fibrinopeptide-b and Disseminated-Intravascular-Coagulation

Topics: Biomarkers; Blood Coagulation Tests; Cerebral Infarction; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Fibrinopeptide B; Humans; Immunoenzyme Techniques; Myocardial Infarction; Peptide Fragments; Pulmonary Embolism; Radioimmunoassay; Thrombophilia; Venous Thrombosis

The mutual relationships between malignant tumours and mechanisms of blood coagulation are presented in a brief survey. In this connection, the mechanisms of a tumour cell entering the circulation through the vessel well and its leaving into the tissues are discussed, the theory of microtrauma being used for explaining these processes. Subsequently, the alterations to be found in the count and function of thrombocytes after contact with a malignant cell and the impact on this cell by blood platelets are represented. As a third factor the activation of blood coagulation which is exercised by substances with a procoagulatory effect produced by the malignant tissue and the frequently observed thrombosis in the course of neoplastic diseases are dealt with in connection with blood level changes of some coagulation factors. In a fourth section the significance of fibrinolysis, its activation and inhibition as well as the production of fibrinolytic activators by neoplasms are discussed.

Topics: Animals; Blood Coagulation Factors; Blood Platelets; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Humans; Neoplasms; Neoplastic Cells, Circulating; Plasminogen Activators; Platelet Aggregation; Thromboembolism

Topics: Amino Acid Sequence; Cathepsin G; Cathepsins; Disseminated Intravascular Coagulation; Fibrin; Fibrinolysin; Fibrinolysis; Fibrinopeptide B; Humans; Neutrophils; Pancreatic Elastase; Plasminogen; Plasminogen Activators; Plasminogen Inactivators; Serine Endopeptidases

Topics: Chemical Phenomena; Chemistry; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Kidney Diseases; Kinetics; Methods; Pulmonary Embolism; Solubility; Thrombin; Thrombophlebitis

A variety of mechanisms may cause intravascular coagulation. Fibrinolysis is nearly always secondary to the initial clotting. In the acute form, ICF is characterized by depletion of platelets and several coagulation factors together with active fibrinolysis. There is a decrease in Factors V and VIII because they are sensitive to coagulation. The stable coagulation factors may be decreased as well because after activation they are removed from the circulation by the liver and reticuloendothelial system. Severe bleeding is the usual accompaniment of the acute syndrome, which may also occur in cancer and infection of all types. The acute syndrome may also occur in prolonged, extensive operations, after transfusion of incompatible blood, heat stroke, acute injury, certain snake bites, and with the administration of certain drugs. The chronic syndrome of intravascular coagulation is much more common and is associated with many diseases, including collagen diseases or immune diseases and malignancy. Many patients with chronic intravascular coagulation have normal or even increased levels of coagulation factors, and these patients have no unusual bleeding. The diagnosis depends on the demonstration of circulating complex of "soluble" fibrin revealed by the ethanol gel and protamine sulfate gelation tests. The secondary fibrinolysis results in elevation of FSP. Many laboratories are investigating the use of other procedures in the diagnosis of intravascular coagulation, including fibrinopeptides A and B, the VIII:C VIIIR:AG ratio, antithrombin III, PF 4, beta-thromboglobulin, D dimer, urinary FSP, and fibrinogen chromatography.

Topics: Animals; Antigens; Antithrombin III; Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Dogs; Factor VIII; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Humans; von Willebrand Factor

Topics: Animals; Antigen-Antibody Complex; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Chromatography, Gel; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Partial Thromboplastin Time; Peptide Hydrolases; Platelet Count; Prothrombin Time; Rabbits; Shwartzman Phenomenon; Thrombin; Thromboplastin

Topics: Adult; Disseminated Intravascular Coagulation; Epitopes; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Molecular Weight; Peptide Hydrolases; Pregnancy; Radioimmunoassay; Solubility; Thrombin

Fibrinogen plays a pivotal role in both the humoral and cellular mechanisms involved in hemostasis. In performing its hemostatic function, fibrinogen in turn is acted on by several independent enzyme systems that either modify its structure or cleave specific fragments of the molecule into the surrounding milieu. Measurements of enzymatically modified fibrinogen or its proteolysis products represent a means whereby the action of these specific enzymes can be quantitated both in vitro and in vivo. Advances in such techniques as protein purification, affinity chromatography, peptide synthesis, and radioimmunoassay technology permit the translation of recently acquired primary structural data on this important protein into sensitive and specific assays for its circulating derivatives. These assay systems are important tools for probing mechanisms of hemostasis and thrombosis.

Topics: Ancrod; Blood Coagulation Tests; Chemical Phenomena; Chemistry, Physical; Chromatography, Gel; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Kinetics; Leukocytes; Peptide Hydrolases; Pulmonary Embolism; Thrombin; Thrombophlebitis

Topics: Disseminated Intravascular Coagulation; Fibrinogen; Fibrinopeptide A; Fibrinopeptide B; Humans; Lupus Erythematosus, Systemic; Pulmonary Embolism; Radioimmunoassay; Thrombin; Thrombophlebitis

Disseminated intravascular coagulation (DIC) is usually diagnosed in sick infants who have prolonged clotting times, depletion of platelets and coagulation factors, and elevated levels of fibrin derivatives. However, the diagnostic accuracy of abnormal coagulation profiles in neonates at risk of DIC has been uncertain. Since DIC is characterized by activation of both the coagulation and fibrinolytic systems, the objective of this study was to determine whether coagulation screening tests correctly identify infants with biochemical evidence of increased thrombin and plasmin generation.. Non-surgical patients in a tertiary care nursery who were sick enough to require an indwelling arterial catheter for monitoring purposes, were enrolled in a prospective cohort study. Blood samples for thrombin/antithrombin III (TAT) complexes and the plasmin-derived fibrinopeptide B beta 1-42 were drawn 36 to 72 h after birth from a free-flowing arterial line. Platelet counts, D-Dimer levels, plasma fibrinogen concentrations and prothrombin times, expressed as International Normalized Ratios or INR, were measured at the same time.. One hundred patients were studied. Fifty-seven infants had elevated levels of TAT (> or = 4 micrograms/l) and B beta 1-42 (> or = 4 nmol/l). The sensitivities of platelets < 150 x 10(9)/l, D-Dimer > 500 ng/ml, fibrinogen < 1.5 g/l, and INR > 1.5 were 39%, 30%, 12%, and 11%, respectively. Corresponding specificities were 88%, 91%, 98%, and 95%.. Abnormal coagulation screens in sick newborn infants strongly support a diagnosis of DIC. However, normal screens do not exclude activation of the coagulation and fibrinolytic systems.

Topics: Antithrombin III; Blood Coagulation Tests; Cohort Studies; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Fibrinopeptide B; Humans; Infant, Newborn; Infant, Newborn, Diseases; Intensive Care, Neonatal; Neonatal Screening; Peptide Hydrolases; Platelet Count; Predictive Value of Tests; Prospective Studies; Prothrombin Time; Thrombin; Treatment Outcome

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

Topics: Adult; Antifibrinolytic Agents; Antigen-Antibody Complex; Antigens; Antithrombin III; Biomarkers; Blood Coagulation Disorders; Case-Control Studies; Craniocerebral Trauma; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Glasgow Coma Scale; Hospitals, General; Humans; Injury Severity Score; Japan; Male; Middle Aged; Multiple Trauma; Partial Thromboplastin Time; Platelet Count; Predictive Value of Tests; Prothrombin Time; Tissue Plasminogen Activator

We measured FPB beta 15-42, and alpha 2 plasmin inhibitor-plasmin-complex (PAC), which are direct indexes of plasmin activity, as well as D-dimer in 204 samples from patients with subarachnoid hemorrhage, trauma, and the patients during cardiopulmonary bypass. In all patients, these molecular markers increased due to secondary fibrinolysis; these increases were significantly higher in DIC patients. There were positive correlations among the molecular markers. The correlation coefficient for FPB beta 15-42 and D-dimer was significantly higher than that for PAC and D-dimer in the DIC patients. In conclusion, it might be better to measure both FPB beta 15-42 and PAC as indexes of plasmin activity in DIC patients, because of the significant difference between the correlation coefficient for PAC and D-dimer, and that for FPB beta 15-42 and D-dimer.

Topics: Adult; alpha-2-Antiplasmin; Antifibrinolytic Agents; Biomarkers; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Fibrinopeptide B; Humans; Male; Middle Aged; Peptide Fragments

We studied blood coagulation and fibrinolysis in 18 DIC patients with multiple organ failure. Blood was collected three times (1st, 3rd, 6th hospital days) from an indwelling arterial line, and FPA, FPB beta 15-42, alpha 2PI-P1-C, D-dimer, t-PA; Ag, and t-PA activity were measured. 1) Continuous FOY infusion (1.40 +/- 0.07 mg/kg/H) resulted in a statistically significant fall of FPA levels, which however, was still above normal. The FPA levels of the patients whose DIC score was not improved or who had massive hematomas were statistically higher than the patients whose DIC score was improved or without hematomas. 2) FPB beta 15-42, alpha 2PI-Pl-C, and D-dimer remained at consistently high levels following onset of the DIC. A significant positive correlations were seen between these indices; between the FPA and FPB beta 15-42, alpha 2PI-Pl-C. 3) The levels of alpha 2PI-Pl-C were found to be higher in the patients with hematomas than those without hematomas. 4) T-PA; Ag level remained at consistently high during all hospital day. On the other hand, t-PA activity level did not change significantly. There was dissociation between the t-PA; Ag and the t-PA activity. 5) The patients whose DIC score were not improved on the 6th hospital day had higher levels of t-PA; Ag than the patients whose DIC score were improved, but there were no differences in the number of the ischemic organs between these patients. In conclusion, regardless of the continuous FOY infusion some patients revealed the continuous production of thrombin.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; alpha-2-Antiplasmin; Antifibrinolytic Agents; Biomarkers; Disseminated Intravascular Coagulation; Female; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Male; Middle Aged; Multiple Organ Failure; Prognosis; Tissue Plasminogen Activator

Hematological and coagulating parameters were examined in 53 patients in an attempt to find possible evidence of disseminated intravascular coagulation after intravascular injection of 5% ethanolamine oleate to sclerose esophageal varices. FDP-E in the peripheral blood measured by latex photometric immunoassay significantly increased from 111.2 +/- 112.9 to 234.2 +/- 178.3 ng/ml and 370.4 +/- 189.5 ng/ml one hour after the first and second sessions of sclerotherapy, respectively (p less than 0.01). The other parameters showed no significant change, except on the first day after sclerotherapy. The increase of FDP-E was closely related to fibrinopeptide A (r = 0.689, p less than 0.01) and fibrinogen (r = 0.585, p less than 0.05), before the sclerotherapy. As repeated intravariceal sclerotherapy over short time intervals can lead to a deterioration of the coagulating system, especially in patients with abnormal preoperative coagulopathy, latex photometric immunoassay for FDP-E is a rapid and useful method of monitoring alterations in the coagulating system.

Topics: Adult; Aged; Blood Coagulation; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Esophageal and Gastric Varices; Female; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Fibrinopeptide B; Humans; Male; Middle Aged; Oleic Acids; Sclerosing Solutions

Topics: Amino Acid Sequence; Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Fibrinopeptide B; Humans; Immunoassay; Molecular Sequence Data; Peptide Fragments; Reference Values; Thrombosis

Topics: Disseminated Intravascular Coagulation; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide B; Humans; Immunoenzyme Techniques

Topics: Adult; Aged; Blood Coagulation; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Gabexate; Guanidines; Humans; Male; Middle Aged; Peptide Fragments

Fibrinopeptide levels were measured in 20 women during transcervical chorionic villus sampling (CVS). Fibrinopeptide A, a sensitive indicator of fibrinogen cleavage by thrombin, significantly increased in five subjects, whereas there was no change in B beta peptide, an indicator of fibrinolysis. The data suggest that modest fibrin formation, uncompensated by fibrinolysis, may be induced in some women by CVS.

Topics: Adult; Biopsy; Chorionic Villi; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Fibrinopeptide B; Humans; Maternal-Fetal Exchange; Peptide Fragments; Pregnancy; Prenatal Diagnosis; Risk Factors

Topics: Acute Disease; Aged; Blood Coagulation; Brain Injuries; Cerebral Hemorrhage; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Humans; Hypertension; Male; Middle Aged; Peptide Fragments

Topics: alpha-2-Antiplasmin; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Factor XIII; Fibrin Fibrinogen Degradation Products; Fibrinolytic Agents; Fibrinopeptide A; Fibrinopeptide B; Humans; Immunoelectrophoresis

Topics: Blood Platelets; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysin; Fibrinopeptide A; Fibrinopeptide B; Humans; Thrombin

Topics: Disseminated Intravascular Coagulation; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Fibrinopeptide B; Hemorrhage; Humans; Models, Chemical; Molecular Weight; Thrombosis

The immunochemical specificity of rabbit antisera to human fibrinopeptide-B (FPB) has been studied by comparing the relative abilities of FPB and of various proteins and peptides containing the NH2-terminal segment of the B beta-chain of human fibrinogen to inhibit the binding of a radioiodinated FPB derivative by each of seven anti-FPB sera. Anti-FBP sera varied in the extent to which they cross-reacted with fibrinogen, the NH2-terminal disulfide knot of fibrinogen (N-DSK), B beta 1(Pyr)-118(Met), B beta 1(Pyr)-42(Arg), and desarginyl-FPB. Anti-FPB sera have been identified that discriminate effectively between FPB and larger FBP-containing peptides; such antisera can be used to measure FPB in the absence of the larger peptides or to demonstrate the presence of larger peptides such as B beta 1(Pyr)-42(Arg) in extracts of clinical plasma samples by means of an increase in FPB immunoreactivity following thrombin treatment. One anti-FPB serum has been identified that is capable of detecting desarginyl-FPB, and this antiserum has been used in the development of a radioimmunoassay for desarginyl-FPB. Thus, by precisely defining the specificity of anti-FPB sera, it has been possible to identify antisera that are useful, not only in the measurement of FPB, but also in the detection of other important related molecules, such as B beta 1(Pyr)-42(Arg) and desarginyl-FPB. The immunochemical detection of these FPB-related peptides should provide useful information concerning the action of proteolytic enzymes, such as plasmin on the NH2-terminal segment of the B beta-chain of fibrinogen, and of carboxypeptidase-B on free FPB, in human plasma.

Topics: Cross Reactions; Disseminated Intravascular Coagulation; Epitopes; Fibrinogen; Fibrinopeptide B; Humans; Immune Sera; Radioimmunoassay

Topics: Animals; Anticoagulants; Disseminated Intravascular Coagulation; Dogs; Epitopes; Fibrinogen; Fibrinopeptide A; Fibrinopeptide B; Heparin; Humans; Radioimmunoassay; Thrombin; Thromboembolism; Thrombosis