fibrin and Leukemia

Topics: Antigens, CD; Biomarkers; Blood Cell Count; Blood Coagulation Tests; Chromosome Aberrations; Disseminated Intravascular Coagulation; Fibrin; Hematologic Diseases; Humans; Leukemia; Solubility

Tissue factor is an ubiquitous phospholipid-protein complex, which triggers blood coagulation through the so-called extrinsic pathway. Reactions initiated by tissue factor bypass many of the early stages of coagulation (contact phase) and involve factors VII, X, V, II and fibrinogen but also factor IX (and VIII) as it was recently demonstrated. So, it appears that tissue factor has a key-role in the haemostasic process as it has been suggested by the mildness or the absence of haemorrhagic syndrome in contact factors deficiencies. Tissue factor activity has been found in many types of cells, especially in white bloods cells. Experimental studies have demonstrated the presence of tissue factor activity in polymorphonuclears, lymphocytes, monocytes (or macrophages). This activity is enhanced by gram-negative endotoxin stimulation, inflammation, cell mediated immunologic phenomena or malignancy. These data are in good agreement with a wild range of features observed in human pathology: fibrin deposits in inflammatory lesions, disseminated intravascular coagulation (DIC) during the course of gram-negative septicemias or acute promyelocytic leukemias, local thrombi at the early phase of graft rejection. The protective effect of a phospholipase C against DIC induced in rats by tissue factor infusion suggests in the future, a specific therapy would be possible in man that, in the frequent clinical conditions involving clotting activation through tissue factor pathway.

Topics: Animals; Blood Coagulation; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Fibrin; Graft Rejection; Humans; Inflammation; Leukemia; Leukocytes; Rabbits; Sepsis; Thromboplastin

Topics: Blood Coagulation; Burns; Chronic Disease; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Tests; Hemostasis; Humans; Leukemia; Purpura, Thrombotic Thrombocytopenic; Thrombin

Topics: Blood Transfusion; Enzyme Inhibitors; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemostatics; Humans; Leukemia; Liver Cirrhosis; Male; Pathology; Physiology; Polycythemia Vera; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Prostatectomy; Prostatic Neoplasms; Prothrombin; Thrombin; Thromboplastin

The lung ball is a special type of pulmonary aspergillosis (PA) occurring often after chemotherapy for leukemia. Histologically the ball, with air crescent sign on roentgenogram, is compatible with necrotizing lung tissue admixed with Aspergilli. The lung ball differs entirely from the common "fungus ball" in its quality, though they are similar in roentgenological appearances. The present two cases were leukemia which showed pulmonary findings in their therapeutic course, resulting in lung resection. In both cases the lung ball was confirmed histopathologically. Immunostaining of the lung tissue for neutrophil elastase showed elastase in various sites in the bronchial wall, pulmonary blood vessels (artery, vein) and cavitary wall. In our previous studies, much importance was attached to the disturbance of the pulmonary circulation caused by fibrin deposition as a factor in the developmental course of the fungus ball type aspergillosis (semi-invasive type). The circulatory disturbance of the lung was recognized also in the present cases. This two-way destruction of the pulmonary tissue, resulting from both neutrophil elastase activities and pulmonary circulatory disturbances, were regarded as the most important factor for the development of the lung ball. There are few studies on aspergillar lung ball with regard to the above respects.

Topics: Aged; Aspergillosis; Diagnosis, Differential; Female; Fibrin; Humans; Leukemia; Leukocyte Elastase; Lung; Lung Diseases, Fungal; Male; Middle Aged; Neutrophils; Pneumonectomy; Radiography, Thoracic

Hypercoagulability is often associated with a variety of disease states, leading to cardiovascular complications. Polyethylenimine (PEI) prolonged prothrombin time, demonstrating its anticoagulant potential. In vitro, PEI at low concentration (nM) significantly blocked thrombin-catalyzed fibrin formation, accounting for its mode of anticoagulation. The uncompetitive inhibition by PEI of fibrin formation was independent of the concentration of fibrinogen (FBG), thrombin, or NaCl. PEI showed no effect on thrombin amidolytic activity, suggesting that the blockade of thrombin interaction with FBG could account for the inhibition on fibrin formation. PEI drastically depressed rabbit brain thromboplastin procoagulation monitored by a single-stage clotting assay using human plasma. In a THP-1 monocytic hypercoagulation model, a 4-h exposure to bacterial endotoxin or Ca(2+) ionophore A23187, respectively, resulted in a 5- or 10-fold enhancement in monocytic tissue factor (mTF) procoagulation. mTF hypercoagulation was offset by PEI included in the assay mixture. PEI showed the potential to arrest mTF hypercoagulation with IC(50) around 1.2 nM. Using a chromogenic assay to dissect the extrinsic pathway, we further assessed whether PEI has any effect on other clotting factors. PEI was not an inhibitor for either FVIIa or FXa, having no effect on not only the amidolytic but also their corresponding functionally catalytic activities. Although PEI upregulated TF-dependent FVII activation under the low-salt condition, the effective downstream inhibition of fibrin formation readily abolished and overrode the upstream enhancement, demonstrating the overall anticoagulation. PEI could present a new class of anticoagulant.

Topics: Anticoagulants; Blood Coagulation; Blood Coagulation Factors; Catalysis; Fibrin; Humans; Leukemia; Monocytes; Polyethyleneimine; Thrombin; Tumor Cells, Cultured

The thrombin activatable fibrinolysis inhibitor (TAFI) influences the pathways regulating fibrin formation and deposition. The enormous TAFI plasma level variability present in adults may be explained by a combination of two polymorphisms in the TAFI gene (+1542C>G; 505G>A). We aimed to correlate these two polymorphisms with plasma TAFI antigen concentrations in healthy children and pediatric oncology patients with and without venous thrombosis who were supplied with Broviac central venous catheters. Polymorphisms were detected by restriction fragment length polymorphism (RFLP) analysis of polymerase chain reaction (PCR) amplification, whereas TAFI concentration was determined using a commercial enzyme-linked immunosorbent assay (ELISA). Samples from 57 controls and 67 pediatric patients (11 venous thrombotic complications) were studied. TAFI levels in healthy children and patients were not influenced by gender or age. Compared with the 505GG carriers (wild type), 505AA carriers as well as heterozygous 505GA carriers each exhibited significantly higher TAFI antigen concentrations. In contrast, the lowest TAFI levels were detected in homozygous carriers of the +1542GG polymorphism. A combination of the genotype 505AA (homozygous carrier) and +1542CC (wild type) was present in 13 probands and resulted in the highest TAFI levels. Although in oncologic patients the risk of thrombosis was markedly increased by the heterozygous factor V 1691G>A mutation, the two TAFI polymorphisms investigated exerted no thrombogenic influence.

Topics: Age Factors; Antigens; Child; Child, Preschool; Factor V; Female; Fibrin; Histone Acetyltransferases; Humans; Infant; Leukemia; Lymphoma, Non-Hodgkin; Male; Neoplasms; Polymerase Chain Reaction; Polymorphism, Single Nucleotide; Reference Values; TATA-Binding Protein Associated Factors; Transcription Factor TFIID

Plasma-soluble fibrin monomer (SFM) level in patients with disseminated intravascular coagulation (DIC) was significantly higher than the level in patients with pre-DIC or in non-DIC patients, and the level in patients with pre-DIC was significantly higher than that in non-DIC patients. There was no significant difference in plasma SFM levels among various diseases underlying DIC. Plasma SFM level in patients with good outcome was significantly decreased after treatment for DIC. The sensitivity of fibrin degradation products and platelet number was high for DIC, but not for pre-DIC. The sensitivity of thrombin-antithrombin III complex, plasmin-plasmin inhibitor complex, and SFM was high for both DIC and pre-DIC. The specificity of these markers was also high. Receiver operating characteristic analysis suggests that plasma SFM level could be the most useful marker for the diagnosis of both DIC and pre-DIC.

Topics: Amino Acid Sequence; Animals; Antibodies, Monoclonal; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Enzyme-Linked Immunosorbent Assay; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Leukemia; Molecular Sequence Data; Neoplasms; Platelet Count; Prognosis; Retrospective Studies; Sensitivity and Specificity; Sepsis

Disseminated intravascular coagulation (DIC) is one of the most critical complications of malignant diseases. It is conventionally diagnosed by a decrease in platelets and an increase in fibrin/fibrinogen degradation products (FDP). Recently, an immunological assay was developed that can directly quantify the amount of soluble fibrin (SF) formed in the blood. This study examined this assay system in the diagnosis of DIC and found that it is a good indicator of both fibrin formation and of DIC. Plasma levels of SF correlated well with the DIC score, which is determined according to the 'DIC Scoring Guideline' proposed by the DIC Study Group under the Japanese Ministry of Public Welfare in 1988. It also correlated well with the serum levels of FDP. Normal values of plasma SF ranged between 0 and 9.50 micrograms/ml. Interestingly, values of SF in females tended to increase with age, for reasons that are not yet determined.

Topics: Adolescent; Adult; Aged; Antithrombin III; Child; Disseminated Intravascular Coagulation; Enzyme-Linked Immunosorbent Assay; Female; Fibrin; Humans; Leukemia; Lipids; Liver; Male; Middle Aged; Neoplasms; Peptide Fragments; Peptide Hydrolases; Prothrombin; Solubility

Fibrin crosslinking was assayed in 22 patients with acute leukemia showing secondary coagulation abnormalities of variable severity. In 9 patients fibrin crosslinking was found to be normal, whereas 10 patients presented impaired polymerization of alpha-chains and 3 of both alpha- and gamma-chains. Only a rough correlation was found between transamidating activity of factor XIII and the fibrin crosslinking pattern in these patients. Moreover, incomplete fibrin crosslinkage occurred at levels of factor XIII far in excess of that required for full polymerization of fibrin in "normal" plasma. This latter finding suggests that, in addition to factor XIII deficiency, other causes are responsible for the high rate of fibrin crosslinking impairment in acute leukemia.

Topics: Acute Disease; Factor XIII; Fibrin; Humans; In Vitro Techniques; Leukemia; Protein Conformation

A 31-year-old man presented with rapid onset of intractable congestive heart failure during the course of chemotherapy for eosinophilic leukemia. Patients with a hypereosinophilic syndrome usually die from complications of eosinophilic infiltration and fibrosis in target organs. The resulting cardiac lesions are a cause of death among these patients. Surgical intervention enabled our patient to survive the immediate medical crisis and has prolonged his life.

Topics: Adult; Endocardium; Eosinophils; Fibrin; Heart Failure; Humans; Leukemia; Male

Topics: Blood Coagulation; Blood Coagulation Disorders; Blood Transfusion; Calcium; Disseminated Intravascular Coagulation; Factor XIII; Factor XIII Deficiency; Female; Fibrin; Fibrinogen; Half-Life; Hemorrhage; Humans; Leukemia; Liver Diseases; Male; Plasma; Pregnancy; Thrombin; Time Factors

In 20 patients with acute leukemia the thrombin-mediated fibrin monomer complexes (SFMC) were determined before and after remission induction chemotherapy for several weeks to assess the extent of hypercoagulability. Increased levels of SFMC were observed in patients with high leukocyte cell counts after induction chemotherapy which may reflect the release of thromboplastic material from destructed leukemic cells. Patients with low leukocyte counts showed only a moderate increase in SFMC. A low concentration of antithrombin III (< 20 mg/100 ml) or a drop from a previously normal value was a prognostic unfavorable sign. An elevated level of plasmin-mediated fibrin-split-products could not be related to the course of therapy.

Topics: Acute Disease; Adolescent; Antineoplastic Agents; Antithrombin III; Blood Coagulation Disorders; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Leukemia; Leukocyte Count; Male; Middle Aged

Topics: Acute Disease; Antithrombins; Blood Cell Count; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Humans; Leukemia; Leukemia, Monocytic, Acute; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Liver Cirrhosis; Lymphatic Diseases; Platelet Adhesiveness; Prothrombin Time; Retinal Detachment; Thrombin; Thrombophlebitis

Topics: Blood Coagulation Tests; Carbon Radioisotopes; Carcinoma; Caseins; Disseminated Intravascular Coagulation; Electrophoresis; Esters; Factor XIII; Fibrin; Fibrinogen; Glycine; Hemagglutination Inhibition Tests; Humans; Leukemia; Sepsis; Serum Globulins; Solubility; Thrombocytopenia

Topics: Aged; Arthritis, Rheumatoid; Blood Cell Count; Blood Platelets; Carbon Radioisotopes; Collagen Diseases; Factor XIII; Female; Fibrin; Fibrinolysis; Heart Failure; Humans; Hypertension, Malignant; Infections; Leukemia; Liver Diseases; Neoplasms; Pulmonary Embolism; Sepsis; Streptokinase

Topics: Adult; Aged; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysis; Hodgkin Disease; Humans; Leukemia; Leukemia, Lymphoid; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Middle Aged; Multiple Myeloma; Myeloproliferative Disorders; Plasminogen; Trypsin Inhibitors

Topics: Acute Disease; Factor XIII; Fibrin; Humans; Leukemia

Topics: Cell Migration Inhibition; Fibrin; Heparin; Humans; In Vitro Techniques; Leukemia; Leukocytes

Topics: Abortion, Missed; Abruptio Placentae; Blood Coagulation Tests; Collagen Diseases; Erythrocytes; Esters; Female; Fibrin; Fibrinolysis; Fluorides; Hemagglutination Inhibition Tests; Humans; Kidney Diseases; Latex Fixation Tests; Leukemia; Ovarian Neoplasms; Pre-Eclampsia; Pregnancy; Pyruvates; Shock; Staphylococcus; Uterine Neoplasms

Topics: Acute Disease; Adenine Nucleotides; Adenosine Diphosphate; Adult; Aged; Blood Platelets; Collagen; Epinephrine; Female; Fibrin; Humans; Kaolin; Leukemia; Leukemia, Monocytic, Acute; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Lymphoma, Non-Hodgkin; Male; Middle Aged; Muramidase; Platelet Adhesiveness; Remission, Spontaneous; Thrombin

Topics: Abortion, Septic; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Ethanol; Female; Fibrin; Hematoma; Humans; Leukemia; Liver Cirrhosis; Methods; Neoplasms; Phlebitis; Postpartum Hemorrhage; Pregnancy; Pregnancy Complications, Hematologic; Sepsis

Topics: Agar; Electrophoresis; Enzyme Activation; Fibrin; Fibrinolysin; Glycoproteins; Humans; Immune Sera; Immunoelectrophoresis; Leukemia; Leukocytes; Peptide Hydrolases; Protease Inhibitors; Trypsin Inhibitors

Topics: Adolescent; Adult; Aged; Blood Coagulation Disorders; Child; Child, Preschool; Enzymes; Female; Fibrin; Fibrinolysin; Fibrinolysis; Humans; In Vitro Techniques; Infant; Leukemia; Male; Middle Aged

Topics: Blood Coagulation Disorders; Fibrin; Fibrinolysis; Heparin; Humans; Leukemia; Neoplasms; Thrombosis

Topics: Alpha-Globulins; Anemia; Biological Assay; Biomedical Research; Blood Coagulation; Blood Coagulation Factors; Calcium; Collagen Diseases; Cysteine; Factor XIII; Fibrin; Hemorrhagic Disorders; Humans; Leukemia; Liver; Liver Diseases; Lymphoma; Neoplasms; Pathology; Serum Globulins; Sulfhydryl Compounds; Thrombin

Topics: Blood Coagulation; Blood Coagulation Tests; Fibrin; Fibrinogen; Humans; Leukemia; Leukemia, Myeloid; Leukocyte Count; Leukocytes

Topics: Aging; Blood Coagulation Tests; Child; Enzymes; Erythroblastosis, Fetal; Fibrin; Humans; Infant; Infant, Newborn; Infant, Premature; Leukemia; Thrombocytopenia

Topics: Anemia; Anemia, Hypochromic; Biomedical Research; Blood Chemical Analysis; Collagen Diseases; Enzyme Inhibitors; Fibrin; Hemophilia A; Hepatitis; Hepatitis A; Jaundice; Jaundice, Obstructive; Leukemia; Liver Cirrhosis; Multiple Myeloma; Nephritis; Nephrotic Syndrome; Physiology; Purpura; Thrombin; Uremia

Topics: Child; Fibrin; Fibrinolysis; Humans; Infant; Leukemia

Topics: Blood Coagulation Tests; Factor IX; Fibrin; Fibrinolysis; Humans; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Medical Records

Topics: Afibrinogenemia; Fibrin; Fibrinogen; Fibrinolysis; Humans; Leukemia; Leukemia, Myeloid; Leukemia, Myeloid, Acute

Topics: Abdomen; Fibrin; Hemorrhage; Humans; Leukemia; Leukemia, Myeloid; Spleen; Splenomegaly

Topics: Fibrin; Fibrinolysis; Leukemia; Lymphoma; Neoplasms

Topics: Fibrin; Fibrinolysis; Hemorrhage; Humans; Leukemia; Leukemia, Myeloid; Syndrome