创伤患者纤维蛋白单体的聚合功能

背景创伤可以引发机体高凝血状态,并可导致显微外科手术失败.目的观察创伤患者治疗前后纤维蛋白单体聚合功能的变化,探索预测创伤后高凝状态和血栓形成的有效辅助手段.设计病例-对照观察,前后对照观察.单位华中科技大学同济医学院协和医院血栓与止血研究室.对象创伤组受检病例为2001-05/2002-01华中科技大学同济医学院协和医院住院的创伤患者34例,男18例,女16例,年龄8～65岁;正常对照组为健康体检者96例,男50例,女46例,年龄21～68岁.所有受检者均无凝血障碍病史,无全身性与凝血相关疾病.方法血浆纤维蛋白单体聚合功能采用血浆纤维蛋白单体聚合功能测定系统进行测定.在蕲蛇毒的作用下,纤维蛋白原转变为纤维蛋白单体并发生聚合反应,伴随纤维蛋白单体聚合反应发生的浊度变化,用光度仪在340 nm连续进行监测,并将电信号输入微机进行分析.创伤组分别于患者创伤后入院时和入院后经过临床清创、手术、缝合、补液及应用抗生素后第3天采集静脉血,测定纤维蛋白单体聚合功能.主要观察指标①纤维蛋白单体聚合速率(反映血浆纤维蛋白原浓度和功能的综合参数).②最大吸光度(反映标本中凝固性血浆纤维蛋白原的量).③纤维蛋白单体聚合速率与最大吸光度的比值(反映血浆纤维蛋白原分子的聚合功能).结果全体受检者均完成相应检测并纳入数据统计中.①创伤组患者纤维蛋白单体聚合反应速率、纤维蛋白原含量、纤维蛋白单体聚合速率与最大吸光度的比值均显著高于正常对照组[创伤组0.87±0.31,(5.81±3.22)g/L,4.61±0.97;正常对照组0.61±0.15,(3.36±1.02)g/L,3.93±0.68,P＜0.01].②治疗3 d后,尽管纤维蛋白单体聚合速率、纤维蛋白原含量有所下降,但仍高于正常组[3.93±0.68,(4.21±1.93)g/L],而纤维蛋白单体聚合速率与最大吸光度的比值无改变(4.68±1.19).结论创伤患者纤维蛋白原水平增高功能增强.创伤患者机体处于高凝状态,有血栓形成趋势.纤维蛋白单体聚合功能测定可作为创伤后预测高凝状态和血栓形成的有效辅助手段.     

血浆纤维蛋白原水平与纤维蛋白单体聚合功能的测定

目的 :建立广州地区健康成人血浆纤维蛋白水平及纤维蛋白原单体聚合功能的正常参考值。方法 :用蕲蛇酶 (Acutulase)水解纤维蛋白 ,用计算机自动检测系统测定。结果 :①纤维蛋白单体聚合反应速率 (FMPV)为 0 498± 0 1 1 0 ;②最大吸光度 (Amax)为 0 2 50± 0 0 5;③纤维蛋白原的浓度 (S)为 2 80±0 65( g/L) ;④FMPV/Amax比值为 1 992± 0 1 80 ;⑤反应延滞时间 (DT)为 2 5± 5(s)。结论 :计算机自动检测系统操作简单快捷 ,测出的纤维蛋白原浓度与传统改良的Clauss法相比 ,无显著性差异。FMPV/Amax比值稳定 ,表明正常人的纤维蛋白单体聚合能力与纤维蛋白的量成正相关。     

缺血性脑血管病患者纤维蛋白单体聚合功能及康复介入的影响

目的　研究缺血性脑血管病患者纤维蛋白单体聚合功能的临床意义及康复介入的影响。方法　检测 110例不同类型缺血性脑血管病患者、及其中 31例脑梗死患者康复介入前后和 5 0例健康人的纤维蛋白单体聚合功能参数。结果　缺血性脑血管病患者较健康人纤维蛋白单体聚合功能各项参数均显著增高(P <0 .0 1) ;缺血性脑血管病患者纤维蛋白原 (Fbg)水平和纤维蛋白单体聚合速率 (FMPV)的异常率较健康人显著增高 (P <0 .0 1) ,Fbg水平异常和纤维蛋白单体聚合功能异常患者缺血性脑血管病的相对危险度 (RR)分别是健康对照组的 4和 31倍 ;脑梗死患者中 ,前循环梗死组FMPV较后循环梗死组和腔隙性脑梗死组显著升高 (P <0 .0 5 ) ;康复介入前脑梗死患者纤维蛋白单体聚合功能显著高于健康对照组 ,康复介入后纤维蛋白单体聚合功能各参数有所降低 ,但与治疗前无显著性差异。结论　纤维蛋白单体聚合功能测定能更全面、客观地反映缺血性脑血管病患者的凝血状态 ,其异常幅度能在一定程度上反应梗死的范围和严重程度。尽管一般的康复介入不能有效改善血液的高凝状态 ,但随着医学技术的不断发展 ,特殊的康复介入对于血液凝血机制的影响值得进一步研究。     

血浆纤维蛋白原单体聚合功能测定及应用

血浆纤维蛋白原单体聚合功能测定及应用符民桂，马西，纪卫东，卢阳测定纤维蛋白原（Ｆｇ）浓度的方法多种多样，但缺乏反映其功能的方法。在凝血酶诱导纤维蛋白单体（Ｆｍ）形成与聚合反应中，反应速度不但取决于凝血酶的活性，而且与纤维蛋白原浓度及其分子功能状态相关...     

缺血性脑血管病康复介入与纤维蛋白单体聚合功能变化的关系

背景：血浆纤维蛋白原(fibrinogen，Fbg)水平的升高是脑血管病的主要危险因素，纤维蛋白单体聚合功能的评价远较Fbg水平的测定具有更重要的临床价值。目的：研究缺血性脑血管病患者纤维蛋白单体聚合功能的临床意义及康复介入对其的影响作用。设计：以患者和正常人为研究对象，病例一对照研究。单位：一所大学医院血液病研究所和神经内科。对象：2001—09／2002—03检测华中科技大学同济医学院附属协和医院神经内科110例不同类型的缺血性脑血管病患者和50例健康人。方法：随机选取31例脑梗死患者进行康复介入，采用血浆纤维蛋白单位聚合功能测定系统进行测定各组血浆纤维蛋白单体聚合功能参数。主要观察指标：纤维蛋白单体聚合功能各项参数的异常情况。结果：缺血性脑血管病患者较健康人纤维蛋白单体聚合功能各项参数均显著增高(P&;lt;0．01)；缺血性脑血管病患者Fbg水平和纤维蛋白单体聚合速率(FMPV)的异常率较健康人显著增高(P&;lt;0．01)，纤维蛋白单体聚合功能异常患者缺血性脑血管病的相对危险度(RR)分别是健康对照组的4～31倍；脑梗死患者中，前循环梗死组FMPV较后循环梗死组和腔隙性脑梗死组显著升高(P&;lt;0．05)；康复介入前脑梗死患者纤维蛋白单体聚合功能显著高于健康对照组，康复介入后纤维蛋白单体聚合功能各参数有所降低，但与治疗前差异无显著性意义。结论：纤维蛋白单体聚合功能测定能更全面、客观的反映缺血性脑血管病患者的凝血状态，能在一定程度上反应梗死的范围和严重程度。尽管一般的康复介入不能有效改善血液的高凝状态，但随着医学技术的不断发展，特殊的康复介入对于凝血机制的影响值得进一步研究．     

纤维蛋白原与纤维蛋白单体聚合功能在亚急性重症乙型肝炎患者中的测定与意义

目的　检测亚急性重症乙型肝炎患者血浆中纤维蛋白原与纤维蛋白单体聚合功能 ,以了解其凝血功能。方法　用蕲蛇酶水解纤维蛋白原和其相关数值。结果　 16例亚急性重症乙型肝炎患者①纤维蛋白原聚合反应速度为 0 312± 0 0 6 5 ;②最大吸光度为 0 175± 0 .0 35 ;③凝固性纤维蛋白含量为 15 0± 30 (mg/dl) ;④纤维蛋白聚合体反应速率 /最大吸光度比值为 1 790± 0 .16 0 ;⑤反应延滞时间为 - 2 1± 5 (s)。结论　亚急性重症乙型肝炎患者的纤维蛋白原反应时间增快 ,但其他各项指标均下调 ,表明患者出血与凝血功能受损有关     

缺血性脑血管病康复介入与纤维蛋白单体聚合功能变化的关系

背景血浆纤维蛋白原(fibrinogen,Fbg)水平的升高是脑血管病的主要危险因素,纤维蛋白单体聚合功能的评价远较Fbg水平的测定具有更重要的临床价值.目的研究缺血性脑血管病患者纤维蛋白单体聚合功能的临床意义及康复介入对其的影响作用.设计以患者和正常人为研究对象,病例-对照研究.单位一所大学医院血液病研究所和神经内科.对象2001-09/2002-03检测华中科技大学同济医学院附属协和医院神经内科110例不同类型的缺血性脑血管病患者和50例健康人.方法随机选取31例脑梗死患者进行康复介入,采用血浆纤维蛋白单位聚合功能测定系统进行测定各组血浆纤维蛋白单体聚合功能参数.主要观察指标纤维蛋白单体聚合功能各项参数的异常情况.结果缺血性脑血管病患者较健康人纤维蛋白单体聚合功能各项参数均显著增高(P＜0.01);缺血性脑血管病患者Fbg水平和纤维蛋白单体聚合速率(FMPV)的异常率较健康人显著增高(P＜0.01),纤维蛋白单体聚合功能异常患者缺血性脑血管病的相对危险度(RR)分别是健康对照组的4～31倍;脑梗死患者中,前循环梗死组FMPV较后循环梗死组和腔隙性脑梗死组显著升高(P＜0.05);康复介入前脑梗死患者纤维蛋白单体聚合功能显著高于健康对照组,康复介入后纤维蛋白单体聚合功能各参数有所降低,但与治疗前差异无显著性意义.结论纤维蛋白单体聚合功能测定能更全面、客观的反映缺血性脑血管病患者的凝血状态,能在一定程度上反应梗死的范围和严重程度.尽管一般的康复介入不能有效改善血液的高凝状态,但随着医学技术的不断发展,特殊的康复介入对于凝血机制的影响值得进一步研究.     

多发性创伤患者纤维蛋白溶解功能的变化

目的探讨多发性创伤患者纤维蛋白溶解功能的变化及其临床意义。方法检测了34例多发性创伤患者伤后24 h内及伤后第3天和30名健康人血液中血浆纤维蛋白原含量（FIB）、纤溶酶原活性（PLG：A）、血浆D-二聚体（DD）、组织型纤溶酶原激活物抗原性（t-PA：Ag）、纤溶酶原激活物抑制剂-1抗原性（PAI-1：Ag）。根据创伤严重程度分为脏器功能不全组16例与脏器功能正常组18例,将24 h内的各检测指标进行比较分析;以及根据预后分为死亡组12例与非死亡组22例的24 h内各检测指标与第3 d的结果比较。结果多发性创伤各组FIB、DD、t-PA：Ag含量明显高于正常对照组,PLG：A明显低于正常对照组（P均〈0.01）,其中脏器功能不全组变化更大,除PAI-1：Ag外其他各指标与脏器功能正常组比较差异均有统计学意义（P均〈0.01）。死亡组第3天FIB、PLG：A、PAI-1：Ag均明显低于24 h内测定的值,DD含量则明显升高（P均〈0.01）,而非死亡组第3天PLG：A、PAI-1：Ag均明显升高,FIB、t-PA：Ag、DD含量下降（P〈0.01或P〈0.05）。结论多发性创伤导致机体继发性纤溶功能亢进,是患者死亡的原因之一。纤溶功能指标的检测有助于临床病情的判断,并为纠正弥散性血管内凝血（DIC）提供实验室依据。     

多发性创伤患者纤维蛋白溶解功能的变化

目的探讨多发性创伤患者纤维蛋白溶解功能的变化及其临床意义。方法检测了34例多发性创伤患者伤后24 h内及伤后第3天和30名健康人血液中血浆纤维蛋白原含量(FIB)、纤溶酶原活性(PLG:A)、血浆D-二聚体(DD)、组织型纤溶酶原激活物抗原性(t-PA:Ag)、纤溶酶原激活物抑制剂-1抗原性(PAI-1:Ag)。根据创伤严重程度分为脏器功能不全组16例与脏器功能正常组18例,将24 h内的各检测指标进行比较分析;以及根据预后分为死亡组12例与非死亡组22例的24 h内各检测指标与第3 d的结果比较。结果多发性创伤各组FIB、DD、t-PA:Ag含量明显高于正常对照组,PLG:A明显低于正常对照组(P均<0.01),其中脏器功能不全组变化更大,除PAI-1:Ag外其他各指标与脏器功能正常组比较差异均有统计学意义(P均<0.01)。死亡组第3天FIB、PLG:A、PAI-1:Ag均明显低于24 h内测定的值,DD含量则明显升高(P均<0.01),而非死亡组第3天PLG:A、PAI-1:Ag均明显升高,FIB、t-PA:Ag、DD含量下降(P<0.01或P<0.05)。结论多发性创伤导致机体继发性纤溶功能亢进,是患者死亡的原因之一。纤溶功能指标的检测有助于临床病情的判断,并为纠正弥散性血管内凝血(DIC)提供实验室依据。     

The soluble fibrin monomer in patients with instable angina

The purpose of the study was to measure the blood level of thrombus precursor protein (TpP), a soluble fibrin monomer, in patients with stable exertional angina (SEA) and healthy people. The study included the examination of 33 patients with SEA (functional class II and III) and 29 practically healthy volunteers (control group). The detection of TpP in blood plasma was performed by solid-phase immune-enzyme analysis ("sandwich" type) using commercial diagnosticum "Kit" ("ABS", USA) and a microplate reader "IEMS Analyzer\Dispenser, with automatic result calculation in "Logistic fif" mode. TpP level in patients with SEA on the average was slightly higher than in control group, but the difference was not significant. TpP blood level was independent of the patients' gender, age, angina functional class and an old myocardial infarction. TpP blood level in patients with SEA depended on the duration of the illness, and proved to be significantly higher (compared with that in control group) in patients with SEA during the first 5 years of the illness, i.e. at early stages of CHD. Solid-phase immune-enzyme analysis ("sandwich" type) is a highly informative and affordable clinical method. TpP level in patients with SEA on the average was slightly higher than in healthy people (1.21 +/- 0.06 mkg/ml and 1.01 +/- 0.12 mkg/ml, respectively), but the difference was significant only in patients during the first 5 years of having SEA (1.41 +/- 0.11 mkg/ml).     

Effect of fibrin monomer on spontaneous platelet aggregation

Fibrin monomer (FM) was shown to cause a considerable increase in artificial shear-induced platelet aggregation. The aggregatory effect of FM was found to be tangibly higher than that in fibrinogen. The mechanism of action of FM on platelet aggregation is hypothesized.     

A novel monoclonal antibody to fibrin monomer and soluble fibrin for the detection of soluble fibrin in plasma

BACKGROUND: Soluble fibrin (SF), composed of fibrin monomer (FM) and fibrinogen, is well known to exist in the circulating blood derived from patients with thrombotic diseases, and its quantification is useful to get some information on the state and degree of intravascular coagulation. However, there was no convenient method for the determination of SF. METHODS: We prepared a novel monoclonal antibody (MoAb) (F405) to FM and SF using desAA-fibrin as the immunogen in the presence of anti-polymerant peptide (Gly-Pro-Arg-Pro, GPRP), and the characterization of the F405 was performed by Western blotting analysis and an enzyme-linked immunosorbent assay (ELISA). We also tried to detect SF in human plasma using an ELISA involving the immobilized F405 and horseradish peroxidase (POD)-labeled anti-fibrinogen polyclonal antibody. RESULTS: The antibody reacted with the fibrin degradation products fragments X, Y and E, but not with fibrinogen or its fragments X, Y, D and E, or the fibrin D-dimer. The epitope recognized by F405 appeared to be the alpha-chain N-terminal region exposed upon removal of the A peptide from the Aalpha-chain because F405 was found to bind to the alpha-chain N-terminal oligo-peptide of fibrin (GPRVVERHQ). Since F405 reacted not only with FM in the presence of GPRP peptide, but also with the SF complex prepared by the addition of thrombin-treated FM to human fibrinogen, we attempted to detect SF in human plasma using ELISA. The analytical range of this method was 1-300 microg/ml. The assay detection limit was < 0.5 microg/ml, and the results of intra- and inter-assay precision studies indicated that this method is accurate and yields reproducible results (< 9.4% and < 10%, respectively). When 56 samples of plasma from patients with disseminated intravascular coagulation (DIC) and 117 control samples from healthy individuals were tested, elevated levels of SF complex were detected in the DIC samples: the mean +/- S.D. of the SF concentration in the DIC and control samples were 63.4 +/- 65.3 microg/ml and 1.9 +/- 1.0 microg/ml, respectively. CONCLUSIONS: The ELISA using F405 is useful for the diagnosis of DIC.     

The effect of glycemic control on plasma soluble fibrin monomer complexes and fibronectin in diabetic patients

We have shown previously that increased concentrations of plasma soluble fibrin monomer complexes (SFMC) and elevated fibronectin (Fn) levels are closely related to the development of diabetic microangiopathy. The purpose of the present study was to explore whether or not changes in plasma glucose levels could have an effect on these protein constituents. Plasma glucose levels of 25 uncontrolled diabetic patients were brought under control with insulin and serial measurements of SFMC and Fn were made over a period of 4 weeks. Glucose values fell from an average of 312 mg/100 ml to 160 mg/100 ml. Ten patients with macroproteinuria (i.e. greater than or equal to 0.5 g/24 hr) showed initially elevated plasma SFMC and Fn concentrations. These levels fell significantly over the 4 week observation period: from 13.6 mg/100 ml to 9.4 mg/100 ml for SFMC and from 38.4 mg/100 ml to 34.5 mg/100 ml for Fn. The remaining 15 patients had nearly normal levels of both SFMC (7.9 mg/100 ml) and Fn (31.1 mg/100 ml) and glycemic control brought no further reduction. The data indicated that a) elevated SFMC and Fn levels are indeed associated with diabetic microangiopathy, especially in the presence of macroproteinuria; and b) adequate glycemic control is capable of normalizing the plasma concentration of these constituents.     

Plasma soluble fibrin monomer complexes in nephrotic syndrome--with reference to hypoalbuminemia

Plasma soluble fibrin monomer complexes (SFMC) in 10 patients with nephrotic syndrome were measured to demonstrate the contribution of hypoalbuminemia to the SFMC formation. The levels of SFMC as well as plasma fibrinogen (Fbg) levels were significantly higher than those in control subjects. There was a negative correlation between the levels of SFMC and serum albumin, and also between Fbg and serum albumin. The increase in SFMC levels which indicates the intravascular generation of thrombin might be correlated to hypoalbuminemia in nephrotic syndrome with hypercoagulability.