thromboplastin and Thrombophlebitis

There is considerable evidence that the hemostatic system is involved in the growth and spread of malignant disease. There is an increased incidence of thromboembolic disease in patients with cancers and hemostatic abnormalities are extremely common in such patients. Antihemostatic agents have been successfully used to treat a variety of experimental tumors, and several clinical trials in humans have been initiated. Although metastasis is undoubtedly multifactorial, intravascular coagulation activation and peritumor fibrin deposition seem to be important. The mechanisms by which hemostatic activation facilitates the malignant process remain to be completely elucidated. Of central importance may be the presence on malignant cells of tissue factor and urokinase receptor. Recent studies have suggested that these proteins, and others, may be involved at several stages of metastasis, including the key event of neovascularization. Tissue factor, the principal initiator of coagulation, may have additional roles, outside of fibrin formation, that are central to the biology of some solid tumors.

Topics: Animals; Anticoagulants; Antineoplastic Agents; Biomarkers; Blood Coagulation Tests; Cell Adhesion; Cysteine Endopeptidases; Disseminated Intravascular Coagulation; Factor Xa; Fibrin; Fibrinolysis; Hemostasis; Heparin; Humans; Monocytes; Neoplasm Metastasis; Neoplasm Proteins; Neoplasms; Neoplasms, Experimental; Neoplastic Cells, Circulating; Neovascularization, Pathologic; Platelet Activation; Platelet Aggregation Inhibitors; Receptors, Thrombin; Thrombophilia; Thrombophlebitis; Thromboplastin; Vitamin K

Over the last years numerous studies have focussed on the in vivo expression of tissue factor (TF) in health and disease. The selective perivascular distribution of TF and the lethal effects of TF knockouts have added strong support to the widely accepted view that TF plays a pivotal role in the initiation of blood coagulation during physiological hemostasis. Inappropriate in vivo expression of TF, particularly by cells that do not express this protein under normal conditions (mainly monocyte-macrophages and endothelial cells), has been documented and is likely responsible for fibrin deposition in a variety of pathological conditions, among which sepsis-associated disseminated intravascular coagulation (DIC) and thromboembolic disease. In malignancy, in vivo expression of TF by tumor cells and/or by host cells has been implicated not only in intratumoral and systemic activation of blood coagulation but also in tumor growth and dissemination.

Topics: Arteriosclerosis; Disseminated Intravascular Coagulation; Humans; Neoplasms; Reference Values; Thrombophlebitis; Thromboplastin; Thrombosis

Thrombosis is the most frequent complication and the second cause of death in patients with overt malignant diseases. Increasing evidence suggests that thrombotic episodes may also precede the diagnosis of cancer by months or years thus representing a potential marker for occult malignancy. Recently, emphasis has been given to the potential risk of cancer therapy (both surgery and chemotherapy) in enhancing the risk for thromboembolic disease. Post-operative deep-vein thrombosis is indeed more frequent in patients operated for malignant diseases than for other disorders. On the other hand, both chemotherapy and hormone therapy are associated with an increased thrombotic risk, which can be prevented by low-dose oral anticoagulation. Possible contributory causes for thromboembolic disease in cancer include the capacity of tumor cells and their products to interact with platelets, clotting and fibrinolytic systems, as well as their interactions with endothelial cells and tumor-associated macrophages. In particular, procoagulant activities of tumor cells have been extensively studied; one of these, cancer procoagulant, could represent a novel marker of malignancy in both solid tumors and acute promyelocytic leukemia (APL). In solid tumors, CP, a vitamin K dependent enzyme could represent the selective target of the antimetastatic effects of warfarin treatment. In APL, CP may contribute to trigger the well known intravascular coagulation syndrome accompanying the early manifestations of the disease and is depressed by all-trans-retinoic acid, an agent capable to determine complete remission with a rapid amelioration of the bleeding syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Antineoplastic Agents; Cysteine Endopeptidases; Disease Models, Animal; Disease Progression; Hormones; Humans; Leukemia, Promyelocytic, Acute; Mice; Mice, Transgenic; Neoplasm Proteins; Neoplasms; Neoplasms, Experimental; Neoplasms, Unknown Primary; Plasminogen Activator Inhibitor 1; Thrombophlebitis; Thromboplastin

Topics: Animals; Anticoagulants; Dose-Response Relationship, Drug; Drug Administration Schedule; Humans; Myocardial Infarction; Prothrombin Time; Rabbits; Thrombophlebitis; Thromboplastin

Topics: Administration, Oral; Animals; Anticoagulants; Cattle; Clinical Trials as Topic; Humans; Prothrombin Time; Rabbits; Random Allocation; Thromboembolism; Thrombophlebitis; Thromboplastin; Warfarin

Topics: Anticoagulants; Blood Coagulation Disorders; Blood Platelets; Disseminated Intravascular Coagulation; Factor X; Fibrin; Fibrinolysis; Humans; Neoplasms; Neovascularization, Pathologic; Thrombophlebitis; Thromboplastin

Thrombophlebitis has been associated with virtually all cancers, especially gastrointestinal, urogenital, and lung neoplasms. Although occurring infrequently in cancer patients, thrombophlebitis may appear before the cancer has become symptomatic and may lead to an earlier diagnosis of cancer. The phlebitic syndrome associated with cancer, although not unique, is distinctive. It is often recurrent and migratory, often involves unusual locations, and is often resistant to anticoagulation therapy. Pulmonary emboli are frequent complications. The pathogenesis of phlebitis in cancer patients is not well understood. Evidence suggests that many cancer patients are hypercoagulable, with abnormalities in platelets, coagulation factors, and the fibrinolytic system. These changes may results from the elaboration of thromboplastin-like substances from the cancer tissue.

Topics: Blood Coagulation; Fibrinolysis; Humans; Neoplasms; Pancreatic Neoplasms; Prognosis; Thrombophlebitis; Thromboplastin

Topics: Arthritis; Blood Coagulation Factors; Collagen Diseases; Diabetes Complications; Endocrine Glands; Glucocorticoids; Humans; Myeloproliferative Disorders; Obesity; Sex Factors; Thromboembolism; Thrombophlebitis; Thromboplastin; Thyroid Diseases

Topics: Animals; Blood Cell Count; Blood Coagulation; Blood Coagulation Factors; Blood Platelets; Complement System Proteins; Disseminated Intravascular Coagulation; Fibrinogen; Fibrinolysis; Humans; Immunoassay; Leukocytes; Plasminogen; Postoperative Complications; Prothrombin Time; Thrombophlebitis; Thromboplastin

Topics: Anticoagulants; Blood Coagulation Tests; Cerebral Hemorrhage; Cerebrovascular Disorders; Coumarins; Heparin; Humans; Middle Aged; Myocardial Infarction; Phenindione; Postoperative Care; Prothrombin Time; Rheumatic Heart Disease; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Administration, Oral; Animals; Anticoagulants; Cattle; Clinical Trials as Topic; Humans; Prothrombin Time; Rabbits; Random Allocation; Thromboembolism; Thrombophlebitis; Thromboplastin; Warfarin

Topics: Anticoagulants; Clinical Trials as Topic; Heart Valve Prosthesis; Humans; Prothrombin Time; Pulmonary Embolism; Quality Control; Reference Values; Thrombophlebitis; Thromboplastin; Warfarin

The British comparative thromboplastin (BCT) was used to monitor the effectiveness of oral anticoagulants in preventing deep vein thrombosis (DVT) in patients undergoing major gynaecological surgery. All patients were screened for DVT with the use of the (125)I-fibrinogen scan.One hundred and forty-five patients aged 40 years or more were randomised into three groups. Group 1 received oral anticoagulant (nicoumalone) treatment, stabilised over five days before surgery and continuing into the second postoperative week. The other patients served as two contrast groups and were managed on a double-blind basis. Group 2 received a subcutaneous low-dose regimen of heparin calcium. Group 3 received subcutaneous saline. Eleven of 48 patients in the saline group, three of 49 patients in the heparin group, and three of 48 patients in the oral anticoagulant group developed DVT as judged by (125)I-fibrinogen scanning. The incidences in groups 1 and 2 were significantly lower than in the saline group. The falls in haemoglobin concentration and incidence of haemorrhage were similar in all three groups.The study showed that oral anticoagulant prophylaxis stabilised preoperatively and low-dose heparin were equally effective in preventing deep vein thrombosis in a moderate-risk group. Immediate preoperative prothrombin ratios of 2.0-2.5 and postoperative ratios of 2.0-4.0 with the BCT gave adequate protection without increased haemorrhagic risk.

Topics: Acenocoumarol; Administration, Oral; Adult; Clinical Trials as Topic; Double-Blind Method; Female; Genitalia, Female; Hemoglobins; Hemorrhage; Heparin; Humans; Middle Aged; Thrombophlebitis; Thromboplastin

Topics: Adult; Aged; Blood Coagulation Tests; Blood Transfusion; Clinical Trials as Topic; Female; Femoral Fractures; Femoral Vein; Fibrinogen; Hematocrit; Heparin; Hip; Humans; Injections, Subcutaneous; Iodine Isotopes; Male; Middle Aged; Myocardial Infarction; Phlebography; Popliteal Vein; Postoperative Complications; Prospective Studies; Radionuclide Imaging; Thrombophlebitis; Thromboplastin; Thrombosis

Topics: Adult; Aged; Anticoagulants; Clinical Trials as Topic; Coumarins; Evaluation Studies as Topic; Female; Fibrinogen; Fibrinolysis; Fluorescein Angiography; Fundus Oculi; Heparin; Humans; Male; Middle Aged; Ophthalmodynamometry; Plasminogen; Retinal Vein; Streptokinase; Thrombophlebitis; Thromboplastin; Visual Acuity

Topics: Adult; Aged; Anticoagulants; Blood Platelets; Female; Femoral Fractures; Humans; Male; Middle Aged; Phlebography; Prothrombin Time; Pulmonary Embolism; Thrombophlebitis; Thromboplastin

Although cancer-associated thrombosis (CAT) is a frequent complication in patients with malignancies, its treatment remains a challenge in daily practice. Here, we report the clinical course of a 51-year-old woman presenting with a highly thrombogenic paraneoplastic coagulopathy. Despite therapeutic anticoagulation with various agents, including rivaroxaban, fondaparinux, and low-molecular-weight heparin, the patient suffered from recurrent venous and arterial thromboembolism. Locally advanced endometrial cancer was identified. Tumor cells showed strong expression of tissue factor (TF), and significant concentrations of TF-bearing microvesicles were detected in patient plasma. Coagulopathy was controlled only by continuous intravenous anticoagulation with the direct thrombin inhibitor, argatroban. Multimodal antineoplastic treatment, including neoadjuvant chemotherapy followed by surgery and postoperative radiotherapy, resulted in clinical cancer remission, which was paralleled by normalization of tumor markers, CA125 and CA19-9, D-dimer levels, and TF-bearing microvesicles. In summary, continuous anticoagulation with argatroban and multimodal anticancer treatment may be necessary to control TF-driven coagulation activation with recurrent CAT in endometrial cancer.. Obwohl die tumorassoziierte Thrombose (CAT) eine häufige Komplikation bei Patienten mit malignen Erkrankungen darstellt, bleibt ihre Behandlung in der täglichen Praxis eine Herausforderung. Wir berichten über den klinischen Fall einer 51-jährigen Patientin, die sich mit einer hochgradig thrombogenen paraneoplastischen Gerinnungsstörung vorstellte. Trotz therapeutischer Antikoagulation mit verschiedenen Präparaten, unter anderem Rivaroxaban, Fondaparinux und niedermolekulares Heparin, entwickelte die Patientin rezidivierende venöse und arterielle Thromboembolien. Es konnte ein lokal fortgeschrittenes Endometriumkarzinom nachgewiesen werden mit starker Expression von Gewebefaktor (Tissue-Faktor, TF) auf den Tumorzellen. Es fanden sich zudem signifikant erhöhte Konzentrationen von TF-tragenden Mikrovesikeln im Plasma der Patientin. Die Koagulopathie konnte nur durch eine kontinuierliche intravenöse Antikoagulation mit dem direkten Thrombininhibitor Argatroban kontrolliert werden. Eine multimodale antineoplastische Behandlung, einschließlich einer neoadjuvanten Chemotherapie mit anschließender Operation und postoperativer Strahlentherapie, führte zu einer klinischen Remission des Tumors, welche mit einer Normalisierung der Tumormarker CA125 und CA19–9, der D-Dimere und der TF-exprimierenden Mikrovesikel einherging. Somit könnte die Kombination aus kontinuierlicher Antikoagulation mit Argatroban und multimodaler Krebstherapie erforderlich sein, um eine TF-vermittelte paraneoplastische Koagulopathie mit rezidivierender CAT bei Patientinnen mit Endometriumkarzinom zu kontrollieren.

Topics: Anticoagulants; Blood Coagulation Disorders; Endometrial Neoplasms; Female; Heparin, Low-Molecular-Weight; Humans; Middle Aged; Neoplasm Recurrence, Local; Thromboembolism; Thrombophlebitis; Thromboplastin; Venous Thromboembolism

Topics: Humans; Immunohistochemistry; Male; Middle Aged; Multiple Myeloma; Syndrome; Thrombophlebitis; Thromboplastin

Lemierre's syndrome presents a classic clinical picture, the pathophysiology of which remains obscure. Attempts have been made to trace genetic predispositions that modify the host detection of pathogen or the resultant systemic reaction.. A 17-year old female, with no previous medical history, was admitted to the intensive care unit for septic shock, acute respiratory distress syndrome and Lemierre's syndrome. Her DNA was assayed for single nucleotide polymorphisms previously incriminated in the detection of the pathogen, the inflammatory response and the coagulation cascade. We observed functional variations in her Toll like 5 receptor (TLR 5) gene and two coagulation variations (Tissue Factor (TF) 603 and Plasminogen-Activator-Inhibitor-1 (PAI-1) 4G-4G homozygosity) associated with thrombotic events.. The innate immune response and the prothrombogenic mutations could explain, at least in part, the symptoms of Lemierre's syndrome. Genomic study of several patients with Lemierre's syndrome may reveal its pathophysiology.

Topics: Adolescent; Female; Fusobacterium Infections; Fusobacterium necrophorum; Humans; Pharyngitis; Plasminogen Activator Inhibitor 1; Polymorphism, Single Nucleotide; Respiratory Distress Syndrome; Shock, Septic; Syndrome; Thrombophlebitis; Thromboplastin; Toll-Like Receptor 5

Peroral administration of peptide Pro-Gly-Pro to 10-11-month-old rats with modeled prethrombotic state normalized functions of the anticoagulation system and produced a potent antiplatelet effect. Peroral administration of Pro-Gly peptide before provocation of thrombin generation and thrombus formation prevented death of animals from thrombosis. Experiments on rats with venous thrombosis induced by stasis and administration of thrombin showed that pretreatment with Pro-Gly peptide decreased the weight of formed thrombi.

Topics: Administration, Oral; Animals; Animals, Outbred Strains; Anticoagulants; Blood Platelets; Disease Models, Animal; Fibrinolysis; Hemostatics; Injections, Intraperitoneal; Male; Oligopeptides; Platelet Aggregation; Platelet Aggregation Inhibitors; Rats; Survival Rate; Thrombophlebitis; Thromboplastin; Thrombosis; Time Factors

The increased risk for deep vein thrombosis (DVT) after orthopaedic surgery has been well documented as well as hypercoagulable state during both total hip arthroplasty (THA) and total knee replacement (TKR). To investigate the influence of the surgical procedure [posterolateral (PL) or lateral (L) approach for THA, use of tourniquet (TQ) or not use of TQ for TKR] on the hypercoagulability and the role of extrinsic pathway activation and endothelial stimulation during orthopaedic surgery we have examined 40 patients (20 patients undergoing primary THA--10 with PL approach and 10 with L approach--and 20 patients undergoing TKR--10 with TQ application and 10 without TQ). Thrombin-antithrombin complexes (TAT), tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombomodulin (TM) and von Willebrand factor antigen (vWF:Ag) were analyzed before and during the orthopaedic surgery. During THA, TAT plasma levels increased more markedly in patients assigned to the L than PL approach (p <0.05); during TKR an elevation of TAT of higher degree (p <0.05) was observed when TQ was not applicated. Blood clotting activation was significantly (p <0.001) more relevant during THA than TKR. No changes in TF and vWF:Ag plasma levels were observed in all patients undergoing THA and TKR. TFPI plasma levels significantly (p <0.05) decreased 1 h after the end of the THA in group PL and group L, whereas they remained unaffected in the two groups of patients undergoing TKR. Similarly TM plasma levels significantly decreased during THA, but not during TKR. In conclusion, these results show that: 1) the site of surgical procedures and the type of approach affect the degree of hypercoagulability, 2) the blood clotting activation takes place in the early phases of orthopaedic surgery, without signs of extrinsic pathway and endothelial activation.

Topics: Aged; Blood Coagulation; Female; Humans; Male; Middle Aged; Orthopedics; Postoperative Complications; Surgical Procedures, Operative; Thrombophlebitis; Thromboplastin

Current biochemical markers of thrombosis, such as d-dimer, are of little value in demonstrating the presence of thrombus postoperatively, as their levels are elevated by surgery. Thrombosis involves adhesive interactions between the endothelium, platelets and leukocytes. The aim of the study was to determine which of a panel of haemostatic and adhesion factors are altered by the presence of thrombus, but not by surgery. These factors were measured in 20 patients with established spontaneous DVTs, 13 patients having hip replacement surgery and 28 control patients. Circulating levels of P-selectin, VCAM-1 and tissue factor were found to be increased when thrombus was present (p <0.018, p <0.0001, p <0.0028 respectively), but were not altered by surgery. The significance of these circulating factors in venous thrombosis remains to be established, but it is conceivable that they are the product of increased leukocyte trafficking and activity. Assay of VCAM-1, in particular, may be of use in the early detection of venous thrombi in postoperative patients.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Female; Humans; Male; Middle Aged; P-Selectin; Predictive Value of Tests; Thrombophlebitis; Thromboplastin; Vascular Cell Adhesion Molecule-1

Topics: Abortion, Habitual; Adult; Animals; Antibodies, Antiphospholipid; Anticoagulants; Antiphospholipid Syndrome; Autoimmune Diseases; Drug Monitoring; Female; Humans; International Normalized Ratio; Intracranial Embolism; Intracranial Thrombosis; Male; Middle Aged; Pregnancy; Recombinant Proteins; Recurrence; Risk; Seizures; Thromboembolism; Thrombophilia; Thrombophlebitis; Thromboplastin; Warfarin

We studied the use of the Ecarin Clotting Time (ECT) as a predictive assay of the antithrombotic effects of argatroban in a new tissue factor-dependent model of venous thrombosis and a model of arterial thrombosis in the rat. Heparin was used as a reference anticoagulant. Infusions of argatroban dose-dependently increased the ECT across the range of doses required for antithrombotic activity in models of venous and arterial thrombosis (1.25-40 microg/kg/min). The TT was only useful as a marker in the case of venous thrombosis, since, in the arterial thrombosis model, the clotting times were >200 s in the majority of animals receiving antithrombotic doses. The aPTT is not sufficiently sensitive to be predictive of an antithrombotic effect in the venous model, and shows only modest increases in the arterial thrombosis model. Heparin did not significantly increase the ECT at antithrombotic doses in the venous thrombosis model, and only increased the ECT by 53% at 40 microg/kg/min in the arterial model, despite a marked antithrombotic effect. Both the TT and aPTT were dose-dependently increased by heparin at doses active in the venous model, whereas both parameters were >200 s at doses active in the arterial thrombosis model. Thus, the ECT provides a predictive marker for the antithrombotic activity of argatroban in both venous and arterial thrombosis, at least in the rat.

Topics: Animals; Antithrombins; Arginine; Arteriovenous Shunt, Surgical; Blood Coagulation Tests; Disease Models, Animal; Male; Pipecolic Acids; Rats; Rats, Inbred Strains; Reference Values; Sulfonamides; Thrombophlebitis; Thromboplastin; Thrombosis; Treatment Outcome

To assess the effect on the desired activated partial thromboplastin time (APTT) of altered practice in the laboratory control of heparin treatment.. Descriptive study of the number of APTTs in the desired range (DR) in 1987 (historical controls) and in 1992/1993. In the latter period, four changes in the implementation of heparin treatment took place: another coagulation analyser was used, laboratory control was intensified with a nomogram as guideline, and the DR was changed form 90-120 to 45-60 s. Furthermore, a standard heparin solution of 417 U/ml was supplied by the hospital pharmacy.. The total amount of APTTs in the desired range increased from 19% in 1987 to 46% in 1992/1993, and the DR was reached in 1987 in 1 day by 14%, and in 1992/1993 by 48% of patients. The mean daily heparin dose was higher in 1992/1993 (34.1 * 1000 U, 95% CI 33.4-34.8) than in 1987 (32.3 * 1000 U, 95% CI 31.5-33.0). The starting dose of heparin of 400 U/kg during the first day, following an initial bolus injection of 70 U/kg, was correct in 44% of patients, too low in 46%, and too high in 10%.. The new policy in the laboratory control of heparin treatment resulted in an increased number of APTTs in the DR, and a shorter time to reach this.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anticoagulants; Female; Follow-Up Studies; Heparin; Humans; Infusions, Intravenous; Male; Middle Aged; Monitoring, Physiologic; Partial Thromboplastin Time; Pulmonary Embolism; Reference Standards; Retrospective Studies; Thrombophlebitis; Thromboplastin

Tissue factor (TF) is a glycoprotein which acts as a trigger of the coagulation cascade. TF expression may be induced at the surface of monocytes and endothelial cells by several stimuli including bacterial endotoxin (LPS) and cytokines (IL 1 beta, TNF alpha) and there is a large body of evidence for the involvement of hypoxia as a primaring factor in the process leading to thrombosis. To define the molecular basis underlying this phenomenon, we evaluated the relative role of platelet activating factor (PAF). PAF primed human monocytes and human umbilical vein endothelial cells (HUVEC) for TF expression following exposure to E coli LPS but was unable to enhance the induction of TF expression by IL 1 beta. The priming effect of PAF with regard to LPS occurred in a time- and dose-dependent manner and was inhibited by the PAF receptor antagonist SR 27417. When HUVEC or monocytes were exposed to an hypoxic environment, a significant rise in LPS-induced TF expression was observed. Hypoxia had no effect on IL 1-induced TF expression. The enhanced LPS-induced TF expression in both cell types was mediated by PAF as indicated by the inhibition obtained with SR 27417, added during hypoxia. Although the importance of hypoxia in the etiology of venous thrombosis has been acknowledged for a long time, evaluation of the relative importance of PAF in the process leading to thrombus formation is still lacking. Stasis-induced thrombosis performed in the rabbit jugular vein was enhanced in a dose-dependent manner by the prior i.v. administration of LPS (0.05 to 100 micrograms/ kg, i.v.). SR 27417 administered simultaneously with LPS prevented thrombus formation with an ED50 value of 0.1 +/- 0.04 mg/kg. These results therefore show that hypoxia promotes LPS-induced TF expression in HUVEC and human monocytes through a PAF-dependent mechanism in vitro and in vivo.

Topics: Animals; Cells, Cultured; Endotoxins; Humans; Hypoxia; Interleukin-1; Lipopolysaccharides; Monocytes; Platelet Activating Factor; Rabbits; Thiazoles; Thrombophlebitis; Thromboplastin; Umbilical Cord

The original activated partial thromboplastin time-based assay for activated protein C (APC)-resistant factor Va (FVa) requires carefully prepared fresh plasma and cannot be used in patients receiving warfarin or in patients with antiphospholipid antibodies. A new test is described here that circumvents these limitations and distinguishes without overlap heterozygotes for APC-resistant FVa from persons with normal FV. A diluted test plasma is incubated with an FV-deficient substrate plasma and tissue factor and then clotted with Ca2+ or Ca2+ plus APC. Test results are independent of the FV level or the dilution of the test plasma used. Of 39 controls, 37 gave normal results. Two controls (5%) gave results indicative of APC resistant FVa and on DNA analysis were found to be heterozygous for FV R506Q. Twenty of 21 randomly selected patients receiving warfarin gave normal results. In the single patient with abnormal results, heterozygous FV R506Q was confirmed by DNA analysis. Two of 15 patients with protein S deficiency and 5 of 29 patients with a lupus anticoagulant had abnormal results. APC resistance caused by FV R506Q was confirmed in the five of these seven patients available for DNA analysis. APC-resistant FVa was also detected in 10 of 21 (46%) stored plasma from unrelated patients with venous thrombosis and negative earlier evaluation for a lupus anticoagulant or a deficiency of protein C, protein S, or antithrombin, which confirms a high incidence of this defect among patients with venous thrombosis.

Topics: Blood Preservation; Calcium; Cryopreservation; DNA Mutational Analysis; Factor Va; Genetic Predisposition to Disease; Heparin; Heterozygote; Humans; Lupus Coagulation Inhibitor; Protein C; Protein S Deficiency; Thrombophlebitis; Thromboplastin; Warfarin

The association of cancer with clinical abnormalities of blood coagulation, including superficial thrombophlebitis, deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC) is well-known, particularly in patients with solid tumors and acute promyelocytic leukemia (APL). Less commonly appreciated is the potential for the development of venous thromboembolic disease (TED) in patients with acute lymphocytic leukemia (ALL). Multiple mechanisms have been implicated for the activation of coagulation in these patients, with an emphasis on the contribution made by the procoagulant properties of the tumor cells themselves. We present two cases of patients with pre-B cell ALL, both of whom developed recurrent TED as the presenting manifestation of their leukemia and/or heralding relapse. The blast cells from one of the patients were studied for the presence of procoagulant activity (PCA) and by Northern blot analysis for tissue factor (TF) messenger RNA (mRNA). Neither PCA nor TF mRNA could be identified in highly purified populations of the lymphoblast cells. We conclude that recurrent TED can be a manifestation of ALL and that mechanisms other than the release of tumor cell procoagulants should be sought to explain the pathogenesis of thrombosis in some patients.

Topics: Adult; Blood Coagulation Factors; Blotting, Northern; Burkitt Lymphoma; Cysteine Endopeptidases; Humans; Male; Middle Aged; Neoplasm Proteins; RNA, Messenger; Thrombophlebitis; Thromboplastin

The aims of the present investigation were to develop a new venous thrombosis animal model with low flow conditions in the venous blood stream and then evaluate this model for testing new anticoagulants. In this model, the vena cava of rats was narrowed with a Doppler flow probe, blood flow velocity continuously recorded and thrombus formation initiated by thromboplastin infusion. Sixty-five minutes following thromboplastin infusion the animals were sacrificed and the following parameters measured: thrombus wet weight, fibrinopeptide A (FpA), activated partial thromboplastin time and platelet number. The new model was evaluated with aspirin, a PGI2 mimetic, heparin and a soluble thrombomodulin analogue. Without thromboplastin infusion no thrombus formation or reduction of blood flow was observed. Controls receiving thromboplastin infusion developed a thrombus, blood flow was arrested, platelet number decreased and FpA was elevated. In contrast, animals pretreated with anticoagulants maintained a residual flow, while thrombus weight, thrombocytopenia and FpA elevation were reduced. The antiplatelet agents were not effective. This study demonstrates that, under low flow conditions, only a combination of blood flow reduction with a hypercoagulable state results in venous thrombus formation. This improved model of venous thrombosis more closely resembles the clinical situation and is applicable for testing anticoagulants.

Topics: Animals; Anticoagulants; Aspirin; Blood Flow Velocity; Constriction; Disease Models, Animal; Epoprostenol; Heparin; Male; Platelet Aggregation Inhibitors; Prostaglandins, Synthetic; Rats; Rats, Wistar; Recombinant Proteins; Thrombomodulin; Thrombophlebitis; Thromboplastin; Vena Cava, Inferior

Venous thrombosis was induced by ligature of the inferior vena cava in rats whose blood was made hypercoagulable by intravenous (IV) administration of tissue thromboplastin. From a dose-response showing that the administration of increasing doses of tissue thromboplastin resulted in a subsequent progressive increase of thrombus weight, two concentrations of tissue thromboplastin were chosen: a high dose (550 microL/kg, IV) where thrombus formation was optimal and a concentration (7 microL/kg, IV) where tissue thromboplastin-hypercoagulability was intermediate. In both experimental conditions, leukopenia provoked by a myelotoxic drug did not influence the development of venous thrombosis. However, after thrombocytopenia induced by an antiplatelet antiserum, a dramatic decrease in thrombus formation was observed in animals that had been pre-challenged with the lower dose of tissue thromboplastin, whereas decrease in platelet count did not affect venous thrombosis under high thrombogenic challenge. When administered orally 2 hours before thrombosis induction, the ticlopidine analogue clopidogrel showed dose-dependent inhibition of thrombus formation in animals that were pre-challenged with a low dose of tissue thromboplastin (ED50 = 7.9 +/- 1.5 mg/kg, orally) but remained ineffective against high tissue thromboplastin-induced venous thrombosis. We further determined the effect of heparin and hirudin, and showed that both of these drugs exhibited a more potent antithrombotic activity after injection of the lower dose of tissue thromboplastin than after injection of a high dose of tissue thromboplastin. Therefore, using our model of stasis and hypercoagulability, platelet activation played a major role in the development of venous thrombosis when the thrombogenitic stimulus was mild.

Topics: Animals; Blood Platelets; Clopidogrel; Disease Models, Animal; Heparin; Hirudins; Leukopenia; Male; Mechlorethamine; Partial Thromboplastin Time; Platelet Aggregation Inhibitors; Rabbits; Rats; Rats, Sprague-Dawley; Thrombocytopenia; Thrombophlebitis; Thromboplastin; Ticlopidine

The main objective of these experiments was to develop and characterize a new experimental model of venous thrombosis, and determine whether a combination of vascular wall damage (crushing with hemostat clamps) and prolonged stasis produced more reproducible clots than prolonged stasis per se. Rabbits were laparotomized, and a segment of the vena cava was dissected free and looped with two silk ligatures, 2.5 cm apart. The proximal tie was ligated 5 min after release of the clamps; the distal tie applied shortly thereafter, trapping a volume of blood in the isolated segment. At 2 hr after ligation, the isolated venous sac was excised and examined for the presence of a clot. Large, well-formed clots, which could be readily transferred and weighed, were invariably observed in the "clamp" and "no clamp" groups, the latter being a sham control. Mean clot weights did not differ in the two groups (23.1 +/- 1.6 versus 30.8 +/- 5.4 mg dry weight, clamped versus no clamp, respectively, p greater than 0.05). However, the precision of the method was improved significantly (p less than 0.005) by clamping as determined by homogeneity of variance testing. Time-course studies showed that a considerable lag period (about 60 min) preceded development of a detectable clot, and that the thrombus evolved rapidly during the interval of 60-90 min postligation. The location of the small clots at 60 min in clamped segments, as well as the failure of prolonged (120 min) stasis without caval isolation to cause substantial thrombi, strongly suggests that clot formation attributed to "stasis per se" is in fact due to focal vascular lesions created at the tie-down points. The present study is also the first report of blockade of localized venous thrombosis by recombinant tissue factor pathway inhibitor (rTFPI). When given as an i.v. bolus 20 min prior to ligation, rTFPI at 400 and 800 micrograms/kg completely blocked formation of the thrombus or greatly reduced its size in five of the six animals tested.

Topics: Animals; Disease Models, Animal; Lipoproteins; Male; Rabbits; Regional Blood Flow; Thrombophlebitis; Thromboplastin; Venae Cavae

Development of thromboplastin (tpl) and plasminogen activator (PA) activity in monocytes and the effects of high doses of corticosteroids (HCD) on these activities were studied in patients undergoing a standardized surgical trauma. Twelve patients who received uncemented total hip prostheses were divided into a nonsteroid group (n = 6) and a steroid group (n = 6). We found no significant differences between the two patient groups regarding tpl or PA activities of peripheral blood mononuclear cells (PBM) isolated during the postoperative phase. However, in the nonsteroid group there was a tendency for increased expression of procoagulant activity and decreased fibrinolytic activity on the 1st postoperative day, favoring the formation of fibrin in the monocyte microenvironment. Further, PBM isolated on the 1st and 2nd day after surgery were significantly less capable of generating tpl activity on endotoxin stimulation than cells isolated preoperatively. This was not the case in the steroid group. These patients had also a tendency for decreased fibrinolysis at the end of the 1st postoperative week, indicating increased imbalance towards a more thrombotic stage after surgery.

Topics: Adrenal Cortex Hormones; Aged; Aged, 80 and over; Blood Coagulation; Female; Fibrinolysis; Hip Prosthesis; Humans; Male; Middle Aged; Monocytes; Plasminogen Activators; Thrombophlebitis; Thromboplastin

We examined thromboplastin activity (TA) of monocytes and release of oxygen-derived free radicals (ODRFs) from monocytes and granulocytes before and after implantation of a hip or a knee prosthesis in 7 patients with rheumatoid arthritis and in 8 patients with arthrosis. Monocyte TA rose threefold on the first postoperative day in the rheumatoid patients, but was unaltered postoperatively in the arthrosis patients. Granulocyte chemiluminescence doubled in the arthrosis group on the second postoperative day, but was unaltered in the rheumatoid patients. Monocyte chemiluminescence was not influenced by the operation. Thus, leukocytes from the rheumatoid patients responded differently from surgical trauma when compared with leukocytes from the arthrosis patients. This difference may have an impact postoperatively.

Topics: Arthritis, Rheumatoid; Granulocytes; Hip Prosthesis; Humans; Joint Diseases; Knee Prosthesis; Monocytes; Thrombophlebitis; Thromboplastin

Antithrombotic potency of recombinant hirudins rHV2, rHV2-Lys47 and rHV2-Arg47 was studied in a model of experimental thrombosis induced by tissue factor in the rat. Venous thrombosis was induced by i.v. injection of 25 mg/kg tissue factor followed by stasis of the inferior vena cava. In this model natural recombinant hirudins, rHV2 and rHV2-Lys47 injected 5 min before thrombo-plastin totally inhibited thrombosis in the same micrograms range as heparin or natural hirudin extracted from leeches. However, the mutant variant rHV2-Arg47 gave a maximal 60% inhibition of thrombosis. Variants rHV2-Lys47 (30 micrograms/kg) and rHV2-Arg47 (157 micrograms/kg) injected 5 min before thromboplastin prevented by 90 to 100% the drop in platelet count observed during the disseminated intravascular coagulation induced by thromboplastin injection. Recombinant hirudins were less anticoagulant than heparin as measured by an APTT on rat plasma. After rat tail transection, rHV2-Lys47 caused a 2-fold smaller prolongation of the bleeding time than an equivalent antithrombotic dose of heparin. Plasmatic elimination of rHV2-Lys47 from rat plasma after i.v. injection had a fast distribution phase with a half-life of 3 min during which 90% of injected rHV2-Lys47 was lost and was followed by a slower elimination phase. Thus recombinant hirudin rHV2-Lys47 appears as a promising potent antithrombotic agent for the prevention of thrombin-dependent venous thrombosis and disseminated intravascular coagulation.

Topics: Animals; Bleeding Time; Disseminated Intravascular Coagulation; Hirudin Therapy; Hirudins; Iodine Radioisotopes; Male; Rats; Rats, Inbred Strains; Recombinant Proteins; Thrombophlebitis; Thromboplastin

To test the possibility that different doses of heparin or other sulfated polysaccharides are required to inhibit thrombosis initiated by different stimuli, we compared the effects of heparin (HEP), pentosan polysulfate (SP54) and dermatan sulfate (DS) on the inhibition of thrombus formation induced by either I) tissue thromboplastin; II) thrombin; or III) factor Xa. Inhibition of thrombus formation induced by the stimuli was measured in a rabbit jugular vein hypercoagulation/stasis model. First, we determined the minimum dose of each sulfated polysaccharide which inhibited tissue thromboplastin-induced thrombus formation by approximately 75%, and then compared the relative effectiveness of this dose to prevent thrombus formation initiated with the other two stimuli. HEP and SP54 were less effective when thrombin was the thrombogenic stimulus, while DS was more effective. HEP was the most effective agent when factor Xa was the stimulus. We conclude that the antithrombotic effectiveness of a given dose of a sulfated polysaccharide may vary depending on the stimulus which initiates thrombus formation.

Topics: Animals; Chondroitin; Dermatan Sulfate; Factor Xa; Female; Fibrinolytic Agents; Heparin; Male; Pentosan Sulfuric Polyester; Polysaccharides; Rabbits; Serine Proteinase Inhibitors; Thrombin; Thrombophlebitis; Thromboplastin

Pathological inhibitors of the coagulation which are recognized by characteristic laboratory findings may cause an increased inclination to haemorrhage, may be clinically mute or also may effect an increased inclination to thrombosis (lupus inhibitors). It is reported on patients with rare coagulation inhibitors, a pathologic antithrombin with normal reptilase time and an antithromboplastin with protracted effect, in which thromboses appeared. The occurrence of thromboses in these patients up to now does not allow the assumption of an effect of these inhibitor substances furthering thrombosis, but only the statement that despite coagulation-analytically recognizable inhibition effects the development of a thrombosis is not prevented. A prophylactic factor substitution in operative interventions is not indicated.

Topics: Adult; Antithrombins; Female; Hemorrhagic Disorders; Humans; Male; Thrombin Time; Thrombophlebitis; Thromboplastin; Thrombosis

Topics: Adult; Blood Coagulation Factors; Female; Humans; Lupus Coagulation Inhibitor; Lupus Erythematosus, Systemic; Pregnancy; Pregnancy Complications; Pulmonary Embolism; Thrombophlebitis; Thromboplastin

Topics: Humans; Prothrombin Time; Reference Standards; Thrombophlebitis; Thromboplastin; Warfarin

Topics: Adolescent; Adult; Aged; beta-Thromboglobulin; Female; Fibrinopeptide A; Fibrinopeptide B; Humans; Leg; Lung; Male; Middle Aged; Platelet Factor 4; Postoperative Complications; Radionuclide Imaging; Thrombin; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Administration, Oral; Anticoagulants; Hemorrhage; Humans; Prothrombin Time; Thrombophlebitis; Thromboplastin

Topics: Heparin; Humans; Postoperative Care; Thrombophlebitis; Thromboplastin

The fibrinolytic responses in the blood during surgical operation have been studied in two groups of patients during intraoperative intermittent compression of the calf. Fibrinolytic activity did not differ significantly between the groups. The postoperative fibrinolytic shutdown was not prevented by intermittent compression of the calf. It is concluded that, whatever the mechanism by which venous thrombosis is prevented by intermittent compression of the calf, it is not by further stimulation of systemic fibrinolysis.

Topics: Dextrans; Evaluation Studies as Topic; Factor X; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Humans; Leg; Male; Postoperative Complications; Pressure; Prothrombin Time; Serum Globulins; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Animals; Blood Coagulation; Cattle; Disseminated Intravascular Coagulation; Ellagic Acid; Factor IX; Factor X; Fibrin; Humans; Lung; Male; Rabbits; Thrombin; Thrombophlebitis; Thromboplastin

A prospective study using an intermittent six hour method of heparin administration with control of subsequent dosage by the activated partial thromboplastin time revealed an over-all incidence of hemorrhagic complications of 12 per cent. If surgical patients are excluded, the incidence of hemorrhage falls to 4 per cent. This may be further reduced by monitoring the activated partial thromboplastin time within the therapeutic range. In no patient did thromboembolism recur while receiving heparin. It is suggested that this method provides adequate control of heparin therapy with an acceptable complication rate and adequate thromboembolic control and is cheaper to use than a continuous infusion.

Topics: Adult; Aged; Blood Coagulation Tests; Female; Hemorrhage; Heparin; Humans; Infusions, Parenteral; Male; Middle Aged; Prospective Studies; Thrombophlebitis; Thromboplastin

Topics: Animals; Blood Coagulation Tests; Cell Adhesion; Dogs; Female; Femoral Vein; Jugular Veins; Male; Neutrophils; Thrombophlebitis; Thromboplastin

The activated partial thromboplastin time is compared with the corresponding prothrombin ratio in 6378 samples of platelet-poor plasma from 446 patients treated for a total of more than 4500 patient/months with oral anticoagulatnts. A relative decrease in the activated partial thromboplastin time following deep vein thrombosis is described, which tends to become less obvious during the first year of treatment and is greater in older patients. Although this relative decrease is also found in patients treated after cerebrovascular accidents, it is not found in patients treated after myocardial infarction or in patients with mitral valve disease treated prophylactically with long-term oral anticoagulants. It is though possible that these changes following deep vein thrombosis might be useful in helping to determine the duration of oral anticoagulant treatment.

Topics: Adult; Blood Coagulation; Female; Heart Valve Diseases; Humans; Male; Middle Aged; Myocardial Infarction; Phenindione; Prothrombin Time; Thrombophlebitis; Thromboplastin; Warfarin

Topics: Arteriosclerosis Obliterans; Aspergillus; Blood Coagulation; Blood Coagulation Tests; Electrocardiography; Fibrinogen; Fibrinolysis; Humans; Immunoelectrophoresis; In Vitro Techniques; Injections, Intravenous; Pelvis; Peptide Hydrolases; Retinal Artery; Thromboangiitis Obliterans; Thrombophlebitis; Thromboplastin; Urticaria

Topics: Aged; Blood Cell Count; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Female; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemoptysis; Humans; Liver Neoplasms; Lung Neoplasms; Male; Middle Aged; Plasminogen; Prothrombin Time; Thrombin; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Tests; Heparin; Humans; Needles; Prothrombin Time; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Blood Coagulation; Blood Coagulation Tests; Clot Retraction; Disseminated Intravascular Coagulation; Half-Life; Hemorrhage; Hemostasis; Heparin; Humans; Infusions, Parenteral; Injections, Intravenous; Injections, Subcutaneous; Pulmonary Embolism; Thrombin; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Aged; Bile Duct Neoplasms; Bile Ducts, Intrahepatic; Blood Coagulation; Chronic Disease; Disseminated Intravascular Coagulation; Fibrinogen; Humans; Male; Prothrombin; Thrombelastography; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Tests; Blood Platelets; Humans; Postoperative Complications; Prognosis; Surface Properties; Thrombin; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Animals; Brain; Drug Stability; Humans; Myocardial Infarction; Phenols; Prothrombin Time; Pulmonary Embolism; Rabbits; South Africa; Thrombophlebitis; Thromboplastin; Warfarin

A bedside test of heparin activity (whole blood activated partial thromboplastin time) was assessed during clinical control of anticoagulation. It correlated closely (r = 0.94) with the whole blood clotting time but had a number of advantages.

Topics: Blood Coagulation Tests; Heparin; Humans; Methods; Pulmonary Embolism; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Adult; Animals; Blood Coagulation; Blood Coagulation Tests; Electrophoresis, Polyacrylamide Gel; Factor VII; Factor X; Female; Humans; Immune Sera; Male; Menopause; Menstruation; Middle Aged; Myocardial Infarction; Neutralization Tests; Prothrombin Time; Rabbits; Sex Factors; Stimulation, Chemical; Thrombophlebitis; Thromboplastin; Time Factors; Warfarin

A prospective, randomized trial is described in which the usefulness of two tests in the control of anticoagulant therapy is compared. Fifty-two patients were controlled by the one-stage prothrombin time and 55 by the activated partial thromboplastin time. There was no significant difference in the incidence of bleeding between the two groups. When bleeding did occur, it was more often reflected by prolongation of the prothrombin time than of the activated partial thromboplastin time. The prothrombin time was found to have some practical advantages over the activated partial thromboplastin time.

Topics: Adult; Age Factors; Aged; Anticoagulants; Blood Coagulation Tests; Hemorrhage; Humans; Methods; Middle Aged; Prothrombin Time; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Anticoagulants; Blood Coagulation Tests; Humans; Myocardial Infarction; Thrombophlebitis; Thromboplastin

Topics: Adolescent; Adult; Aged; Blood Coagulation Tests; Female; Hemorrhage; Heparin; Humans; Infusions, Parenteral; Male; Middle Aged; Prospective Studies; Pulmonary Embolism; Radiography; Radionuclide Imaging; Recurrence; Thromboembolism; Thrombophlebitis; Thromboplastin; Time Factors

Topics: Adolescent; Adult; Aged; Blood Coagulation Tests; Female; Heparin; Humans; Injections, Intravenous; Male; Middle Aged; Prospective Studies; Pulmonary Embolism; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Adolescent; Adult; Aged; Anticoagulants; Blood Cell Count; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Child; Child, Preschool; Factor V; Factor VII; Factor VIII; Factor X; Female; Fibrinogen; Glucocorticoids; Humans; Infant; Male; Middle Aged; Nephrotic Syndrome; Prothrombin; Renal Veins; Thromboembolism; Thrombophlebitis; Thromboplastin

Arterial thrombosis and renal vein thrombosis occurred in two men and one woman, respectively, treated with steroids for the nephrotic syndrome. Raised serum cholesterol occurred in one patient only. Though bleeding, clotting, and prothrombin times, as well as the platelet counts, were normal, the rate of thromboplastin generation was increased in all three patients. Adding heparin to the plasma of one patient slowed the rate, and suggested that the raised rate could be due to removal or suppression of such normal circulating coagulation inhibitors. The thromboplastin generation test seems to be useful in diagnosing and managing such hypercoagulable states, and may help in further investigations of their causes.

Topics: Adult; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Cholesterol; Female; Heparin; Humans; Male; Nephrotic Syndrome; Prednisolone; Thrombophlebitis; Thromboplastin; Thrombosis

Topics: Administration, Oral; Anticoagulants; Blood Coagulation Tests; Humans; Myocardial Infarction; Prothrombin Time; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Disorders; Child; Erythrocyte Aggregation; Female; Humans; Infant; Infant, Newborn; Kidney Cortex Necrosis; Male; Meningitis, Meningococcal; Renal Veins; Thrombocytopenia; Thrombophlebitis; Thromboplastin

Topics: Abortion, Septic; Blood Coagulation Disorders; Embolism, Amniotic Fluid; Female; Fetal Death; Fibrinolysis; Gelatin; Hemorrhagic Disorders; Humans; Hydrogen-Ion Concentration; Placenta; Placenta Diseases; Plasma Substitutes; Pregnancy; Pregnancy Complications; Pulmonary Embolism; Shock, Hemorrhagic; Shock, Septic; Streptokinase; Thrombophlebitis; Thromboplastin; Thrombosis

Topics: Arteriosclerosis; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Extracorporeal Circulation; Fibrin; Fibrinolysis; Hemorrhage; Heparin; Heparin Antagonists; Humans; Hyperlipidemias; Hypersensitivity; Natriuresis; Osteoporosis; Protamines; Prothrombin Time; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Female; Fibrin; Fibrinogen; Fibrinolysis; Heparin; Humans; Middle Aged; Purpura, Thrombocytopenic; Thrombophlebitis; Thromboplastin

Topics: Adult; Aged; Anticoagulants; Blood Coagulation Tests; Female; Heart Valve Diseases; Humans; Male; Middle Aged; Myocardial Infarction; Phenindione; Prothrombin Time; Pulmonary Embolism; Thrombophlebitis; Thromboplastin; Warfarin

Topics: Analysis of Variance; Blood Coagulation Tests; Blood Flow Velocity; Blood Platelets; Blood Specimen Collection; Fibrinogen; Humans; Leg; Phlebography; Physical Examination; Thrombophlebitis; Thromboplastin

Topics: Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Blood Specimen Collection; Female; Hematocrit; Humans; Male; Middle Aged; Thrombelastography; Thrombophlebitis; Thromboplastin

Topics: Adolescent; Adult; Blood Coagulation Disorders; Blood Coagulation Factors; Child; Child, Preschool; Factor VII; Factor VIII; Factor XIII; Female; Humans; Infant; Kaolin; Lymphoma, Non-Hodgkin; Male; Prothrombin Time; Pulmonary Embolism; Thrombocytopenia; Thrombophlebitis; Thromboplastin; Wiskott-Aldrich Syndrome

Topics: Adenocarcinoma; Blood Coagulation Tests; Carcinoma, Bronchogenic; Carcinoma, Squamous Cell; Coumarins; Female; Heparin; Humans; Male; Smoking; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Disorders; Blood Platelet Disorders; Humans; Thromboembolism; Thrombophlebitis; Thromboplastin; Thrombosis

Topics: Blood Coagulation Disorders; Child; Chromatography; Factor V; Female; Humans; Thrombophlebitis; Thromboplastin

Topics: Angiography; Deoxyribonuclease I; Drug Therapy; Fibrinolysis; Fibrinolytic Agents; Geriatrics; Infusions, Intravenous; Infusions, Parenteral; Streptodornase and Streptokinase; Streptokinase; Thrombophlebitis; Thromboplastin; Thrombosis; Urokinase-Type Plasminogen Activator

Topics: Adolescent; Blood Coagulation Tests; Blood Platelets; Child; Cholecystitis; Coronary Disease; Duodenal Ulcer; Geriatrics; Glycine max; Hemophilia A; Humans; Lecithins; Myocardial Infarction; Phosphatidylcholines; Polycythemia Vera; Thrombophlebitis; Thromboplastin

Topics: Humans; Thrombophlebitis; Thromboplastin

Topics: Dicumarol; Heparin; Humans; Thrombophlebitis; Thromboplastin; Thrombosis; Venous Thrombosis

Topics: Humans; Thrombophlebitis; Thromboplastin

Topics: Thrombophlebitis; Thromboplastin; Veins; Venous Thrombosis

Topics: Carcinoma; Humans; Neoplasm Recurrence, Local; Stomach Neoplasms; Thrombophlebitis; Thromboplastin