.27)μmol/L和(1.47±0.42)μmol/L(P<0.001)。治疗30d后,服用抗血小板药的各组血浆LPA含量都明显降低[分别为(2.48±0.30)、(1.96±0.24)和(1.33±0.21)μmol/L;P<0.01~0.05)],各组缺血发作次数分别为3.78±0.93、2.20±1.10和1.53±0.81(P<0.01~0.05)。结论:TIA患者血浆LPA含量明显增高。氯吡格雷与阿司匹林联合应用能降低血浆LPA含量和减少缺血发作次数。     

不同抗栓干预对心房颤动患者体内血小板活化的影响

目的 观察不同抗栓干预对非瓣膜性心房颤动(nonvalvular atrial fibrillation,NVAF)患者血浆溶血磷脂酸(lysophosplmidic acid,LPA)含量变化的影响,为临床抗栓治疗提供依据.方法 经临床和辅助检查确诊的235例未接受抗栓治疗的NVAF患者,随机分为阿司匹林+双嘧达莫组(n=76,阿司匹林100 mg/d,双嘧达莫100 mg/d)、阿司匹林+固定剂量华法林组(n=79,阿司匹林100 mg/d,华法林1.25mg/d)和调整剂量华法林组(n=80,INR 1.5～2.1).根据患者年龄,每组再分为<60岁组、60～75岁组和≥76岁组.测定治疗前、治疗后2周和6周时血浆LPA含量,比较含量变化.结果 阿司匹林+固定剂量华法林组血浆LPA含量降低较阿司匹林+双嘧达莫组和调整剂量华法林组更为显著(P均<0.01).<60岁组经阿司匹林+双嘧达莫治疗后2周和6周,血浆LPA含量较治疗前显著降低(P均<0.01).<60岁组经阿司匹林+固定剂量华法林治疗后2周和6周,血浆LPA含量较治疗前显著降低(P均<0.01).60～75岁组经阿司匹林+固定剂量华法林治疗后2周和6周,血浆LPA含量较治疗前显著降低(P均<0.01).各年龄组患者经调整剂量华法林(INR 1.5～2.1)治疗后2周和6周,血浆LPA含量均较治疗前显著降低.结论 不同抗栓治疗方式对不同年龄组NVAF患者体内血小板活化均有不同程度的影响.<60岁组可给予阿司匹林+双嘧达莫治疗,75岁以下的患者可给予阿司匹林+固定剂量华法林治疗,>75岁的患者推荐应用调整剂量华法林(INR1.5～2.1)治疗.     

阿司匹林对缺血性脑血管病患者血浆溶血磷脂酸含量的影响

目的观察缺血性脑血管病患者应用阿司匹林后能否降低血浆溶血磷脂酸(LPA)含量.方法1400例患者纳入本研究,其中803例诊为可能的缺血性脑血管病,343例为缺血性脑血管病.36名健康志愿者为对照组.LPA含量采用层析技术结合改良无机磷定量方法测定.结果缺血性脑血管病组血浆LPA含量(3.11±1.55 μmol/L)显著高于对照组(1.77±1.04μmo1/L,P＜0.001).服用阿司匹林(80 mg,1次/d)1个月可显著降低血浆中LPA含量.停服阿司匹林后1个月LPA含量再次升高(3.90±1.09μmol/L),明显高于服用阿司匹林时(1.93±0.85 μmok/L,P＜0.001).结论血浆LPA含量升高与血小板活化密切相关,口服阿司匹林可降低血浆LPA含量,这可能是阿司匹林预防缺血性卒中的机制之一.     

短暂性脑缺血发作ABCD2评分与血浆LPA水平的相关性研究

目的探讨短暂性脑缺血发作（TIA）ABCD2评分与血浆溶血磷脂酸（LPA）水平的关系。方法测定98例TIA患者（TIA组）和62例健康体检者（对照组）血浆LPA水平,TIA组按ABCD2评分分为高危组、中危组和低危组,比较三组间治疗前后血浆LPA水平及1个月内发作次数。结果 TIA组血浆LPA水平高于对照组（P〈0.01）;高、中、低危组间治疗前后血浆LPA水平及发作次数差异均有统计学意义（P〈0.01）。结论 ABCD2评分与血浆LPA水平密切相关,联合二者更有助于TIA的指导治疗和风险评估。     

短暂性脑缺血发作病人血浆溶血磷脂酸含量变化及其临床意义

目的研究短暂性脑缺血发作（TIA）病人血浆溶血磷脂酸（LPA）含量变化的特点及其临床意义。方法选取经临床和辅助检查确诊的TIA病人51例（TIA组）,测定其血浆中LPA含量变化,另选择年龄匹配的50名健康体检者作为对照组。结果TIA组病人于症状发作后24h内血浆LPA含量为（4.58±0.71）μmol/L,显著高于正常对照组的（1.36±0.41）μmol/L（P〈0.001）。结论LPA有可能作为一个指示体内凝血和血栓形成启动的分子标记物,而且有可能进一步用于指导临床抗血小板治疗。     

血液内溶血磷脂酸浓度与氯吡格雷治疗短暂性脑缺血发作疗效的关系

目的探讨血液内溶血磷脂酸(lysophosphatidic acid,LPA)浓度与氯吡格雷治疗短暂性脑缺血发作(transi-ent ischemic attack,TIA)疗效的关系。方法选择TIA患者77例,根据血液内LPA浓度分为LPA增高组(>3.2μmol/L,49例)和LPA正常组(≤3.2μmol/L,28例),用氯吡格雷75 mg/d进行治疗,随访1个月,观察TIA患者的发作频率以及发展成为脑梗死的发生率。结果 LPA增高组患者治疗前和治疗后LPA浓度明显高于LPA正常组,LPA增高组患者治疗后LPA浓度较治疗前明显降低(P<0.05)。经过1个月的氟吡格雷治疗,LPA增高组患者中,1个月内平均发作(1.53±0.34)次,共有8例发展成为脑梗死,发生率为16.3%,而LPA正常组患者中,1个月内平均发作(2.17±0.52)次,有7例发展成为脑梗死,发生率为25.0%。结论氯吡格雷治疗高血浓度LPA的TIA患者疗效优于正常血浓度LPA的TIA患者。     

银丹心脑通对短暂性脑缺血发作患者血浆内皮素和降钙素基因相关肽的影响

目的 观察银丹心脑通软胶囊防治短暂性脑缺血发作(TIA)的效果.方法 将120例TIA患者随机分为观察组和对照组,各60例.两组均给予阿司匹林及尼莫地平等基础治疗,观察组加用银丹心脑通软胶囊,两组随访观察28 d.观察两组治疗前后血浆内皮素(ET)和降钙素基因相关肽(CGRP)的含量变化.结果 病例组ET高于正常组.治疗4周后,观察组ET下降(P＜0.01),CGRP上升.结论 银丹心脑通软胶囊可有效抑制内皮细胞损伤,降低ET释放,改善脑血流量,增强脑供氧,阻止TIA演变为脑梗死的进程.     

短暂性脑缺血发作患者纤维蛋白原和C-反应蛋白的检测及其临床意义

目的:观察短暂性脑缺血发作(TIA)患者卒中危险程度与血浆纤维蛋白原(FIB)含量和C-反应蛋白(CRP)水平的关系并探讨其临床意义。方法:60例TIA患者按TIA后预测短暂脑卒中危险性的ABCD评分系统,被分为高危卒中组(ABCD评分>4分,32例),非高危卒中组(TIA组,ABCD评分≤4分,30例),另30例健康体检者作为健康对照组。分别测量各组对象的血浆FIB、血清CRP水平并作比较。结果:高危卒中组血浆FIB水平[(4.6±1.2)g/L]、血清CRP水平[(32.12±6.3)mg/L]明显高于TIA组[(3.6±0.2)g/L、(6.20±4.5mg/L)]及健康对照组[(3.1±0.3)g/L、(5.4±4.8)mg/L],P<0.05或P<0.01。Pearson直线相关分析表明,高危卒中组血浆FIB与血清CRP水平呈正相关(r=0.61,P<0.01)。结论:不同卒中危险程度短暂性脑缺血发作患者血浆纤维蛋白原和血清C-反应蛋白水平存在显著差异。C-反应蛋白与纤维蛋白原可作为早期预测短暂性脑缺血发作患者发生脑卒中风险的生化指标。     

溶血磷脂酸作为缺血性脑血管病早期预警因子的观察

目的探讨溶血磷脂酸在缺血性脑血管病早期的预警价值。方法对1226例发病48 h的脑梗死和短暂性脑缺血发作患者与719例健康人的血浆进行溶血磷脂酸(LPA)检测,总结其特点。结果观察组(脑梗死、短暂性脑缺血发作)血浆LPA水平均明显升高,显著高于对照组(健康人群)。结论 LPA是血小板活化早期释放的物质,可作为缺血性脑血管病的早期预警因子。     

抗血小板药物与血浆溶血磷脂酸水平的对比研究

目的探讨在心脑血管疾病一、二级预防中起重要作用的抗血小板药物与血浆溶血磷脂酸(LPA)水平的关系。方法随机选择有缺血性脑卒中危险因素及临床症状、需要二级预防的患者502例(治疗组),给予阿司匹林等抗血小板药物进行治疗,治疗前后进行症状自我评分,测定血浆LPA水平,检测抗血小板药物降低血浆LPA的效能及与临床症状的相关性。另选同期健康体检者79例作为对照组。比较两组血浆LPA水平。结果治疗组治疗前血浆LPA水平明显高于对照组[(5.17±2.03)μmol/L vs(2.72±2.70)μmol/L,P0.01]。治疗组服用阿司匹林1个月后LPA水平明显下降[(5.17±2.03)μmol/L vs(3.21±1.57)μmol/L,P0.01]。阿司匹林治疗导致血浆LPA下降程度与症状自我评分降低呈正相关(r=0.290,P0.01)。联合应用抗血小板药物血浆LPA也相应降低。结论 LPA可能作为较有价值的实验室指标来判断阿司匹林等抗血小板药物的效果。对服用阿司匹林100 mg/d反应欠佳的患者可以考虑联合使用抗血小板药物。     

短暂性脑缺血发作患者颅内外动脉狭窄与血浆溶血磷脂酸水平的相关性研究

目的探讨短暂性脑缺血发作（TIA）患者颅内外动脉狭窄程度和其血浆溶血磷脂酸（LPA）水平的相关性。方法选择2010年1月至2013年10月入住我院神经内科并明确诊断为TIA的患者97例,所有患者行头及颈CT血管成像（CTA）检查以评估颅内外血管病变情况。根据患者血管狭窄程度分为四组：无狭窄组、轻度、中度及重度狭窄组。采用定磷法测定所有TIA患者的血浆LPA水平,对可能有意义的影响因素进行有序Logistic回归分析。结果脑血管造影检查发现无颅内外动脉狭窄的患者11例,有颅内外血管狭窄的86例,其中轻度狭窄者39例,中度狭窄者32例,重度狭窄并闭塞者的患者15例。单因素分析结果表明,年龄、糖尿病、血浆LPA水平等因素在不同颅内外动脉狭窄程度的TIA患者之间有显著性差异（F=6．933,P=0．000;X2=16．413,P=0．001;F=4．456,P=0．006）。Logistic回归分析显示年龄、糖尿病与TIA患者颅内外血管狭窄程度独立相关,血浆LPA水平与TIA患者颅内外血管狭窄程度也存在一定的关联,取LPA2．5μmol／L为界值,LPA〉2．5μmol／L是TIA患者存在颅内外血管狭窄的独立预测因子（OR：2．277,P=0．061）,高血压、卒中史也与TIA患者颅内外动脉狭窄程度存在相关性,但各组间差异均无统计学意义（P〉0．05）。Spearman等级相关分析显示,LPA水平与颅内外动脉狭窄程度呈正相关（r=0．347,P=0．000）,校正年龄、糖尿病、高血压、卒中史等因素后相关性仍存在（r=0．214,P=0．039）。结论TIA患者血浆LPA水平与颅内外动脉狭窄病变等级存在相关性,颅内外血管狭窄程度越高,LPA水平也就越高。血浆IJPA水平或可作为TIA患者存在颅内外血管狭窄的独立预测因子。     

Microparticle-associated P-selectin reflects platelet activation in preeclampsia

Platelet activation in preeclampsia is reflected by elevated levels of platelets exposing P-selectin. In plasma, a non-cell bound (soluble) form of P-selectin is present. Elevated levels of this soluble form have been reported in preeclampsia. Plasma P-selectin may consist of two fractions: microparticle (MP)--associated P-selectin and non-MP--associated P-selectin. In the present cross-sectional study, we investigated to which extent plasma P-selectin is MP--associated and whether such MP are elevated in preeclamptic patients. Preeclamptic patients (n=10) were matched with normotensive pregnant women (n=10) and non-pregnant controls (n=10). Plasma P-selectin was measured by ELISA. MP were isolated, double labelled with anti-CD61 (GPIIIa) and anti-CD62P (P-selectin) and subsequently analyzed with flowcytometry. Plasma P-selectin concentration was elevated in preeclamptic patients compared to non-pregnant controls (p=0.007), but not compared to normotensive pregnant women (p=0.210). Plasma P-selectin is partially MP--associated (3-5%). In pregnancy, the fraction of P-selectin exposing platelet-derived MP (PMP) (10.9%) was increased compared to non-pregnant controls (8%). This fraction further increased in preeclamptic patients (15.4%), and significantly differed from normotensive pregnant women (p=0.02). A minor fraction of plasma P-selectin is associated with PMP. The fraction of PMP exposing P-selectin is increased in preeclamptic patients and to a lesser extent in normotensive pregnancy. Because MP associated P-selectin exclusively originates from platelets, this fraction indicates platelet activation. Platelet activation is prominent in preeclampsia and this study proves that at least a part of the plasma P-selectin originates from platelets.     

Altered plasma lipid pattern in falciparum malaria.

Plasma levels of HDL, LDL, total cholesterol and triglycerides were measured in 60 patients with falciparum malaria (37 severe cases and 23 mild) and in 83 healthy individuals, to study malaria-induced changes in plasma lipids. Triglyceride levels were lower in the patients than in the controls but the difference was significant only for those with severe malaria (P < 0.001). In contrast, the levels of all the other plasma lipids were significantly higher (P < 0.001) in those with severe malaria than in those with mild malaria, and in the mild malaria cases compared with the controls. Initially LDL cholesterol was estimated by the Friedwald formula, but this gave negative values in a few cases of severe malaria. Plasma lipoproteins were therefore also measured by nephelometry; the estimated levels of S particles, corresponding to LDL, were then found to be lower in all malaria cases than in the controls (P < 0.001) but never negative. Interestingly, levels of L particles in the patients with severe malaria were significantly elevated compared with the other patients and controls (P < 0.001), indicating impaired metabolism of chylomicrons. Plasma albumin, considered a negative acute phase protein (i.e. its level decreases as a consequence of the acute phase response), was reduced significantly and was directly correlated to HDL cholesterol levels (r = 0.715 and r = 0.895, respectively) in both mild and severe malaria. Follow-up of 22 of the severe malaria cases three weeks after treatment indicated that, while triglycerides had returned to similar levels to those in the controls, total cholesterol levels were still elevated and could give misleading results if lipid profiles were used, immediately after malaria infection, to assess an individual's risk of developing atherosclerosis.     

Hypothalamic-pituitary-adrenal axis activity in patients with rheumatoid arthritis

OBJECTIVE: To study the hypothalamic-pituitary-adrenal (HPA) axis in patients with rheumatoid arthritis (RA). METHODS: Fifty patients with RA participated in 3 groups: recent onset active RA (n = 20), longstanding active RA (n = 20) and long-standing RA in remission (n = 10), and were compared with 20 healthy controls. The activity of the HPA-axis was assessed under basal conditions and in response to stress (insulin tolerance test, ITT). In addition, patients with recent onset RA underwent a corticotropin releasing hormone (CRH) test and a dexamethasone suppression test. Plasma levels of interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha) and IL-6 were also measured. RESULTS: Basal plasma, salivary and urinary cortisol levels and plasma adrenocorticotropic hormone (ACTH) levels were not different between patients with RA and healthy controls. During the ITT, cortisol levels were consistently lower in RA patients than in healthy controls. ACTH levels during the ITT were not different between patients with RA and healthy controls. ACTH and cortisol responses to CRH were assessed only in patients with recent onset RA and were found to be within normal limits. Basal circulating plasma IL-6 levels were significantly higher in patients with active RA than in the other groups. CONCLUSION: Under the standardized conditions of the ITT, patients with RA have decreased plasma cortisol levels compared to healthy controls, despite elevated levels of IL-6. The defect is probably located at the adrenal level and may be of pathogenetic significance for the development of chronic arthritis.     

血浆中特定磷脂与慢性脑供血不足的相关研究

目的探讨慢性脑供血不足(CCCI)与血浆中特定的磷脂(AP)的相关性,以评价AP是否可以作为诊断CCCI的标准之一。方法选择CCCI患者1212例为CCCI组,同期选择无CCCI症状者202例为对照组,用比色法测定AP。采用ROC曲线下面积等评估测定AP的准确性。结果与对照组比较,CCCI组血浆AP水平显著升高[(6.27±0.69)Uυs(4.37±0.79)U,P<0.01]。CCCI组血浆AP水平与年龄无相关性(r=0.001,P=0.902)。用血浆AP作为CCCI的诊断方法的准确性较高,其ROC曲线下面积为0.961(95%CI:0.946～0.976,P<0.01)。AP正常界值=5.39 U时,敏感性为92.1%,特异性为89.1%。结论 CCCI患者具有血浆AP水平升高的生化特性。AP可能是诊断CCCI的一个较好的分子标记物。