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PubMed2002

Classic risk factors, hypercoagulability and migraine in young women with cerebral lacunar infarctions.

OBJECTIVE: Lacunar cerebral infarctions (LACI) in young women is a rare condition which pathogenesis is still not fully recognized. We explored the presence of classic risk factors, hypercoagulability and migraine in young women with LACI. METHODS: Charts of 192 consecutive premenopausal women suffering cerebrovascular insult [125 (65%) haemorhagic, 58 (30%) ischaemic and 9 (5%) unclassified] during a period of 5 years were reviewed. Sixteen out of 58 (27%) patients with ischaemic stroke were identified to have LACI and included in a study. RESULTS: Ten and seven out of 16 LACI women had at least one classical risk factor (hypertension, hyperlipidaemia, smoking or oral contraceptives) or migraine, respectively. LACI patients had slight hypercoagulable state indicated by shorter thrombin and thromboplastin times, higher fibrinogen and higher t-PA antigen than 47 age matched controls (all P < 0.05). In addition in LACI patients with migraine the trend toward more pronounced hypercoagulable state in comparison to LACI patients without migraine was found. The combination of migraine, at least one classic risk factor and hypercoagulability was present in 5/16 (31.25%) of patients. CONCLUSIONS: The combination of slightly to moderately expressed classic risk factors, hypercoagulability and migraine might be a risk profile for LACI in young women. Further studies are needed to clarify risk profile, rather than isolated risk factors, for LACI in a specific group as young women are.

Adolescent↗
PubMed2005

A hypothesis-generating study to evaluate platelet activity in diabetics with chronic kidney disease.

BACKGROUND: It is well described that diabetes mellitus is a hypercoagulable state. It is also known that patients with renal dysfunction have impaired platelet aggregation and function. It is not well described how renal dysfunction affects the hypercoagulability associated with diabetes. This post-hoc sub-group analysis compares platelet function, clot structure and thrombin generation time at baseline, and following enoxaparin exposure in three groups of subjects. METHODS: 30 total subjects were evaluated in the three groups: Group I: normal controls (n = 10), Group II: subjects with renal dysfunction but without diabetes (n = 13), and Group III: subjects with concomitant diabetes and renal dysfunction (n = 7). For each subject, platelet contractile force (PCF), clot elastic modulus (CEM) and thrombin generation time (TGT) were simultaneously measured in whole blood at baseline, and following increasing enoxaparin antifactor Xa activity exposure. The group means for each parameter were determined and compared using one-way analysis of variance, with post-hoc Tukey-Kramer test. RESULTS: At baseline, subjects in Group III (diabetics with concomitant renal dysfunction) display significantly enhanced platelet activity, as measured by PCF (p = 0.003) and CEM (p = 0.03), relative to the non-diabetic Groups I and II. Subjects in Group II (renal dysfunction without diabetes) had significantly prolonged TGT values relative to controls when the antifactor Xa activity concentration reached 0.5 (p = 0.007), 1.0 (p = 0.005) and 3.0 IU/mL (p < 0.0001), respectively. There were no differences between Group II and Group III with respect to TGT at these antifactor Xa activity concentrations. When the antifactor Xa activity concentration reached 3.0 IU/mL, Groups II and III formed significantly less rigid blood clots (CEM p = 0.003) and also trended toward reduced PCF (p = 0.06) relative to Group I. CONCLUSION: This hypothesis-generating sub-group analysis suggests that at baseline, patients with concomitant diabetes and renal dysfunction have significantly enhanced platelet activity (PCF), and form more rigid blood clots (CEM) compared to controls and subjects with renal dysfunction but no diabetes. This may suggest that the presence of renal dysfunction does not ameliorate the hypercoagulable state associated with diabetes. Secondly, it appears that subjects with renal dysfunction but without diabetes have an enhanced response to enoxaparin relative to controls.

Journal Article↗
PubMed1999

Thrombophilia as a multigenic disease.

BACKGROUND AND OBJECTIVE: Venous thrombosis is a common disease annually affecting 1 in 1000 individuals. The multifactorial nature of the disease is illustrated by the frequent identification of one or more predisposing genetic and/or environmental risk factors in thrombosis patients. Most of the genetic defects known today affect the function of the natural anticoagulant pathways and in particular the protein C system. This presentation focuses on the importance of the genetic factors in the pathogenesis of inherited thrombophilia with particular emphasis on those defects which affect the protein C system. INFORMATION SOURCES: Published results in articles covered by the Medline database have been integrated with our original studies in the field of thrombophilia. STATE OF THE ART AND PERSPECTIVES: The risk of venous thrombosis is increased when the hemostatic balance between pro- and anti-coagulant forces is shifted in favor of coagulation. When this is caused by an inherited defect, the resulting hypercoagulable state is a lifelong risk factor for thrombosis. Resistance to activated protein C (APC resistance) is the most common inherited hypercoagulable state found to be associated with venous thrombosis. It is caused by a single point mutation in the factor V (FV) gene, which predicts the substitution of Arg506 with a Gln. Arg506 is one of three APC-cleavage sites and the mutation results in the loss of this APC-cleavage site. The mutation is only found in Caucasians but the prevalence of the mutant FV allele (FV:Q506) varies between countries. It is found to be highly prevalent (up to 15%) in Scandinavian populations, in areas with high incidence of thrombosis. FV:Q506 is associated with a 5-10-fold increased risk of thrombosis and is found in 20-60% of Caucasian patients with thrombosis. The second most common inherited risk factor for thrombosis is a point mutation (G20210A) in the 3' untranslated region of the prothrombin gene. This mutation is present in approximately 2% of healthy individuals and in 6-7% of thrombosis patients, suggesting it to be a mild risk factor of thrombosis. Other less common genetic risk factors for thrombosis are the deficiencies of natural anticoagulant proteins such as antithrombin, protein C or protein S. Such defects are present in less than 1% of healthy individuals and together they account for 5-10% of genetic defects found in patients with venous thrombosis. Owing to the high prevalence of inherited APC resistance (FV:Q506) and of the G20210A mutation in the prothrombin gene, combinations of genetic defects are relatively common in the general population. As each genetic defect is an independent risk factor for thrombosis, individuals with multiple defects have a highly increased risk of thrombosis. As a consequence, multiple defects are often found in patients with thrombosis.

3' Untranslated Regions↗
PubMed1998

[Clinical analysis of intracranial venous embolism during pregnancy and puerperium].

OBJECTIVE: To study the cause and clinical manifestation of intracranial venous embolim during pregnancy and puerperium, and its early diagnosis and treatment. METHODS: 18 cases of intracranial venous embolism confirmed by Computed Tomography (CT) were eligible for this retrospective study. RESULTS: Of all the cases, 8 cases occurred before delivery and 10 post partum; 10 cases complicated by pregnancy induced hypertension and 8 cases postpartum hemorrhage. Headache occurred most frequently, followed by coma and seizure. Blood rheologic assay showed hypercoagulable states in 6 cases. For 11 cases treated with urokinase, 10 were cured, while in the remaining patients, 3 of 6 cured. CONCLUSIONS: The results show that hypercoagulability states were related to intracranial venous embolism. Coma and seizure were the main characters. CT was an important diagnostic measure. Lowering intracranial pressure, anticoagulation, dethrombosis and timely ending pregnancy were the main treatment measures. The early use of urokinase may exert better effect.

Adult↗
PubMed2003

The coagulation system.

Congenital and acquired hypercoagulable states arise from an imbalance between procoagulant and anticoagulant activity. Although these imbalances are present throughout the entire vascular tree, thrombotic lesions are usually localized in discrete segments of the veins or arteries and in certain organ systems. Thus, hypercoagulable states are likely to be associated with focal defects in the vascular wall to produce thrombosis. Many recently described factors are associated with hypercoagulability. Because thrombosis is a disease in which genetic and acquired risk factors interact dynamically, a thorough history, family history, and physical examination should be performed before ordering an extensive and costly coagulation panel.

Antiphospholipid Syndrome↗
PubMed2002

Tissue factor and tissue factor pathway inhibitor levels in unstable angina patients during short-term low-molecular-weight heparin administration.

High tissue factor (TF), tissue factor pathway inhibitor (TFPI) levels and a hypercoagulability state have been documented in unstable angina patients. We evaluated whether short-term enoxaparin administration (100 IU/kg b.i.d. for 3 d) reduces the high TF levels and the hypercoagulability state, and whether it influences the fibrinolytic system in 20 unstable angina patients. On d 3, we observed a significant reduction in TF levels both 1 h and 4 h after the morning injection (-25.6% and -21.7%; P < 0.001 respectively) in comparison with the base-line levels. Both 1 and 4 h after the morning injection on the d 3, TFPI levels significantly (P < 0.001) increased (+96.4%, +96.9% respectively) with respect to the base-line values. After enoxaparin administration, at all observation times, thrombin-antithrombin complexes and prothrombin fragment F1 + 2 levels were significantly (P < 0.001) lower with respect to base-line levels. We observed a slight but significant increase in tissue plasminogen activator antigen levels in preinjection samples, as well as 1 h and 4 h after enoxaparin administration, in comparison with the base-line values. This study provides evidence that low-molecular-weight heparin (LMWH) administration, in addition to a reduction of hypercoagulability and a mild fibrinolytic activation, is associated with decreased TF levels, so indicating a novel mechanism of interference of LMWH with the haemostatic system.

Adult↗
PubMed1996

Clinical significance of the FV:Q506 mutation in unselected oncology patients.

PURPOSE: A common germline mutation in the factor V gene (FV:Q506) has been associated with hypercoagulability in families with heritable predisposition to thrombosis. We examined the prevalence and clinical significance of the FV:Q506 mutation in cancer patients. PATIENTS AND METHODS: We performed a retrospective cohort study by examining 353 consecutive, unselected patients in a general hematology/oncology clinic. We ascertained risk factors, obtained the clinical clotting history, and determined the heterozygous or homozygous presence of the FV:Q506 allele for each patient. RESULTS: We detected a germline mutation in 5.4% (19 of 353) of patients, of whom 18 were heterozygous and 1 was homozygous for the FV:Q506 mutant allele. In 17 of 18 heterozygous patients, there was no history of venous thrombosis or catheter-associated thrombosis. These asymptomatic patients included 13 patients who had been diagnosed with cancer or leukemia for a mean of 66.2 months (median 69) and had received a variety of local and systemic treatments. In contrast, 1 of 18 heterozygous and 1 of 1 homozygous patients had developed deep vein thrombosis that was associated, respectively, with either recurrent thrombotic events or a strong family history for pulmonary embolus. CONCLUSIONS: Routine screening for the FV:Q506 mutation in cancer patients without a personal or family history for venous thrombosis is not helpful in guiding management. In contrast, an episode of venous thrombosis in a patient with a mutant germline FV:Q506 allele was associated with recurrent thrombotic events. These findings suggest that patients heterozygous for the FV:Q506 allele may require an independent "susceptibility" element to manifest a venous hypercoagulable state. In addition, only 2 of 25 clinic patients with a venous clot carried the FV:Q506 allele suggesting this genetic defect plays a minor role in the hypercoagulable state of cancer.

Adult↗
PubMed2004

Changes in the blood coagulation, fibrinolysis, and cytokine profile during laparoscopic and open cholecystectomy.

BACKGROUND: It has long been known that a hypercoagulability state develops after surgery. A surge in circulating cytokine levels is also commonly found in the postoperative period. These cytokines have all been shown to be capable of inducing a hypercoagulability state. Recently laparoscopic cholecystectomy (LC) has been introduced, and its advantages over the open procedure seem related to the reduced surgical trauma. LC is associated with a diminished acute-phase response compared with the open procedure. Our present knowledge on the influence of laparoscopic upon coagulation and fibrinolysis is incomplete and based on a few studies. METHODS: The aim of this prospective, nonrandomized study was to investigate hemostatic system alterations in patients who undergo open and laparoscopic cholecystectomy. In addition we also measured the plasma cytokine profile to explore any relationship between changes in plasma cytokine levels and postoperative coagulation profile. Between September 1999 and April 2002, 71 patients were nonrandomly assigned to open (group 1) or laparoscopic cholecystectomy (group 2). All patients from group 1 were operated by a surgical team different from ours, who prefers the OC procedure. The patients with acute cholecystitis were excluded. Prothrombin fragment 1.2 (F1.2), thrombin-antithrombin (TAT), fibrinogen, soluble fibrin, antithrombin III (AT), protein C, plasminogen, and D-dimer levels were measured at baseline and at 1, 24, 48, and 72 h postoperatively. Serial serum levels of IL-1beta and IL-6 were measured by colorimetric enzyme-linked immunosorbent assay (ELISA). RESULTS: Plasma levels of F1.2, TAT, fibrinogen, soluble fibrin, and D-dimer increased significantly in group 1. Plasma levels of AT, protein C, and plasminogen decreased in both groups. In the OC group, the serum IL-3 and IL-6 levels began to significantly increased as early as 1 h from the beginning of the operation, revealing a peak at the sixth hour. When IL-6 and IL-1 levels were markedly elevated also, F1.2, fibrinogen, and soluble fibrin levels were increased. CONCLUSIONS: Only mild hypercoagulability was observed in patients who had undergone laparoscopic cholecystectomy. The cytokine surge was correlated with hypercoagulability. There was in fact a positive correlation between IL-6 level and hypercoagulability. The correlation between cytokine levels and coagulation activation may be related to the type of surgery performed. Further studies are required to investigate these issues.

Adult↗
PubMed2002

Hematologic aspects of liver transplantation for Budd-Chiari syndrome with special reference to myeloproliferative disorders.

BACKGROUND: Patients who undergo orthotopic liver transplantation (OLT) for Budd-Chiari syndrome (BCS) traditionally have been anticoagulated with warfarin postoperatively. Because a significant proportion of BCS patients are found to have an underlying myeloproliferative disorder (MPD), antiplatelet therapy may be a more rational treatment strategy for this subgroup. METHODS: All patients who underwent OLT for the diagnosis of BCS at our institution through March 2000 were included in this analysis. Posttransplant therapy consisted of hydroxyurea and aspirin for those with MPDs. Standard anticoagulation or no antithrombotic treatment was given to BCS patients with other causes. Major posttransplantation complications (thrombosis and bleeding) and mortality were determined. RESULTS: Seventeen patients underwent OLT for BCS at our institution. The mean follow-up was 68.4 months. Two of seventeen patients died; one patient died of recurrent thrombosis (124 months after OLT) and the other patient died of acute hepatitis B (7 months after OLT). Twelve patients (71%) had evidence of a MPD. Two of the MPD patients were treated with warfarin before the initiation of hydroxyurea and aspirin therapy. The remaining 10 MPD patients were placed on only hydroxyurea and aspirin after OLT. Anagrelide was used in place of hydroxyurea in two patients because of cytopenias caused by the latter agent. The mean follow-up of this group of 10 patients was 59.9 months. Only one patient experienced recurrent thrombosis, which occurred more than 10 years after the original transplant. There were no major bleeding complications and posttransplant liver biopsies were well tolerated. CONCLUSIONS: Antiplatelet therapy that consists of hydroxyurea and aspirin is a safe and effective alternative to anticoagulation to prevent recurrent thrombosis in MPD patients with BCS after liver transplantation. For patients with a hypercoagulable state corrected by OLT, antithrombotic therapy probably is not required. For those patients with conditions not corrected by OLT or with idiopathic BCS, anticoagulation or other therapy to control the hypercoagulable state should be given.

Adolescent↗
PubMed1989

Hypercoagulability in arterial disease.

Isolated human monocytes generate tissue factor when stimulated with endotoxin. Tissue factor generation provides a marker for activation of the monocyte and of the clotting system. Determination of the recalcification time of blood after incubation with endotoxin detects minute changes in coagulability. This clotting assay was utilized to assess the presence of a hypercoagulable state in patients with peripheral arterial occlusive disease when compared with healthy volunteers. Citrated blood was incubated with endotoxin for two hours, CaCl2 was added, and the recalcification time determined. Hypercoagulability was indicated by shortened recalcification time. The recalcification time +/- standard deviation for saline (control) and endotoxin-activated samples from 19 healthy volunteers was 6.55 +/- 0.8 and 5.69 +/- 0.7 minutes, respectively, whereas it was 4.93 +/- 1.2 and 4.55 +/- 0.9 minutes for 31 patients with peripheral arterial occlusive disease (p less than .001 for each). This hypercoagulable state can accentuate the arterial occlusive process in patients with peripheral vascular disease and may prove to be of diagnostic, therapeutic, and prognostic significance.

Arterial Occlusive Diseases↗
PubMedDate not supplied

Relationship of urokinase type plasminogen activator, plasminogen activator inhibitor type 1 and activated protein C in fibrinolysis of human placenta.

Suppression of the fibrinolytic activity plays an important role in the prevention of hemorrhage during pregnancy and labor. A hypofibrinolytic and hypercoagulable state may be established in the placenta during pregnancy. However, little infraction is present in the normal placenta. This evidence shows that placenta maintains the fibrinolytic activity in spite of hypercoagulable state. As there is a high amount of APC in the placenta, APC is thought to be involved in fibrinolysis of placenta. Thus, we studied the role of APC on fibrinolysis in placenta. (1) uPA activity of cell membrane reappears after incubation with uPA/PAI-1 complex and a large amount of APC by flow cytometry, (2) APC was made PAI-1/APC complex after incubation of uPA/PAI-1 complex with APC. Our results suggest that APC is the important substance for fibrinolysis in the placenta by decreasing of PAI activity.

Blotting, Western↗
PubMed1993

[Prophylactic use of concentrated antithrombin III preparation in children with nephrotic syndrome].

Decreased plasma level of antithrombin III was assumed to be one of the major factors underlying hypercoagulable state in nephrotic syndrome. Concentrated antithrombin III preparation was given to 8 children with nephrotic syndrome with a plasma antithrombin III activity of less than 70%, to evaluate the effect on hypercoagulable state. Plasma antithrombin III activity was elevated to more than 70% in 7 of 8 children after treatment, while plasma levels of plasmin-alpha 2 plasmin inhibitor complex and FDP-D dimer were not significantly decreased. One patient developed brain infarction after the treatment, suggesting that prophylactic administration of concentrated antithrombin III preparation is not fully protective against thrombotic complications in nephrotic syndrome.

Adolescent↗
PubMed1981

Rheological and clotting changes in the immediate post-myocardial infarction period.

Several coagulative, fibrinolytic, and rheologic indices were studied in a large group of patients with acute myocardial infarction. The results were compared with those obtained in a normal control group. Changes of blood and plasma viscosity, fibrinogen, and fibrinolytic activity, compatible with a hypercoagulable state, were found in the immediate post-infarction period. However, elevated AT III levels as compared to control group were observed. This could be interpreted as a reactive response to the hypercoagulable state. Significant correlations could be observed between blood viscosity and Ht, plasma viscosity and fibrinogen, fibrinogen and fibrinolytic levels and between fibrinogen and ESR.

Adult↗
PubMed2005

D-dimer levels, constitutional thrombophilia, and venous thrombosis prediction: clinical aspects and implications.

The negative predictive value of D-dimers in the diagnosis of a recent venous thromboembolism (VTE) episode is well established. The plasma level of D-dimer is usually increased in hypercoagulable states. The measurement of D-dimer could be of clinical interest in patients with constitutional thrombophilia as there is no close relationship between the clinical expression and the genotype indicating the existence of a hypercoagulable state. Moreover, the predictive value of D-dimer testing in patients with thrombophilia has been questioned. The review of the literature and results of a recent study of our group are presented. Decreased levels of D-dimer are observed in patients receiving an oral anticoagulant treatment versus untreated patients. In contrast, no significant difference was observed between those with and those without thrombophilia among treated or untreated patients. Patients with constitutional thrombophilia are supposed to have an increased risk of postoperative VTE. The review of the existing literature could not confirm this opinion but this could be due to the fact that most patients receive a prophylactic treatment. Thus, there is an indirect evidence of its efficacy in these patients.

Administration, Oral↗
PubMed2003

Hemodilution during off-pump coronary artery bypass grafting: can we improve flow and reduce hypercoagulability?

BACKGROUND: The aim of this study was to compare intraoperative coronary graft flows performed on pump and off pump and to evaluate the effects of hemodilution on coronary graft flows in off-pump coronary artery bypass grafting (CABG) patients by using transit time flow measurements (TTFM). METHODS: Three hundred patients undergoing only CABG procedures were enrolled in a prospective randomized manner into 3 groups. Group 1 consisted of 100 patients undergoing operations with standard cardiopulmonary bypass techniques. Group 2 consisted of 100 patients scheduled for revascularizations using off-pump techniques. Group 3 consisted of 100 patients who underwent operations with offpump techniques under controlled hemodilution (hematocrit levels kept between 25% and 28%). TTFM were performed with the coronary Flometer system. Mean flows, pulsatility indices, and flow patterns were evaluated. Twenty-five patients in each group were randomly assigned for control angiography 6 days postoperatively. Thromboelastographic (TEG) measurements were performed for each patient before and after surgery to evaluate the patient's coagulation status. RESULTS: The mean number of anastomoses was higher in group 1 than in groups 2 and 3 (P < .05). Mean arterial pressures and heart rates were similar between groups during measurements. Hematocrit values were higher in group 2 than in groups 1 and 3 (P < .05). Mean flows for left anterior descending coronary artery and right coronary artery territories were significantly lower in group 2 patients (P < .05). For the circumflex artery territory, mean flows did not reach statistically significant levels despite lower flows again in group 2. The pulsatility indices were similar in all 3 groups for all 3 coronary territories. Postoperative coronary angiographic results revealed similar graft patencies among the 3 groups (not significantly different). Postoperative TEG patterns failed to show a hypercoagulable state in off-pump patients. CONCLUSION: Off-pump CABG patients with hemodilution had significantly higher graft flows than off-pump CABG patients without hemodilution. Although we failed to show the existence of a hypercoagulable state for patients in the offpump group, an examination of the TTFM findings suggests that hemodilution may help to improve graft patency in offpump CABG patients during the early postoperative period.

Blood Coagulation Disorders↗
PubMed1990

Superficial migratory thrombophlebitis and factor XII deficiency.

A patient with painful migratory erythematous nodules for 7 years is presented. The nodules, which were localized on the lower and upper extremities, progressed to palpable cords. Multiple venograms showed no evidence of deep vein thrombosis. Skin biopsy specimens were diagnostic of superficial thrombophlebitis. There was no evidence of internal malignancy. Extensive evaluation for an underlying hypercoagulable state was remarkable for a factor XII level 17% of normal. The patient was unresponsive to a wide range of treatments. The recalcitrant nature of his disease and lack of deep venous involvement are unique. An underlying hypercoagulable state should be considered when the diagnosis of superficial migratory thrombophlebitis is considered.

Adult↗
PubMed2003

Long-term outcome of infrainguinal bypass grafting in patients with serologically proven hypercoagulability.

OBJECTIVE: The purpose of this study was to test the hypothesis that the long-term outcome of infrainguinal bypass grafting in patients with congenital or acquired hypercoagulability is inferior to the results in patients without documented clotting disorders. METHODS: The study was a retrospective analysis of consecutive patients from January 1994 to January 2001. RESULTS: Five hundred eighty-two infrainguinal bypass grafts were created in 456 patients. Indication for surgery was limb-threatening ischemia in 84%; prosthetic conduits were implanted in 38%. Seventy-four grafts were created in 57 patients with one or more serologically proven hypercoagulable states, including heparin-induced platelet aggregation (n = 37), anticardiolipin antibodies (n = 11), lupus anticoagulant (n = 8), protein C or S deficiency (n = 7), antithrombin III deficiency (n = 3), and factor V Leiden mutation (n = 1). Patients with hypercoagulability were younger (63 +/- 2 years versus 69 +/- 1 years; P =.007), more likely to have undergone prior revascularization attempts (38% versus 21%; P =.003), and more likely to have chronic anticoagulation therapy after surgery (46% versus 25%; P =.001). After 5 years (median follow-up, 19 months), patients with hypercoagulability had poorer primary patency (28% +/- 7% versus 35% +/- 5%; P =.004), primary assisted patency (37% +/- 7% versus 45% +/- 6%; P =.0001), secondary patency (41% +/- 7% versus 53% +/- 6%; P =.0001), limb salvage (55% +/- 8% versus 67% +/- 6%; P =.009), and survival (61% +/- 8% versus 74% +/- 4%; P =.02) rates. Multivariate analysis identified only prosthetic conduit choice (P =.0001), hypercoagulability (P =.0003), and limb salvage indication (P =.01) as independent predictors of graft failure. CONCLUSION: Patients with serologically proven hypercoagulability have inferior long-term patency, limb salvage, and survival rates after infrainguinal bypass. The high prevalence rate (13%) of diverse hypercoagulable states in this patient population supports serologic screening, especially in referral practices.

Aged↗
PubMed1989

[Tumor metastasis and the fibrinolytic system].

Metastatic spread of malignant tumor appears to correlate with activation of the fibrolytic system. The role of fibrinolysis in growth and metastasis was examined in Lewis lung carcinoma of mice. The inhibition of fibrinolysis or proteases decreased the primary tumor growth and pulmonary metastasis, whereas the activation of fibrinolysis or proteases increased the number of metastatic foci in the lung. Electronmicroscopically, thrombus formation in the primary site prevented tumor invasion and metastasis formation. Plasminogen activator (PA) content of excised tumors was determined by SDS-PAGE, and major PA was found to be urokinase (UK) type. Immunohistochemical study with specific antisera was done. When tumor cells possessed a high level of UK, laminin and type IV collagen, components of the basement membrane, disappeared from tumor tissues. These findings suggest that PA through protease cascade plays a role in tumor invasion and metastasis. Clinically, patients with advanced cancer are usually in a hypercoagulable state with elevated fibrinogen, and fibrin deposition around tumor mass is a serious problem in cancer chemotherapy. UK infusion prior to 5-fluorouracil increased tissue concentration of antitumor agent. However, development of consumption coagulopathy characterized by progression from hypercoagulable state to disseminated intravascular coagulation has also been found in several cases.

Animals↗