创伤弧菌脓毒症大鼠肝组织因子和组织因子途径抑制物的基因表达及抗生素的影响

目的 研究创伤弧菌(VV)脓毒症大鼠肝组织的组织因子(TF)和组织因子途径抑制物(TFPI)基因表达及抗生素头孢哌酮钠联用乳酸左旋氧氟沙星对其的影响.方法 110只雄性SD大鼠随机(随机数字法)分为正常对照组(NC组,10只)、创伤弧菌脓毒症组(VV组,分5个哑组,每亚组10只)、创伤弧菌脓毒症药物干预组(AA组,分5个亚组,每亚组10只).构建创伤弧菌脓毒症模型及药物干预模型.RT-PCR检测大鼠肝组织TF mRNA和TFPI mRNA的基因表达水平.应用SPSS 12.0进行t检验、方差分析等处理.结果 与NC组相比,VV组染菌后2 h,6 h,9 h,12 h,16 h TF mRNA表达均明显升高(P<0.05),其中染菌6 h表达最高;从组染菌后9 h,12 h的TF mRNA仍明显高于NC组(P<0.05),后逐渐减少.VV组与AA组的肝组织TFPI mRNA与NC组相比,均无明显改变(P>0.05).与相同时间点的VV组相比,AA组16 h TF mRNA明显降低(P相似文献   

TF及TFPI在急性白血病患者血浆中检测的临床意义

目的：检测急性白血病（AL）患者化疗前后血浆中组织因子（TF）及组织因子途径抑制物（TFPI）的含量变化,探讨血浆TF及TFPI在AL病情进展、疗效观察、预后判断中的意义,为AL患者发生凝血功能异常提供临床诊断和治疗依据。方法：选择2009年7月—2010年2月间住院的各型初诊AL患者48例,正常对照组20例,采集空腹外周肘静脉血,应用酶联免疫吸附法（ELISA）检测AL患者血浆中TF及TFPI的含量,同时检测其他的临床相关指标,比较血浆TF及TFPI含量在AL患者化疗前后的变化。结果：初诊的AL患者经治疗缓解后血浆TF和TFPI含量均较治疗前明显下降,差异有统计学意义;急性早幼粒细胞白血病（APL）患者化疗前血浆TF和TFPI含量均明显高于其他类型AL,APL患者化疗前后血浆TF和TFPI含量均有明显差异;合并DIC组的AL患者血浆TF和TFPI含量均明显高于不合并DIC组的AL,且化疗前后血浆TF和TFPI含量有显著差异。结论：初诊的AL患者血浆中TF和TFPI的含量均明显增高,而治疗缓解后降低,提示血浆中TF和TFPI含量变化与疾病的发生、进展及临床疗效有一定关系;血浆中TF和TFPI含量的升高与DIC的发生密切相关,在一定程度上对DIC的疗效判断具有预示作用。     

组织因子途径抑制物活性测定及其临床应用

目的 探索组织因子途径抑制物（ＴＦＰＩ）活性测定及其临床应用,方法 采用简易稀释凝血活酶时间方法 对８２例肝脏病,２３例糖尿病,１０２例恶性肿瘤,４６例肾脏病患者进行ＴＦＰＩ活性检测,结果 除了急性肝炎,其他各类疾病ＴＦＰＩ活性均高于正常对照,急性白血病患者治疗前后ＴＦＰＩ活性也有显著差异,结论：ＴＦＰＩ的活性测定能反映各类疾病中的血管病变的严重性,并能对疾病转归作了判断。     

The relationship of TFPI, Lp(a), and oxidized LDL antibody levels in patients with coronary artery disease

OBJECTIVES: The aim of the present study was to determine and correlate tissue factor pathway inhibitor (TFPI), lipoprotein (a) (Lp(a)), oxidized low-density lipoprotein (LDL) antibody (oLAB), and thiobarbituric acid reactive substances (TBARS; as a marker of lipid peroxidation) levels in patients with coronary artery disease (CAD) and in a control group. DESIGN AND METHODS: Peripheral blood samples from patients with coronary heart disease were provided by the Department of Cardiology. Serum oLAB, Lp(a), plasma total TFPI, and plasma-free TFPI levels were determined by ELISA. Serum TBARS levels were determined by a spectrophotometric method using thiobarbituric acid. RESULTS: The CAD and the control group were matched for age and sex. Serum Lp(a), oLAB, and plasma total TFPI levels in patients with coronary heart disease were found to be significantly higher than in the control group (P < 0.001). But there was no difference in plasma-free TFPI levels between patients with CAD and the control group (P > 0.05). In patients with single (P < 0.05), double, and triple vessel (P < 0.01) disease, the mean serum Lp(a) levels were significantly higher than in the control group. On the other hand, in patients with single vessel disease (P < 0.05), double vessel disease (P < 0.05), and triple vessel disease (P < 0.001), plasma total TFPI levels were found to be significantly higher than in the control group. We also found a significant positive correlation (r = 0.28, P < 0.05) between serum Lp(a) and plasma total TFPI levels in CAD. In the patient group, TBARS, total cholesterol, triglyceride (TRG), and LDL cholesterol levels were found to be significantly higher than those in the control group. In addition, high-density lipoprotein (HDL) cholesterol levels were found to be significantly lower than the control group. CONCLUSIONS: These results suggest that elevated plasma levels of total TFPI, Lp(a), and oLAB may be useful diagnostic and monitoring markers in patients with CAD.     

Temporal expression of alternatively spliced forms of tissue factor pathway inhibitor in mice

Summary.  Background: Mouse tissue factor pathway inhibitor (TFPI) is produced in three alternatively spliced isoforms that differ in domain structure and mechanism for cell surface binding. Tissue expression of TFPI isoforms in mice was characterized as an initial step for identification of their physiological functions. Methods and Results: Sequence homology demonstrates that TFPIα existed over 430 Ma while TFPIβ and TFPIγ evolved more recently. In situ hybridization studies of heart and lung did not reveal any cells exclusively expressing a single isoform. Although our previous studies have demonstrated that TFPIα mRNA is more prevalent than TFPIβ or TFPIγ mRNA in mouse tissues, western blot studies demonstrated that TFPIβ is the primary protein isoform produced in adult tissues, while TFPIα is expressed during embryonic development and in placenta. Consistent with TFPIβ as the primary isoform produced within adult vascular beds, the TFPI isoform in mouse plasma migrates like TFPIβ in SDS-PAGE and mice have a much smaller heparin-releasable pool of plasma TFPIα than humans. Conclusions: The data demonstrate that alternatively spliced isoforms of TFPI are temporally expressed in mouse tissues at the level of protein production. TFPIα and TFPIβ are produced in embryonic tissues and in placenta while adult tissues produce almost exclusively TFPIβ.     

中晚期肿瘤患者围术期血浆TF和TFPI水平变化及意义

目的　观察中、晚期肿瘤患者围术期血浆组织因子 (TF) ,组织途径抑制物 (TFPI)水平的变化 ,旨在了解患者在围术期机体的凝血活性状态 .方法　采集 58例恶性肿瘤患者作为观察组I,1 6例良性肿瘤患者作为观察组II及 2 0例非肿瘤手术患者作为正常对照组 ,运用ELISA法检测血浆TF和TFPI的水平。结果　恶性肿瘤患者血浆TF水平较正常对照组术前明显升高 (P <0 .0 5) ,术中继续有轻微升高 (P <0 .0 1 )的现象 ,肺癌患者术中升高较明显 (自身术前 ,术后比较P <0 .0 5〉。术后除肺癌患者仍高于对照组外 ,其他基本恢复正常 .良性肿瘤患者在整个围术期无明显变化。而血浆TFPI水平术中有轻微升高 ,术前、术后及良性肿瘤患者与正常对照组比较没有明显的差异。结论　恶性肿瘤患者术前血浆具有较高表达的TF水平较对照组 ,术中继续有轻微升高 ,肺癌患者升高更明显 ,且术后仍处于较高的水平。TFPI术中有轻微的升高。这也许能解释为什么肺癌等恶性肿瘤患者围术期尤其术后易发生深部静脉血栓栓塞及肿瘤转移和复发。     

急性心肌梗死患者组织因子及组织因子途径激活抑制物水平的变化

目的探讨急性心肌梗死(AMI)患者组织因子(TF)及组织因子途径激活抑制物(TF-PI)的变化及临床意义。方法用ELISA法分别检测50例AMI患者及20例健康对照的外周血TF及TFPI的抗原水平。比较15例支架手术患者冠状窦内及外周血的TFPI水平。比较并发糖尿病和/或高脂血症AMI患者与无并发症者的TFAg及TFPIAg水平。结果AMI患者的TFAg及TFPIAg较正常人均明显升高(P<0.01);支架患者冠状窦内的TFPI水平明显低于其外周血(P<0.01);有并发症患者的TF及TFPI水平均明显高于无并发症患者(分别为P<0.01和P<0.05)。结论AMI患者外周血凝血活性增高,并发糖尿病和/或高脂血症AMI患者的凝血活性较无并发症患者高,血栓形成使冠状动脉腔内的TFPI消耗而降低。     

腔隙性脑梗死患者血浆组织因子和组织因子途径抑制物抗原水平的测定

目的探讨腔隙性脑梗死(lacunarinfarct,LI)患者血浆组织因子(tissue factor,TF)和组织因子途径抑制物(tissuefactor pathwayinhibitor,TFPI)测定的临床意义以及组织因子途径在LI发病中的作用.方法择确诊的LI患者63例,采用酶联免疫吸附的方法测定血浆TF和TFPI相关指标抗原水平,与正常对照组比较并对不同危险因素患者组之间的结果进行分析.结果①与正常对照组比较,LI患者组血浆TF抗原水平显著增高(217.4±101.3pg/ml对140.9±27.1pg/ml,P=0.0003)、游离TFPI抗原水平降低(41.4±16.7 ng/ml对30.0±18.6 ng/ml,P=0.005);②合并高血压、糖尿病和血脂异常LI患者血浆TFPI相关指标的改变不同;③LI患者血浆t-TFPI和tr-TFPI抗原水平与血浆TF抗原水平相关.结论LI患者血浆组织因子途径改变表现为凝血活性增高和抗凝活性减低.     

冠心病患者血浆TF、TFPI水平的变化及其临床意义

目的　观察冠心病患者血浆组织因子 (TF)、组织因子途径抑制物 (TFPI)水平的变化及其临床意义。方法　 79例临床确诊的冠心病患者 ,其中急性心肌梗死 (AMI组 ) 32例、不稳定型心绞痛 (UAP组 ) 2 7例、稳定型心绞痛 (SAP组 ) 2 0例 ,15例健康对照组作为对照组。采用发色底物法测定血浆TF、TFPI活性。结果　与对照组、SAP组比较 ,AMI组血浆TF、TFPI显著增高 ,三组差异具有显著性意义 (P<0 0 5 ) ;AMI组血浆TF活性与UAP组比较差异无统计学意义 (P >0 0 5 ) ,但TFPI活性较UAP组明显升高 ,两者差异具有显著性意义 (P <0 0 5 )。UAP组血浆TF活性较健康对照组及SAP组明显升高 ,三组间差异具有显著性意义 (P <0 0 5 ) ,UAP组血浆TFPI活性较健康对照组及SAP组差异无统计学意义 (P >0 0 5 ) ;SAP组血浆TF、TFPI活性较健康对照组差异无统计学意义 (P >0 0 5 )。结论　 (1)AMI、UAP患者存在异常激活的高凝状态 ,TF触发的外源性凝血途径在冠脉内血栓形成上发挥重要作用。 (2 )AMI、UAP患者体内TF、TFPI系统存在严重失衡     

Hereditary and acquired protein S deficiencies are associated with low TFPI levels in plasma

Summary. Background: Protein S and tissue factor pathway inhibitor (TFPI) act together in down‐regulating coagulation. Objective: To investigate the TFPI/protein S system in hereditary and acquired protein S deficiency. Methods: Plasma antigen levels of protein S and full‐length TFPI were determined in heterozygous type I protein S‐deficient individuals (n = 35), patients on oral anticoagulant treatment (OAT) (n = 29), oral contraceptive (OC) users (n = 10) and matched controls. Thrombin generation was determined using calibrated automated thrombography. Results: Full‐length TFPI levels were lower in type I protein S‐deficient individuals (76.8 ± 33.8%) than in age‐ and sex‐matched controls (128.0 ± 59.4%, P < 0.001). Among protein S‐deficient individuals with thrombosis, those on OAT had not only lower total protein S levels (25.7 ± 8.2% vs. 54.7 ± 8.2%, P < 0.001), but also lower full‐length TFPI levels (52.6 ± 15.0% vs. 75.4 ± 22.9%, P = 0.009) than those not on OAT. Similarly, OC users had lower protein S (73.8 ± 11.5% vs. 87.9 ± 10.8%, P = 0.005) and full‐length TFPI levels (73.7 ± 27.7% vs. 106.4 ± 29.2%, P = 0.007) than non‐users. When triggered with tissue factor, plasma from protein S‐deficient individuals generated 3–5‐fold more thrombin than control plasma. The difference was only partially corrected by normalization of the protein S level, full correction requiring additional normalization of the TFPI level. Protein S‐immunodepletion experiments indicated that free protein S and full‐length TFPI form a complex in plasma, and the protein S/TFPI interaction was confirmed by surface plasmon resonance analysis. Conclusions: Full‐length TFPI binds to protein S in plasma and is reduced in genetic and acquired protein S deficiency. The concomitant TFPI deficiency substantially contributes to the hypercoagulable state associated with protein S deficiency.     

血液透析对维持性血液透析患者血浆组织因子、组织因子途径抑制物活性的影响

目的　观察血液透析过程对维持性血液透析 (maintenancehemodialysis,MHD)患者血浆中组织因子 (tissuefactor,TF)及其调节物 -组织因子途径抑制物 (tissuefactorpathwayinhibitor,TFPI)活性的影响。方法　应用发色底物法检测了 4 3名慢性肾衰竭患者的血浆组织因子、组织因子途径抑制物活性 ,其中 2 0例为未进行血液透析的终末期肾病 (end -stagerenaldisease ,ESRD)患者 (肾衰竭组 ) ,2 3例为慢性MHD患者在一次透析开始前 (透析前组 )和透析结束时 (透析后组 )的血浆TF、TFPI活性指标。同时观察透析过程中肝素对血浆TF、TFPI活性的影响。并对 2 3名健康自愿者 (正常对照组 )进行了血浆TF、TFPI活性的测定。结果　①TF活性在肾衰竭组和透析前组均较正常对照组明显升高 ,分别为 [(1.1790± 0 .2 937)nmvs (0 .30 5 5±0 .190 1)nm ;(0 .884 8± 0 .5 4 6 1)nmvs (0 .30 5 5± 0 .190 1)nm ,(P均 <0 .0 1) ];肾衰竭组高于透析前组 ,但差异无显著性 (P >0 .0 5 ) ;②TFPI活性在透析前组和肾衰竭组均较对照组轻度升高 ,且肾衰竭组TFPI活性低于透析前组 ,但P均 >0 .0 5 ,无统计学意义 ;③一次透析过程中 ,透析后组TFPI活性明显高于透析前组[(2 .110 5± 1.36 37)u/mlvs (1.3347± 0 .84 19)u/ml,(P <0 .0 5 )     

心肺复苏后组织因子和组织因子途径抑制物的动态变化和临床意义

目的 观察院内心肺复苏后不同时间点组织因子(TF)和组织因子途径抑制物(TFPI)水平的动态变化特点并探讨其临床意义.方法 选择2005年9月至2007年9月温州医学院附属第一医院急诊科收治的年龄>16岁明确心搏停止时间的心肺复苏患者24例,依据是否达到自主循环恢复标准随机分为ROSC和末ROSC两组,分别记录小同患者心搏停止的病因和临床特点,并用ELISA方法 检测心肺复苏(CPR)后30 min,60 min,6 h,24 h,48 h血清TF和TFPI抗原浓度,10例来自健康体检的健康自愿者为对照组.计量数据用均数±标准差((-x)±s)来表示,两组计量数据的比较采用独立样本t检验,三组及以上计量数据比较采用单因素方差分析法,计数数据的比较采用旧格表精确x2榆验,以P<0.05为差异具有统计学意义.结果 与对照组比较,ROSC组患者在CPR 30 min血TF水平显著升高(P<0.01),在CPR 6 h达高峰,在CPR48 h时已下降;与对照组及ROSC组同时点比较,末ROSC组血TF水平更是显著升高(P<0.01).与对照组比较,在CPR后30 min,ROSC和未ROSC两组血清TFPI水平差异无统计学意义(P>0.05),60 min后ROSC组血清TFPI水平逐渐升高并有显著差别(P<0.01或<0.05).与对照组比较,未ROSC组和ROSC组患者在CPR 30 min时的TF/TFPI水平均显著性升高(P<0.01),且前者显著高于后者(P<0.01),在ROSC组IF/TFPI值在CPR后6 h有显著升高(P<0.01),在48 h下降.结论 血清TF和TFPI水平在院内心肺复苏的患者中明显升高,CPR后半小时的TF和TF/TFPI的水平可用于判断预后.     

Atorvastatin or transgenic expression of TFPI inhibits coagulation initiated by anti‐nonGal IgG binding to porcine aortic endothelial cells

Summary. Background: Intravascular thrombosis remains a barrier to successful xenotransplantation. Tissue factor (TF) expression on porcine aortic endothelial cells (PAECs), which results from their activation by xenoreactive antibodies (Abs) to Galα1,3Gal (Gal) and subsequent complement activation, plays an important role. Objectives: The present study aimed to clarify the role of Abs directed against nonGal antigens in the activation of PAECs to express functional TF and to investigate selected methods of inhibiting TF activity. Methods: PAECs from wild‐type (WT), α1,3‐galactosyltransferase gene‐knockout (GT‐KO) pigs, or pigs transgenic for CD46 or tissue factor pathway inhibitor (TFPI), were incubated with naïve baboon serum (BS) or sensitized BS (with high anti‐nonGal Ab levels). TF activity of PAECs was assessed. Results: Only fresh, but not heat‐inactivated (HI), naïve BS activated WT PAECs to express functional TF. Similarly, PAECs from CD46 pigs were resistant to activation by naïve BS, but not to activation by fresh or HI sensitized BS. HI sensitized BS also activated GT‐KO PAECs to induce TF activity. TF expression on PAECs induced by anti‐nonGal Abs was inhibited if serum was pretreated with (i) an anti‐IgG Fab Ab or (ii) atorvastatin, or (iii) when PAECs were transgenic for TFPI. Conclusions: Anti‐nonGal IgG Abs activated PAECs to induce TF activity through a complement‐independent pathway. This implies that GT‐KO pigs expressing a complement‐regulatory protein may be insufficient to prevent the activation of PAECs. Genetic modification with an ‘anticoagulant’ gene (e.g. TFPI) or a therapeutic approach (e.g. atorvastatin) will be required to prevent coagulation dysregulation after pig‐to‐primate organ transplantation.     

抗组织因子途径抑制物单克隆抗体的制备及鉴定

目的：制备抗组织因子途径抑制物（ＴＦＰＩ）单克隆抗体。方法：用微量ＴＦＰＩ脾内包埋免疫ＢＡＬＢ／ｃ小鼠，取脾细胞与ＳＰ２／Ｏ细胞融合，建立了２株稳定分泌抗ＴＦＰＩ单克隆抗体（ＭｃＡｂ）的杂交瘤细胞株，分别命名为４Ｆ４和４Ｆ８。对其中的一株４Ｆ８进行研究，其杂交瘤细胞染色体众数为９３，分泌的抗体为ＩｇＧ１。以简易正辛酸法从腹水纯化ＭｃＡｂ４Ｆ８，ＳＤＳ－ＰＡＧＥ检测其纯度，Ｗｅｓｔｅｒｎｂｌｏｔｉｎｇ分析显示其可特异性地识别分子量为３４８００的抗原分子。对纯化的抗体以改良过碘酸钠氧化法用辣根过氧化物酶标记后，采用双夹心ＥＬＩＳＡ法检测正常人血浆ＴＦＰＩ含量。结果：稀释的凝血酶原时间（ＰＴ）测定，ＭｃＡｂ４Ｆ８可缩短其凝固时间，且呈量效关系，ＭｃＡｂ４Ｆ８还可使乏因子Ⅸ血浆稀释的ＰＴ明显缩短。正常人血浆ＴＦＰＩ含量为１０３．２±１１．５μｇ／Ｌ，结果与美国Ｄｉａｇｎｏｓｔｉｃａ公司的ＴＦＰＩＥＬＩＳＡ试剂盒所测结果（９８．４±１０．３μｇ／Ｌ）相近（ｒ＝０．９２）。结论：ＭｃＡｂ４Ｆ８有潜在的药用价值，并可望为我国ＴＦＰＩ的研究提供精确的检测手段。     

Elevated plasma levels of neuropeptide Y in female fibromyalgia patients

Neuropeptide Y(NPY) co-exists with norepinephrine in the sympathetic nervous system, and NPY may represent the sympathetic-neuronal output. Fibromyalgia syndrome (FMS) patients have perturbations in the hypothalmic-pituitary-adrenal (HPA) axis and in the sympathetic stress axis as well. As opioid peptides, monoamines and sex steroids are integrated in the regulation of stress, it is interesting to further explore the role of NPY in FMS patients, as they show many symptoms that are related to perturbations of those systems. In this study, plasma NPY levels were assessed in subgroups of FMS patients: cyclic (regular menstrual cycles), non-cyclic (post-menopausal), depressed and non-depressed patients. In order to examine whether pain and other symptoms seen in FMS patients are correlated to the NPY levels, the patients were also registering 15 different symptoms daily during 28 days. Sex and age-matched healthy controls were recruited for comparisons. Non-parametric tests were used for the statistical analyses. The results showed that the NPY levels were significantly elevated in the patients compared to the controls. In the luteal phase of the cyclic patients, the levels of the peptide were higher than in the corresponding controls. For the non-cyclic patients, there was a positive correlation between physical symptoms and NPY levels, however, pain per se did not reach the significant level of correlation. The non-depressed patients had the same levels of NPY as the depressed FMS patients, who also had a positive correlation between anxiety and NPY levels. These results suggest that FMS patients have an altered activity in the NPY system, most likely due to prolonged and/or repeated stress, and that the hormonal state and time of the menstrual cycle also may be of importance in the complex pathophysiologic mechanism behind the development of FMS.     

Low tissue factor pathway inhibitor (TFPI) together with low antithrombin allows sufficient thrombin generation in neonates

Summary.  Neonates have an excellent hemostasis despite, in comparison to adults, markedly decreased and delayed ability to generate thrombin. Only 30–50% of peak adult thrombin activity can be produced in neonatal plasma by means of conventional in vitro assays. We show that in contrast to conventional activation, activation with small amounts of lipidated tissue factor (<10 pmol L⁻¹) results in shorter clotting times and faster activated factor X- and thrombin generation in neonates compared with adults due to the concomitant action of low tissue factor pathway inhibitor and antithrombin. The concentrations of both inhibitors in cord plasma are approximately 50% of the respective adult values. After addition of 2.5 pmol L⁻¹ lipidated tissue factor, cord plasma clotted ∼90 s earlier than adult plasma and the amount of free thrombin generated was ∼90% of adult value (291 ± 14 vs. 329 ± 16 nmol L⁻¹ min⁻¹, P  < 0.01). Our results might help to explain the clinically observed excellent hemostasis of neonates despite low levels of procoagulant factors.     

创伤弧菌脓毒症血浆组织因子和组织因子途径抑制物的改变及抗菌药物的影响

目的探讨大鼠创伤弧菌(VV)脓毒症血浆中组织因子(TF)和组织因子途径抑制物(TFPI)的改变以及头孢哌酮钠与乳酸左氧氟沙星联用对其的影响。方法制作大鼠VV脓毒症模型(VV组)和VV脓毒症药物干预模型(AA组),使用ELISA法测定各组大鼠血浆中TF和TFPI的含量。结果与正常对照组(NC组)相比,VV组在染菌后9 h、12 h血浆TF显著升高(P＜0．05),各时间点血浆TFPI含量无显著改变(P＞0．05);9 h、12 h的TFPI/TF比值有显著性下降(P＜0．05)。AA组染菌后9 h、12 h血浆TF明显高于NC组(P＜0．05),TFPI/TF比值在抗菌药物干预后逐渐上升,16 h时点该比值明显高于NC组(P＜0．05)。与相同时间点的VV组比较,AA组染菌后12 h血浆TF明显减低(P＜0．05),12 h、16 h血浆TFPI明显升高(P＜0．05),9 h、12 h、16 h的TFPI/TF比值亦明显升高(P＜0．05)。结论创伤弧菌脓毒症时血浆TF含量显著升高,但同期TFPI并无明显减低或升高,TFPI/TF比值减低;头孢哌酮钠联用乳酸左氧氟沙星可减低血浆TF含量,提高TFPI/TF比值。创伤弧菌脓毒症时存在明显的促凝和抗凝作用的失衡,抗菌药物干预后可使促凝和抗凝平衡被逐渐恢复。     

Poor anticoagulant response to tissue factor pathway inhibitor in patients with venous thrombosis

Summary.  Tissue factor pathway inhibitor (TFPI) is of major importance in regulating the coagulation triggering effects of tissue factor. An association between TFPI deficiency and thrombosis has still not been clearly demonstrated. We evaluated the anticoagulant activity of exogenous TFPI added either to the plasma of patients with venous thrombosis ( n  = 118) or to the plasma of healthy controls similar in terms of mean age and sex ratio ( n  = 107). A poor anticoagulant response to TFPI, defined as TFPI resistance, was observed in 4.7% of controls and in 11.0% of patients. TFPI resistance was associated with an almost threefold increase in the risk of thrombosis and could therefore represent a novel hemostatic risk factor for venous thrombosis.     

急性缺血性脑卒中患者脂蛋白相关磷脂酶 A2和同型半胱氨酸水平的变化及影响因素

目的研究急性缺血性脑卒中患者血脂蛋白相关磷脂酶A2（ Lp-PLA2）、同型半胱氨酸（ HCY）水平的变化及影响因素。方法将192例符合筛选标准的急性缺血性脑卒中患者设为卒中组,79例健康体检者设为对照组,前者又根据美国国立卫生院卒中量表（ NIHSS）评价神经功能缺损程度,分为轻度（＜4分）、中度（4～15分）和重度（＞15分）三个组;采血检测血浆Lp-PLA2水平、血清HCY水平、血常规和血生化。结果①脑卒中组Lp-PLA2、HCY水平显著高于对照组,而且重度组高于中度组,中度组高于轻度组,差异均有统计学意义（ P＜0．05）;②脑卒中组血白细胞（WBC）、中性粒细胞（NE）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL）、脂蛋白a[Lp（a）]、葡萄糖（Glu）水平显著高于对照组;高密度脂蛋白（HDL）低于对照组（P＜0.05）;③多重线性回归分析显示,Lp-PLA2与年龄、肥胖、NIHSS评分、HCY呈正相关,HCY与性别、吸烟、NIHSS评分、LP（ a）呈正相关。结论急性缺血性脑卒中血Lp-PLA2和HCY水平均增高,两者显著相关,联合检测可为临床的治疗和二级预防提供一定的帮助。