Fibrinolytic study in plasma and ascitic fluid of cirrhotic patients before and after ascites concentration; reinfusion technique

Management of cirrhosis with massive ascites involves particular difficulties. The introduction of a peritoneovenous shunt and reinfusion of concentrated ascitic fluid techniques allows increased diuresis and improves renal function. However, these procedures have frequently been associated with disseminated intravascular coagulation and/or activation of fibrinolysis. Factor VIII activity, antigen and ristocetin cofactor, plasminogen, antiplasmin, plasminogen activator activity and plasmin-antiplasmin complex were investigated both in the ascitic fluid and plasma of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicated that no hyperfibrinolysis was seen in the plasma of cirrhotic patients and that activation of fibrinolysis exists in ascites. Significantly higher levels of plasmin-antiplasmin complex and plasminogen activator activity were found in ascitic fluid than in plasma. In post-reinfusion much higher levels of all three Factor VIII components were observed in cirrhotic plasma than in normal plasma. In conclusion, activation of fibrinolysis could explain coagulation complications occurring after ascites reinfusion. Antifibrinolytic treatment could render the concentration-reinfusion technique more acceptable.     

A DIC-like picture on plasma and ascitic fluid of cirrhotic patients

Ascitic fluid reinfusion in severe cirrhosis has frequently been associated with intravascular coagulation (DIC). A low-grade DIC has been postulated to be present in liver cirrhosis. PT, APTT, fibrinogen, plasminogen, antiplasmin, fibrin degradation producers (FDP), euglobulin lysis time, tissue plasminogen activator, and fibrinopeptide A were investigated both in the plasma and ascitic fluid of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicate that increased thrombin formation associated with hyperfibrinolysis is present in the plasma of cirrhotic patients. In ascitic fluid very high levels of thrombin and fibrinolysis activation were found. We conclude that (1) a DIC-like picture exists in ascites and (2) after ascites reinfusion procedures, ascitic fluid is the principal factor in the pathogenesis of DIC. During ascitic fluid reinfusion heparin treatment could be used successfully.     

急性脑血栓形成患者血浆及脑脊液纤溶指标的观察

目的：研究急性脑血栓形成患者血浆及脑脊液组织型纤溶酶原激活物(t-PA)及其抑制物(PAI-1)和D-二聚体含量的变化及其临床意义。方法：采用双抗体夹心固相酶联免疫吸附法(ELISA)检测35例急性脑血栓形成患者(血栓组)的血浆和其中3l例的脑脊液t—PA、PAI-l和D-二聚体的抗原含量，与35例无心脑、肝肾及血液疾病患者(对照组)血浆和其中20例脑脊液进行比较。结果：血栓组血浆及脑脊液中t-PA、PAI-1和D-二聚体含量均高于对照组；脑脊液中t-PA、PAI-l和D-二聚体的含量分别与血浆中含量呈正相关。结论：急性脑血栓形成患者纤溶活性明显下降,t-PA及PAI-l参与了脑血栓形成的病理过程。     

脑梗死患者止凝血系统功能改变的研究

目的探讨脑梗死患者治疗前后D-二聚体（D-Dimer）、抗凝血酶活性（AT1A）、组织型纤溶酶原激活物（t—PA）、纤溶酶原激活物抑制物-1（PAI-1）及血管性血友病因子（vWF）的变化趋势,评估上述指标在脑梗死治疗监测中的临床价值。方法采用SYSMEXCA7000型血液凝固仪测定血浆D-Dimer、tPA、PAI-1和AT1A;采用ELISA法测定vWF。结果与健康对照组比较,脑梗死患者组治疗前D-Dimer、PAI-1、vWF显著增高（P〈0．01）,t-PA显著降低（P〈0．01）,AT：A无显著性改变（P〉0．05）。脑梗死患者治疗后血浆D-Dimer、PAI-1、vWF较治疗前显著降低（P〈0．01）,tPA显著增高（P〈0．01）,AT：A在治疗前后无明显改变（P〉0．05）;GCS〉8分组和GCS≤8分组血浆胁Dimer、PAI-1、vWF明显下降（P〈0．01）,t-PA显著增高（P〈0．01）,而AT：A无明显差异（P〉0．05）。结论纤溶系统指标和vWF在脑梗死患者治疗前后发生显著改变且与病程发展相关。     

糖耐量减低患者纤溶受抑的临床观察

目的探讨糖耐量减低(IGT)及IGT合并急性冠状动脉综合征(ACS)患者纤溶受抑状态。方法97例患者随机分成3组,IGT组33例,IGT+ACS组32例,ACS组32例;正常对照组20例。检测血浆中组织型纤溶酶原激活剂(t-PA),纤溶酶原激活物抑制剂-1(PAI-1)及D-二聚体的水平,并计算出PAI-1/D-二聚体的比值。结果IGT组、IGT+ACS组和ACS组血浆t-PA、PAI-1和D-二聚体浓度均显著高于正常对照组(P<0.05,P<0.01);IGT组和IGT+ACS组血浆D-二聚体水平增高幅度则显著低于ACS组(P<0.05,P<0.01);IGT组和IGT+ACS组的PAI-1/D-二聚体比值分别比正常对照组及ACS组明显增高(P<0.01)。结论IGT患者存在纤溶受抑状态,血浆D-二聚体的水平结合PAI-1/D-二聚体比值能反映患者纤溶受抑的状态及预后。     

Plasminogen activators and plasminogen activator inhibitor in malignant and non-malignant ascitic fluid

Ascitic fluid from tumour patients (hepatoma, gastric cancer, gallbladder cancer, colorectal cancer, ovarian cancer) and from non-malignant diseases (liver cirrhosis, congestive heart failure) were compared with respect to their content of determinants of the fibrinolytic system, tissue-type plasminogen activator antigen (t-PAag) and activity (t-PAact), urokinase-type plasminogen activator antigen (u-PA) and plasminogen activator inhibitor activity (PAI). Furthermore, SDS-polyacrylamide slab-gel electrophoresis (SDS-PAGE) was performed to evaluate molecular weight distribution of the detectable fibrinolytic parameters. In malignant ascites, PAI activity was three to four times higher, and increased complex formation of PAI with t-PA could be demonstrated, compared with non-malignant ascitic fluid. Tissue-type plasminogen activator antigen and activity showed a similar concentration in ascites of both study groups. Urokinase-type plasminogen activator antigen was detectable neither in ascites of malignant nor in ascites of non-malignant origin. It is concluded that t-PA is the physiological plasminogen activator in ascites and that increased PAI levels followed by increased complex formation between t-PA and PAI might reflect a reaction of the peritoneum.     

射频导管消融术后部分凝血与纤溶指标的变化

目的观察射频导管消融术(RFCA)对患者术后部分凝血与纤溶指标变化的影响,以及术后恢复时间。方法对56例接受RFCA治疗的患者,在RFCA前、心内电生理检查后、成功消融后即刻、术后第2天和第7天抽取静脉血,测定D-二聚体(DD)、血管内血友病因子(vWF)、血浆组织纤溶酶原(t-PA)和组织纤溶酶原抑制物(PAI-1)含量。结果与术前比较,血浆DD、vWF浓度以及血浆PAI-1含量在心内电生理检查后、消融成功后即刻和术后第2天均显著上升(P0.01),并于第7天降至术前水平(P0.05),而t-PA含量在心内电生理检查后,消融成功后即刻和术后第2天显著下降(P0.01),并于第7天降至术前水平(P0.05)。结论 RFCA可引起血液中部分凝血与纤溶物质水平显著增加,术前、术后对其监测有利于指导抗凝药物应用和预防血栓栓塞的发生。     

急性冠状动脉综合征病人血清CRP与纤溶活性变化

目的探讨急性冠状动脉综合征（ACS）病人血清C-反应蛋白（CRP）与纤溶活性变化。方法检测并比较47例ACS病人、41例稳定型心绞痛（SA）病人和40例正常人（正常对照组）CRP、纤维蛋白原（FIB）、血脂、D-二聚体浓度，组织型纤溶酶原激活物（tPA）、纤溶酶原激活物抑制物-1（PAI-1）活性及自细胞（WBC）总数。结果与SA组及正常对照组比较，ACS组病人CRP、FIB、WBC、D-二聚体及PAI-1明显升高（F=6．027～2543．668，q=3．571～16．098，P〈0．05、0．01），tPA降低（F=4．138，q=3．043～3．913，P〈0．05）；CRP与D-二聚体及PAI-1活性呈正相关（r=0．326、0．393，P〈0．05、0．01），与tPA活性呈负相关（r=-0．387，P％0．05）。结论ACS病人炎症标志物水平增高及纤溶活性降低，CRP水平升高与纤溶活性降低密切相关。炎症反应及纤溶活性降低在ACS的发生发展中具有重要作用。     

心绞痛患者介入术后血小板活化及纤溶功能的变化

目的 研究冠心病不稳定心绞痛患者经皮冠状动脉腔内成形术（PTCA）和冠状动脉内支架术（stent)后外周循环中血小板活化及纤溶功能的变化。方法 由外周静脉采血，采用ELISA检测PTCA和stent术前后血浆血小板表面α-颗粒膜蛋白（GMP-140），血管性假血友病因子（VWF），组织纤溶酶原激活剂（t-PA)，纤溶酶原激活剂抑制物-1（PAI-1），D-二聚体（D-D）的含量。结果 31例不稳定型心绞痛患者PTCA术后10min血浆血小板膜表面GMP-140及D-二聚体明显增高。术后24h虽明显下降，但血小板膜表面GMP-140尚未降至正常，PAI-1术后24h亦明显增高。结论 冠心病不稳定型迟缓绞痛患者PTCA和stent术后确有血小板活化和纤溶活性受损。     

Fibrinolysis in patients with an abdominal aortic aneurysm with special emphasis on rupture and shock.

BACKGROUND: A ruptured abdominal aortic aneurysm (AAA) is associated with high mortality. Postoperative complications such as hemorrhage, multiple organ failure, myocardial infarction, and thromboembolism are common. An active and balanced hemostatic system is essential to avoid bleeding as well as thrombosis. When these activities are not properly regulated the patient is at risk of developing either excessive bleeding or thrombosis-related complications. Previous studies have shown a state of activated coagulation in patients with ruptured AAA. However, there are conflicting results regarding the fibrinolytic response. OBJECTIVES: The aim of the present study was to investigate the fibrinolytic state pre-operatively in patients with ruptured and non-ruptured AAA in relation to the clinical outcome with special regard to the influence of shock. METHODS: A prospective study was performed on 95 patients who underwent surgery for a ruptured AAA with shock (n = 43), a ruptured AAA without shock (n = 12), and a non-ruptured AAA (n = 40). Forty-one controls without an aneurysm were matched to the AAA patients according to age, gender and smoking habits. Plasma levels of tissue plasminogen activator antigen (tPAag), and plasminogen activator inhibitor type-1 (PAI-1) were measured as markers of fibrinolytic activity. D-dimer, a marker of fibrin turnover, was also measured. RESULTS: D-dimer was significantly higher in patients with a non-ruptured AAA compared with controls without AAA. There were significantly higher levels of D-dimer, tPAag, and PAI-1 in patients operated for ruptured compared with non-ruptured AAA. tPAag was also significantly higher in ruptured AAA patients with shock compared with without shock. No deaths occurred in patients operated on for a non-ruptured AAA or ruptured AAA without shock. There were 12 deaths after repair of a ruptured AAA with shock, of which two patients died from bleeding and the remaining 10 from multiple organ failure and cardiac failure. CONCLUSION: Our results indicate a state of activated coagulation in patients with a non-ruptured AAA, the state being intensified by rupture. The present data show normal fibrinolytic activities in patients with a non-ruptured AAA, but increased systemic fibrinolysis, as demonstrated by elevated tPAag level, in patients with a ruptured AAA. The elevated PAI-1 level indicates a simultaneous inhibition of the systemic fibrinolysis. Furthermore, the hyperfibrinolytic state was reinforced by shock in this study. However, the clinical outcome, with a relatively high incidence of thrombosis-related deaths, indicate a prothrombotic state instead of a hyperfibrinolytic state as a major point of attention in patients with shock as a result of a ruptured AAA.     

纤溶和凝血功能变化与2型糖尿病微血管病变的关系

目的探讨凝血与纤溶功能变化在糖尿病微血管病变中的临床意义。方法纤溶酶原激活物抑制物-1（PAI-1）活性采用发色底物法,纤维蛋白原（Fg）采用免疫浊度法测定。结果糖尿病无微血管病变组血浆PAI-1和Fg水平高于小常对照组（P〈0．05）,糖尿病微血管病变组血浆PAI-1和Fg水平明显高于无微血管病变组及正常对照组（P〈0．01）。结论2型糖尿病患者存在血液的高凝及低纤溶状态,在发生2型糖尿病微血管病变后更为明显,检测2型糖尿病患者血浆中PAI-1和Fg水平,对糖尿病微血管病变的预防和治疗具有一定的临床意义。     

Relationship of waist and hip circumference with coagulation and fibrinolysis in postmenopausal women

The contribution of obesity to the occurrence of cardiovascular events may not be wholly related to its influence on traditional risk factors. Coagulation and fibrinolysis may also influence cardiovascular risk, but the relationship of adiposity with these processes is unclear. The aim of the present study was to investigate the relationships of BMI (body mass index), waist circumference, hip circumference and WHR (waist-to-hip ratio) with VIIc (factor VII activity), plasma markers of thrombin generation [F1+2 (prothrombin fragment 1+2)], fibrin formation [SF (soluble fibrin)] and fibrin turnover (D-dimer), and PAI-1 (plasminogen activator inhibitor-1; a marker of fibrinolytic inhibitory capacity). The study cohort was 80 healthy postmenopausal women who were not diabetic, current smokers or taking hormone therapy and who had a fasting sample of blood collected. VIIc, F1+2, SF and PAI-1 were all positively correlated with BMI, waist circumference and WHR, whereas D-dimer was positively correlated with waist circumference and WHR, but not BMI. WHR was the strongest correlate of all the markers except for PAI-1, which was most closely related to BMI. Hip circumference became a negative correlate of F1+2 and D-dimer after adjusting for waist circumference. The relationships of WHR with F1+2 and SF, but not with VIIc and D-dimer, were independent of traditional risk factors. The positive association between waist circumference and markers of thrombin generation, fibrin production and fibrin turnover suggests that abdominal adiposity may contribute to atherothrombosis by activating intravascular coagulation. In contrast, a larger hip circumference appears to have a protective affect against coagulation activation.     

Vagus nerve stimulation inhibits activation of coagulation and fibrinolysis during endotoxemia in rats

BACKGROUND: Sepsis and endotoxemia are associated with concurrent activation of inflammation and the hemostatic mechanism, which both contribute to organ dysfunction and death. Electrical vagus nerve stimulation (VNS) has been found to inhibit tumor necrosis factor (TNF)-alpha release during endotoxemia in rodents. OBJECTIVE: To determine the effect of VNS on activation of coagulation and fibrinolysis. METHODS: Rats received a sublethal i.v. dose of lipopolysaccharide (LPS) after electrical VNS or sham stimulation. Activation of coagulation and fibrinolysis, as well as cytokine release, was measured before LPS injection and 2, 4 and 6 h thereafter. Results: LPS induced activation of the coagulation system (increases in the plasma concentrations of thrombin-antithrombin complexes and D-dimer, and a decrease in antithrombin) and biphasic changes in the fibrinolytic system [early rises of plasminogen activator activity and tissue-type plasminogen activator, followed by a delayed increase in plasminogen activator inhibitor type 1 (PAI-1)]. VNS strongly inhibited all LPS-induced procoagulant responses and more modestly attenuated the fibrinolytic response. In addition, VNS attenuated the LPS-induced increases in plasma and splenic concentrations of the proinflammatory cytokines TNF-alpha and interleukin-6 (IL-6), while not influencing the release of the anti-inflammatory cytokine IL-10. CONCLUSION: These data illustrate a thus far unrecognized effect of VNS and suggest that the cholinergic anti-inflammatory pathway not only impacts on inflammation but also on the coagulant-anticoagulant balance.     

The extent of diffuse intravascular coagulation and fibrinolysis in patients with liver cirrhosis.

Twenty-five patients with different stages of liver cirrhosis were evaluated with regard to the degree of liver synthesis reduction, the extent of the decrease of blood coagulation factors and/or alterations of the fibrinolytic system. For the assessment of the residual level of liver synthesis we used pseudo-cholinesterase and serum albumin as references. We did not find a correlation between these quantities and antithrombin III or fibrinogen, but highly significant inverse correlations with tissue plasminogen activator activity and D-dimer concentration. We found considerable alterations in the concentrations of the coagulation and fibrinolysis factors, with the exception of fibrinogen and plasminogen activator inhibitor. Significant increases were seen for thrombin-antithrombin III complex, tissue plasminogen activator activity and D-dimer, while significant decreases were seen for antithrombin III and alpha 2-antiplasmin, compared with a group of healthy volunteers. In the group of patients with liver cirrhosis and reduced liver synthesis, as documented by lowered pseudo-cholinesterase and serum albumin, the reduction of both antithrombin III and alpha 2-antiplasmin was most prominent. Intravascular coagulation was negligibly small. For the fibrinolytic system, the increase of tissue plasminogen activator, the decrease of the fibrinolysis inhibitor (alpha 2-antiplasmin) and the elevated D-dimer concentration seem to be important. These results suggest an acceleration of fibrinolysis and the prolonged presence of cross-linked fibrin degradation products.     

吡格列酮对老年高血压并胰岛素抵抗病人纤溶系统的影响

目的评价吡格列酮对老年高血压并胰岛素抵抗病人纤溶功能的影响。方法24例老年高血压并胰岛素抵抗病人口服吡格列酮15mg／d,共16周．服药前后分别测定血浆纤溶酶原激活物抑制物-1（PAO-1）、组织型纤溶酶原激活物、二聚体和纤维蛋白原含量,同时测定空腹胰岛素、空腹血糖和24h动态血压。结果吡格列酮治疗后血浆纤溶酶原激活物抑制物-1、二聚体抗原水平明显下降（P〈0．01）,组织型纤溶酶原激活物抗原水平明显增加（P〈0．01）,胰岛素敏感指数显著提高（P〈0、01）,空腹胰岛素和纤维蛋白原明显降低（P〈0．01）;24h平均收缩压和舒张压均降低（P〈0．05）。多因素分析结果表明治疗前空腹胰岛素水平对PAI-1的降低影响最大（P〈0．01）。结论吡格列酮能有效改善老年高血压并胰岛素抵抗病人纤溶系统功能,提高胰岛素敏感性,降低收缩压和舒张压;空腹胰岛素水平是影响病人纤溶功能的主要因素。     

慢性心力衰竭患者血浆组织型纤溶酶原激活物和纤溶酶原激活物抑制物-1含量变化及其临床意义

目的　研究慢性心力衰竭 (CHF)患者血浆组织型纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制物 1(PAI 1)含量的变化及其临床意义。方法　用酶联免疫吸附法 (ELISA)检测 6 0例CHF患者 (CHF组 )和 2 0例健康体检者 (正常对照组 )血浆t PA及PAI 1抗原含量。结果　CHF组血浆t PA和PAI 1平均含量都明显高于对照组 (P<0 .0 1)。CHF患者血浆PAI 1含量增高随心功能恶化而愈加明显。结论　CHF患者纤溶功能明显下降 ,可用血浆t PA、PAI 1含量作为判断病情的参考指标之一。     

Pregnancy outcome and fibrinolytic, endothelial and coagulation markers in women undergoing uterine artery Doppler screening at 23 weeks

Summary.  Background:  Pre-eclampsia (PET) and/or fetal growth restriction (FGR) remain a major cause of maternal and fetal morbidity and mortality. In pregnancy, fibrinolysis is controlled by the maternal endothelium and placenta, both of which are central to the pathogenesis of PET/FGR. Clinically, uterine artery Doppler screening at 23 weeks is used to predict PET/FGR. An abnormal uterine artery Doppler finding is defined as early diastolic bilateral uterine artery notching (BN) in the waveform. However, about 50% of mothers with BN do not develop PET/FGR. Objectives:  We investigated fibrinolytic changes and uterine artery Doppler findings in the second trimester, and related them to pregnancy outcome; in particular assessing whether fibrinolytic markers could discriminate between normal and abnormal outcome in mothers with BN. Patients/methods:  Plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), plasminogen activator inhibitor-2 (PAI-2), plasmin-α₂ antiplasmin (PAP), D-dimers and markers of endothelial dysfunction were measured with Doppler ultrasound at 23 weeks. Results:  Those with BN had decreased PAP and D-dimer levels, and raised PAI-1 and thrombomodulin levels. Mothers with BN and PET/FGR had significantly increased t-PA levels and reduced PAI-2 levels. Conclusions:  BN at 23 weeks of gestation is associated with increased PAI-1 levels. Within the BN group, mothers who developed PET/FGR had increased t-PA levels and decreased PAI-2 levels, although there was no net change in fibrinolysis as measured by D-dimer levels. No single fibrinolytic marker is helpful in determining pregnancy outcome in those with BN, but t-PA and PAI-2 are worthy of study in a multifactorial algorithm.     

Increased erythrocyte glutathione peroxidase activity and serum tumor necrosis factor-alpha in HIV-infected patients: relationship to on-going prothrombotic state

A condition of oxidative stress, due to perturbation of oxidant/antioxidant balance, has been suggested to play a role not only in the pathogenesis of human immunodeficiency virus (HIV) infection, but also in the promotion of a thrombophilic condition. Because various hemostatic dysfunctions usually considered as risk factors for thrombotic events were reported in HIV infection, this study was undertaken to investigate whether the oxidative phenomenon could promote a prothrombotic state in such condition. Erythrocyte glutathione peroxidase (GSH-Px), the major free-radical scavenger enzyme, and serum tumor necrosis factor-alpha (TNF-alpha) were evaluated in 33 consecutive HIV-infected out-patients and 35 matched HIV-negative healthy controls at a distance of any acute episode. Thrombin generation was explored by measuring the plasma levels of prothrombin fragment 1 + 2 (F1 + 2), whereas fibrin degradation products (D-dimer) and plasminogen activator inhibitor (PAI-1) activity were evaluated as indices of plasmin activity and fibrinolytic derangement. The anticoagulant pathway was investigated by measuring the plasma levels of antithrombin and protein C. Erythrocyte GSH-Px activity and serum TNF-alpha were significantly higher in HIV-infected patients when compared to controls. F1 + 2, D-dimer, and PAI-1 activity were increased in HIV-infected patients by comparison with controls. Normal antithrombin, but decreased protein C, was instead detected in HIV-infected patients. In the latter patients, serum TNF-alpha negatively correlated with both erythrocyte GSH-Px activity and plasma D-dimer. On the other hand, a positive correlation was shown between F1 + 2 and D-dimer and between D-dimer and GSH-Px activity. Furthermore, a trend toward increasing levels of GSH-Px with increasing PAI-1 activity was reported. These findings suggest a relationship between erythrocyte oxidative stress and the hypercoagulable condition during HIV infection.     

Posttrauma coagulation and fibrinolysis.

OBJECTIVE: To determine the effects of disseminated intravascular coagulation (DIC) and head injury on posttrauma coagulation and fibrinolysis. DESIGN: Case-control study. SETTING: General ICU (tertiary care center) in a city hospital serving a population of 150 million people. PATIENTS: Forty trauma victims: 15 with DIC; 25 without DIC. INTERVENTIONS: Measurement of six types of coagulation and fibrinolytic molecular markers (fibrinopeptide A, fibrinopeptide B beta 15-42, plasmin antiplasmin complex, D-dimer, tissue plasminogen activator antigen concentration, tissue plasminogen activator activity) immediately after trauma, 3 days later, and 6 days later. Anticoagulant treatment with gabexate mesilate at 1.45 +/- 0.06 mg/kg/hr. MEASUREMENTS AND MAIN RESULTS: Fibrinopeptide A, fibrinopeptide B beta 15-42, plasmin antiplasmin complex, and D-dimer showed high values immediately after trauma and exceeded normal activity for the first 6 days. When trauma was complicated with DIC, the molecular markers showed significantly higher values than those for non-DIC patients on all days. In the head-injured patients, such effect was not noted. Tissue plasminogen activator antigen concentration and tissue plasminogen activator activity were within a normal physiologic range of variation. By contrast, tissue plasminogen activator antigen concentration increased significantly after trauma in patients with DIC. When anticoagulant treatment was found effective, it caused a reduction in fibrinopeptide A. CONCLUSIONS: a) Fibrinolytic shut-down and its reactivation cannot be confirmed after trauma. b) Head injury does not lead to an increase in posttrauma coagulation or fibrinolytic activity. c) DIC enhances posttrauma coagulation and fibrinolytic activity and plasminogen activator inhibitor activity can be inferred in DIC patients. d) Increase in tissue plasminogen activator antigen concentration without tissue plasminogen activator activation may be a prognostic factor indicative of DIC and its chances of improvement, and fibrinopeptide A as an assessment criterion for the effectiveness of anticoagulant treatment.