肝病患者血浆抗凝血酶Ⅲ活性测定

抗凝血酶Ⅲ(Antithrombin-Ⅲ,AT-Ⅲ)是人体内一种重要的抗凝血物质,占人体总抗凝血能力的50%～60%。本文采用凝固时间法测定几种肝病患者血浆AT-Ⅲ活性并与健康人进行比较,结果报道如下。1资料与方法1.1实验对象健康对照组:选择我院门诊健康体检者178例,经体格检查、B超、心电图、血常规、尿常规、肝功能、血脂、肾功能等检查均正常者。其中男75例,女103例;年龄18～58岁。肝病组:选择我院初诊肝病患者195例,其中急性肝炎56例,慢性肝炎88例,肝硬化39例,重症肝炎12例。诊断标准按2000年9月中华医学会传染病与寄生虫病学分会,肝病学分会联合…     

糖尿病足患者血浆D-二聚体、纤维蛋白原水平及抗凝血酶Ⅲ活性

目的:比较不同严重程度糖尿病足患者血浆D-二聚体(D-D)、纤维蛋白原(Fbg)水平及抗凝血酶Ⅲ(AT-Ⅲ)活性。方法:选取本院疮面修复科2012年4月～2013年3月107例糖尿病足患者为观察对象,按其严重程度分为0～2级(A组)、3～4级(B组)两组,另选体检健康者45例为对照(C组),检测以上对象血浆D-二聚体(D-D)、纤维蛋白原(Fbg)水平及抗凝血酶Ⅲ(AT-Ⅲ)活性,并比较各组间各指标的差异。结果:B组血浆D-D、Fbg水平显著高于A组和C组;B组AT-Ⅲ活性显著低于A组,更低于C组。结论:血浆D-D、Fbg水平和AT-Ⅲ活性的联合检测对于判断糖尿病足患者体内高凝状况及监测糖尿病足的发生、发展有重要的临床价值。     

类风湿患者DD和AT-Ⅲ检测的临床意义

目的检测类风湿关节炎（RA）患者血浆D-二聚体（DD）及抗凝血酶Ⅲ（AT-Ⅲ）表达水平,探讨其在RA中的临床意义。方法选择RA患者36例为RA组,正常对照组30例,测定其血浆DD、AT-III及血浆C反应蛋白（CRP）水平。结果 RA组患者血浆DD水平为（289.36±71.75）μg/L,显著高于正常对照组的（132.25±38.63）μg/L;血浆AT-III水平为（56.2±12.70）%,明显低于对照组的（92.40±3.80）%,差异均有统计学意义（P〈0.05）。相关性分析显示,RA组患者血浆DD、AT-III水平与DAS28评分具有相关性（r=0.32,P〈0.01;r=-0.72,P〈0.01）。RA组患者经治疗病情缓解后（DAS28〈2.6）血浆DD水平为（141.38±32.75）μg/L,显著低于治疗前的（289.36±71.75）μg/L,差异有统计学意义（P〈0.01）,与正常对照组比较差异无统计学意义（P〉0.05）;RA组患者经治疗病情缓解后血浆AT-III水平为（96.20±4.20）%,显著高于治疗前的（56.2±12.7）%,差异有统计学意义（P〈0.01）,与正常对照组比较差异无统计学意义（P〉0.05）。结论血浆DD及AT-III水平与RA患者的病情活动有关,可反映心血管病变危险性,对RA患者的病情判断及预后估计有重要的评判价值。     

抗凝血酶因子Ⅲ的分子生物学研究进展

AT-Ⅲ是人血浆中重要的丝氨酸蛋白酶抑制剂,由9个α-螺旋结构,3个β-折叠,一个反应中心环组成。天然AT-Ⅲ与肝素结合使半掩埋的RCL排出分子表面,AT-Ⅲ分子处于高抑制活性构象。AT-Ⅲ基因位于1q23-25,长度为19kb。外显子I前后的DNA序列调控AT-Ⅲ基因的表达。基因的缺失、变异将导致AT-Ⅲ分子在血浆中的浓度低下或功能异常,引发血栓性疾病。     

D-D、Fb和AT-Ⅲ在脑梗死不同时期的变化及相关性分析

目的：探讨血浆D-二聚体（D-D）、纤维蛋白原（Fb）和抗凝血酶Ⅲ（AT-Ⅲ）在脑梗死（CI）不同时期的变化及其临床意义。方法：根据临床特征,对260例CI患者进行分组,其中CI急性期组80例、进展期组41例、非进展期组65例、康复期组74例;90例体检健康者为正常对照组。采用SYSMEX CA7000血凝仪分别检测其血浆D-D、Fb和AT-Ⅲ水平。结果：CI急性期、进展期、非进展期患者D-D、Fb含量均明显高于正常对照组（P〈0.01）,AT-Ⅲ低于正常对照组（P〈0.01）;脑梗死组中,D-D与AT-Ⅲ呈负相关（P〈0.01）,D-D与Fb呈正相关（P〈0.01）,AT-Ⅲ与Fb无相关性。结论：CI患者D-D、Fb、AT-Ⅲ变化显著,D-D升高伴随AT-Ⅲ含量降低,提示D-D、Fb、AT-Ⅲ共同参与了梗死发生发展的病理生理过程,可作为CI临床危险分级和病情监测的指标。     

子痫前期重度患者FⅧ、FⅨ、AT-Ⅲ的测定分析

目的通过对子痫前期重度患者、正常妊娠妇女凝血功能及肝功能指标检测分析,探讨该疾病血管内皮细胞损伤、凝血系统激活及肝功能受损情况。方法通过使用凝固法,发色底物法,免疫法检测30例正常妊娠足月妇女、25例早发型重度子痫前期、35例晚发型重度子痫前期患者入院未用药前FVIII,FⅨ、AT-III,D-Dimer指标,并采用全自动生化分析仪测定其ALT、AST肝功能指标。结果早发型重度子痫前期组、晚发型重度子痫前期与正常对照组比AT-Ⅲ下降,FⅨ、D-D、ALT、AST升高,且差异具有统计学意义(P<0.01)。结论子痫前期重度尤其是早发型患者存在严重的血管内皮细胞损伤、血液高凝状态,随着病情的发展出现一定程度的肝功能损伤。     

肾综合征出血热患者血小板功能、肝素样物质、AT-Ⅲ∶α的变化及相互关系

测定了５５例肾综合征出血热（ＨＦＲＳ）患者血小板计数、血小板粘附功能、血小板聚集功能、血浆肝素样物质含量及抗凝血酶－Ⅲ活性（ＡＴ－Ⅲ∶α）。结果表明，ＨＦＲＳ患者有显著的血小板计数降低，血小板粘附、聚集功能减弱，血肝素样物质含量增高与ＡＴ－Ⅲ∶α下降（Ｐ＜０．０５），在病程的极期与危重型患者，上述改变更为显著。相关分析表明，在ＡＴ－Ⅲ∶α＞８０％的患者，血肝素样物质含量与血小板计数、血小板粘附率及血小板聚集率之间的相关系数分别为－０．４３４４，－０．７１５７，－０．５５４７（Ｐ值均＜０．０１）。提示，ＨＦＲＳ患者血肝素样物质含量的增高可能是血小板数量减少与粘附、聚集功能减弱的原因之一，而这一影响作用在ＡＴ－Ⅲ∶α＞８０％的患者尤为显著。     

冠心病患者血浆组织因子、组织因子途径抑制物水平及抗凝血酶-Ⅲ活性的研究

目的 :检测不同类型冠心病 (CHD)患者血浆组织因子 (TF)、组织因子途径抑制物 (TFPI)抗原水平及抗凝血酶 Ⅲ(AT Ⅲ)活性的变化并探讨其临床意义。方法 :TF抗原 (TF Ag)、TFPI抗原 (TFPI Ag)均采用双抗夹心ELISA法测定 ,AT Ⅲ活性采用发色底物法。结果 :急性心肌梗死 (AMI)组、不稳定型心绞痛 (UAP)组和稳定型心绞痛 (SAP)组TF抗原水平治疗前后均显著高于对照组 (P <0 .0 5 ) ,陈旧性心肌梗死(OMI)组治疗前后与对照组水平接近 (P >0 .0 5 ) ;各组治疗前后TFPI抗原水平均高于对照组 (P <0 .0 5 ) ;各组治疗前AT Ⅲ活性均显著低于对照组 (P <0 .0 5 ) ,治疗后 ,AMI组和UAP组AT Ⅲ活性升高至对照组水平 (P >0 .0 5 ) ,SAP组和OMI组仍低于对照组 (P <0 .0 5 )。结论 :AMI及心绞痛患者发作期 ,外源性凝血途径被启动 ,TF过度表达 ,TFPI反馈性增高 ,AT Ⅲ活性因被过多拮抗和消耗而降低 ,血液处于高凝状态。     

动脉粥样硬化性脑梗死患者血浆抗凝血酶Ⅲ的变化及其机制

 目的：探讨抗凝血酶Ⅲ（AT-Ⅲ）在动脉粥样硬化性脑梗死患者中的变化及其机制。方法：采用发色底物法检测55例动脉粥样硬化性脑梗死患者血浆中AT-Ⅲ活性,并与神经系统损伤程度、一般生化项目进行相关性分析;应用酶联免疫吸附法（ELISA）测定血浆肿瘤坏死因子（TNF-α）和白细胞介素6（IL-6）水平;酶免疫法（EIA）测定患者血浆中免疫复合物的含量;流式细胞术检测外周血单核细胞数量及表型,并与正常组55例体检者进行对照。采用ELISA法分析免疫复合物刺激外周血单核细胞后TNF-α和IL-6分泌的变化;Western blotting法观察TNF-α和IL-6对人脑血管内皮细胞AT-Ⅲ表达的影响。结果：动脉粥样硬化性脑梗死患者血浆中AT-Ⅲ活性明显降低（P<005）,且与神经系统功能损伤程度呈负相关（P<005）,与收缩压、舒张压、空腹血糖、胆固醇、甘油三酯、低密度脂蛋白、同型半胱氨酸呈负相关,与高密度脂蛋白呈正相关（P<005）;同时,患者血浆中TNF-α和IL-6水平明显升高（P<001）,伴随免疫复合物含量增多（P<001）;流式细胞术分析发现,患者外周血CD14+CD16+和CD14+CD32+单核细胞数量无明显变化（P>005）,而CD14+CD64+单核细胞数量显著增多（P<005）。经免疫复合物刺激后,外周血单核细胞TNF-α和IL-6分泌明显升高（P<001）,而TNF-α或IL-6与人脑血管内皮细胞共孵育后,均可下调其AT-Ⅲ蛋白表达水平（P<005或P<001）。结论：AT-Ⅲ在动脉粥样硬化性脑梗死患者血浆中明显降低,是脑梗死发病的危险因素之一,且与病情严重程度相关,其可能的机制是免疫复合物通过CD14+CD64+单核细胞介导促炎细胞因子的产生。升高AT-Ⅲ活性对缺血脑组织具有保护作用。     

青光眼患者血浆肾素活性、AT- Ⅱ RIA的变化

青光眼是目前致盲的主要病因之一，因此，探索其发病机制显得尤为重要。有报道血液流变学、微量元素，前列腺素均与青光眼的发生有关。肾素(Renin)、血管紧张素Ⅱ(AT-Ⅱ)作为血管活性物质在调节机体血压，水和电解质平衡方面的作用已早为人知。但有关PRA和AT-Ⅱ与青光眼的关系尚无文献报道。现将结果报告如下。     

抗凝血酶Ⅲ、D-二聚体与纤维蛋白原在 下肢静脉血栓形成中的临床应用

目的 探讨抗凝血酶Ⅲ（AT-Ⅲ）、D-二聚体（D-D）与纤维蛋白原（Fbg）对下肢静脉血栓形成的临床应用价值。方法 选取2018年1月~12月我院收治的下肢静脉血栓患者100例设为观察组,另选取同期100名健康体检者设为对照组。观察组给予什么治疗方法,比较两组AT-Ⅲ、D-D与Fbg变化及其对下肢静脉血栓的诊断率。结果 术前观察组AT-Ⅲ低于对照组[（82.82±9.17）% vs（101.4±7.66）%],D-D与Fbg高于对照组[（23.49±14.82） g/mL vs（0.37±0.12） g/mL]、[（4.65±1.12）g/L vs（2.52±0.51）g/L],差异有统计学意义（P＜0.05）。观察组术后6 d AT-Ⅲ高于术后3 d[（90.61±7.68）% vs（89.13±29.01）%],但差异无统计学意义（P＞0.05）;D-D与Fbg低于术后3 d[（2.80±0.95） g/mL vs（12.35±8.01） g/mL]、[（2.75±1.01）g/L vs（3.58±1.07）g/L],差异有统计学意义（P＜0.05）。三项联合检测对下肢静脉血栓的诊断率高于AT-Ⅲ、D-D和Fbg单项检测,差异有统计学意义（P＜0.05）。结论 检测AT-Ⅲ、D-D和Fbg是判断机体抗凝水平和血栓形成较为简便且快速的方法,可以作为下肢静脉血栓形成早期诊断与治疗的指标,且三项联合检测可提高下肢静脉血栓诊断率。     

Haemostasis and antithrombin III in the full-term newborn foal

Thirty-three Standardbred foals received a physical examination and had blood drawn for anti-thrombin III (AT III), immunoglobulin G (IgG), and haemostasis evaluation between 24 and 72 h of age. Based on physical examination, a normal haemogram within reference intervals and serum IgG concentration >600 mg/dl, 19 foals remained in the study. AT III values for protein concentration (mg/dl) and activity (mg/dl and percentage thrombin inhibition) were determined by rocket immunoelectrophoresis and chromogenic substrate assay, respectively, and compared to the reference intervals for adults. In 19 healthy, full-term foals, the mean plasma AT III activity for percentage thrombin inhibition (75.9%), mean amount of active AT III (19.2 mg/dl) and the mean plasma AT III concentration (28.7 mg/dl) were significantly (P<0.05) lower than the reference interval of adult values. The mean active AT III concentration for both foals (19.2 mg/dl) and adults (24.6 mg/dl) was significantly (P<0.05) less than their AT III concentration, 28.7 and 44.3 mg/dl, respectively. Fibrinogen degradation products (FDPs) were increased in 100% of the foals, with 12 of 19 (63%) having FDPs >10 <40 g/dl). Platelet count, prothrombin time, activated partial thromboplastin time and fibrinogen did not differ significantly from those of adult values.These findings support the view that haemostasis in the full term foal is characterised as a hypercoagulable state by the significant decrease in plasma AT III activity and concentration and increase in split products of fibrin and fibrinogen.     

Antithrombin III-Veränderungen nach Herzinfarkt

Summary The antithrombin III (AT III) activity and the AT III concentration were investigated in 62 consecutive patients with acute myocardial infarction (AMI). To identify the reactant pattern of AT III in postaggressive situations, we also determined labile and acute phase proteins. Firstly, 29 patients were nourished orally and then 33 patients were fed by i.v. hyperalimentation (additional caloric intake of approximately 1,000 cal). AT III activities and concentrations as well as prealbumin and retinol-binding protein decreased concomittantly and significantly whereas haptoglobin, C-reactive protein and fibrinogen increased significantly after AMI. The changes cannot be interpreted as being alterations of the haematocrit. The alterations of AT III correlated significantly with the changes of labile proteins but not with the acute phase reactant proteins. The AT III decrease in the postinfarctional phase may promote a prethrombotic state. In addition it can be concluded from our results that AT III reacts as (nutritive-dependent) labile protein, which is lowered in postaggressive situation and does not increase as an acute phase reactant. This is in accordance with results from recent animal experiments.

     

Effect of Antithrombin III on Local Hemostasis in the Kidneys during Experimental Nephritis

Administration of antithrombin III-enriched plasma to rabbits with acute Masugi nephritis inhibited prothrombinase formation and increased the release of component C3 from the kidneys. This treatment had a cytoprotective effect and was probably followed by dissociation of antigen--antibody complexes.     

Decreased production or increased turnover of antithrombin III in severe acquired coagulopathy?

Summary During the course of severe coagulopathy in an infant suffering from septicaemia and shock, antithrombin III levels were determined repeatedly before and during substitution therapy with human antithrombin. By mathematical analysis of these data, using a biexponential function, the plasma elimination half-life of the antithrombin III was estimated to be 7.5–10.5 h. Compared with known plasma half-lives of radioactively labelled antithrombin III in adults the increase was five-to ten-fold. This indicates that the significantly decreased levels of antithrombin III in this case of coagulopathy were at least partly due to an accelerated consumption of antithrombin III. The estimation of the plasma elimination half-life of antithrombin III helps to differentiate decreased production from increased consumption in cases of severe coagulopathy. Thus, a more precise diagnosis of disseminated intravascular coagulation can be made whilst taking advantage of substitution therapy and avoiding the hazards of radioactive tracer proteins.     

Antithrombotic activity of Russian Antithrombin III preparation on the model of induced venous thrombosis

Antithrombotic activity of Russian preparation Antithrombin III was studied on rat model of induced venous thrombosis. Optimal doses of antithrombin and heparin preventing thrombus growth were determined. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 142, No. 7, pp. 75–77, July, 2006     

Modulation of hemostatic balance with antithrombin III replacement therapy in a case of liver cirrhosis associated with recurrent venous thrombosis

Patients with liver failure can present both thrombotic and hemorragic complications because of the deficiency in coagulation factors and inhibitors (protein C and S, antithrombin III) and impairment of fibrinolytic balance. Here we report the case of a 63-year-old man with liver cirrhosis, recurrent thrombosis, and features of low-grade consumption coagulopathy, showing severe antithrombin III deficiency (about 30% of normal values). Treatment with antithrombin III (2000 U/day) and low doses of heparin (5000 U b.i.d.) was successful in modulating the coagulation system toward an antithrombotic effect. After discharge from hospital the ambulatory treatment with antithrombin III concentrates (2000 U twice a week) allowed the attainment of antithrombin III activity of about 60% and prevented the patient from recurrence of venous thrombosis.Abbreviations AT-III Antithrombin III - DIC Disseminated intravascular coagulation - TAT complexes Thrombin-antithrombin III complexes - PAI-1 Plasminogen activator inhibitor-1