thromboplastin and Afibrinogenemia

Inherited thrombophilia can be defined as a genetically determined predisposition to the development of thromboembolic complications. Since the discovery of activated protein C resistance in 1993, several additional disorders have been described and, at present, it is possible to identify an inherited predisposition in about 60 to 70% of patients with such complications. These inherited prothrombotic risk factors include qualitative or quantitative defects of coagulation factor inhibitors, increased levels or function of coagulation factors, defects of the fibrinolytic system, altered platelet function, and hyperhomocysteinemia. In this review, the main inherited prothrombotic risk factors are analyzed from epidemiological, laboratory, clinical, and therapeutic points of view. Finally, we discuss the synergism between genetic and acquired prothrombotic risk factors in particular conditions such as childhood and pregnancy.

Topics: Afibrinogenemia; Blood Coagulation Factor Inhibitors; Blood Coagulation Factors; Child, Preschool; Coagulation Protein Disorders; Female; Fibrinolysis; Genetic Predisposition to Disease; Heparin Cofactor II; Humans; Male; Pregnancy; Risk Factors; Thrombophilia; Thromboplastin

For many years, the laboratory investigation of patients with thrombophilia has lagged behind that of patients with bleeding diathesis. Improved understanding of the mechanisms that control and regulate coagulation, and the resultant recognition of new defects, have greatly stimulated clinical laboratory interest in this area. Assays to detect resistance to activated protein C; deficiencies of antithrombin, protein C, and protein S; and the presence of antiphospholipid antibodies are widely available and should form part of the investigation of patients that present with idiopathic thrombosis. Such a work-up will likely provide an explanation for thrombosis in 40 to 60% of patients. Abnormalities of fibrinogen and fibrinolysis may explain still more, although such defects are currently considered rare. In addition, presently unrecognized defects almost certainly exist, and the identification of such individuals will undoubtedly improve our understanding of the hemostatic mechanism. Laboratory tests to define the hypercoagulable state are continually being developed. They include whole blood coagulation and platelet function tests and novel activation markers. However, acceptance of these approaches by clinical laboratories has been slow.

Topics: Afibrinogenemia; Antiphospholipid Syndrome; Antithrombins; Blood Coagulation Tests; Factor V; Fibrinolysis; Homocysteine; Humans; Lipoproteins; Lupus Coagulation Inhibitor; Monocytes; Platelet Activation; Protein C; Protein S; Protein S Deficiency; Prothrombin; Thrombomodulin; Thrombophilia; Thromboplastin

Topics: Afibrinogenemia; Blood Coagulation; Blood Coagulation Tests; Diagnosis, Differential; Disseminated Intravascular Coagulation; Fibrinolysis; Hemostasis; Humans; Models, Biological; Syndrome; Thromboplastin; Toxemia

Topics: Afibrinogenemia; Anti-Infective Agents; Antigens; Blood Coagulation Disorders; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemagglutination Inhibition Tests; Heparin; Humans; Prothrombin Time; Radioimmunoassay; Thrombin; Thrombocytopenia; Thromboplastin

Topics: Abortion, Induced; Abruptio Placentae; Afibrinogenemia; Amniotic Fluid; Anticoagulants; Blood Coagulation Disorders; Embolism; Embolism, Amniotic Fluid; Female; Fetal Death; Fibrinolysis; History; Humans; Obstetrics; Postpartum Hemorrhage; Postpartum Period; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Thromboplastin

Conventional clotting tests are not expeditious enough to allow timely targeted interventions in trauma, and current point-of-care analyzers, such as rotational thromboelastometry (ROTEM), have limited sensitivity for hyperfibrinolysis and hypofibrinogenemia.. To evaluate the performance of a recently developed global fibrinolysis capacity (GFC) assay in identifying fibrinolysis and hypofibrinogenemia in trauma patients.. Exploratory analysis of a prospective cohort of adult trauma patients admitted to a single UK major trauma center and of commercially available healthy donor samples was performed. Lysis time (LT) was measured in plasma according to the GFC manufacturer's protocol, and a novel fibrinogen-related parameter (percentage reduction in GFC optical density from baseline at 1 minute) was derived from the GFC curve. Hyperfibrinolysis was defined as a tissue factor-activated ROTEM maximum lysis of >15% or LT of ≤30 minutes.. Compared to healthy donors (n = 19), non-tranexamic acid-treated trauma patients (n = 82) showed shortened LT, indicative of hyperfibrinolysis (29 minutes [16-35] vs 43 minutes [40-47]; p < .001). Of the 63 patients without overt ROTEM-hyperfibrinolysis, 31 (49%) had LT of ≤30 minutes, with 26% (8 of 31) of them requiring major transfusions. LT showed increased accuracy compared to maximum lysis in predicting 28-day mortality (area under the receiver operating characteristic curve, 0.96 [0.92-1.00] vs 0.65 [0.49-0.81]; p = .001). Percentage reduction in GFC optical density from baseline at 1 minute showed comparable specificity (76% vs 79%) to ROTEM clot amplitude at 5 minutes from tissue factor-activated ROTEM with cytochalasin D in detecting hypofibrinogenemia but correctly reclassified >50% of the patients with false negative results, leading to higher sensitivity (90% vs 77%).. Severe trauma patients are characterized by a hyperfibrinolytic profile upon admission to the emergency department. The GFC assay is more sensitive than ROTEM in capturing hyperfibrinolysis and hypofibrinogenemia but requires further development and automation.

Topics: Adult; Afibrinogenemia; Blood Coagulation Disorders; Fibrinolysis; Humans; Prospective Studies; Thrombelastography; Thromboplastin; Wounds and Injuries

Fibrinogen depletion via catalysis by snake venom enzymes as a therapeutic strategy to prevent or treat thrombotic disorders was utilized for over four decades, with ancrod being the quintessential agent. However, ancrod eventually was found to not be of clinical utility in large scale stroke trial, resulting in the eventual discontinuation of the administration of the drug for any indication. It was hypothesized that ancrod, possessing thrombin-like activity, may have unappreciated robust coagulation kinetics. Using thrombelastographic methods, a comparison of equivalent tissue factor initiated thrombin generation and Calloselasma rhodostoma venom (rich in ancrod activity) on plasmatic coagulation kinetics was performed. The venom resulted in thrombi that formed nearly twice as fast compared to thrombin formed clots, and there was no difference in fibrinolytic kinetics initiated by tissue-type plasminogen activator. In plasma containing iron and carbon monoxide modified fibrinogen, which may be found in patients at risk of stroke, the coagulation kinetic differences observed with venom was still more vigorous than that seen with thrombin. These phenomena may provide insight into the clinical failure of ancrod, and may serve as an impetus to revisit the concept of fibrinogen depletion via fibrinogenolytic enzymes, not those with thrombin-like activity.

Topics: Afibrinogenemia; Ancrod; Animals; Blood Coagulation; Crotalid Venoms; Fibrinogen; Fibrinolysis; Humans; Kinetics; Thrombelastography; Thrombin; Thromboplastin

Normal haemostasis is maintained by a controlled balance between coagulation and fibrinolysis, involving thrombin and plasmin the respective key enzymes. Simultaneous evaluation of both enzymes facilitates, therefore, an overall understanding of normal and pathological haemostasis. Combined thrombin and plasmin generation (T/P-G) assays have been recently described, and we have adapted the technique to investigate the interplay between coagulation and fibrinolysis in patients with various haemostatic disorders. Our modified T/P-G was initiated by the addition of a mixture of optimised lower concentrations of tissue factor and tissue-type plasminogen activator. Thrombin generation (TG) and plasmin generation (PG) were monitored simultaneously using individual fluorescent substrates in separate microtitre wells. The relationship between coagulation and fibrinolysis was demonstrated by analysing the effects of thrombin inhibitors, activated protein C and thrombomodulin. The most evident impairments in TG were observed with plasma samples deficient of coagulation factors participating in the prothrombinase complex. Defects in PG were observed with deficiencies of factor (F)V, FX, fibrinogen, and plasminogen. TG appeared to be a prerequisite for the initiation of PG, and overall PG was governed by fibrinogen concentration. TG in patients with haemophilia A correlated with levels of FVIII activity, but there was no significant relationship between PG and FVIII:C, confirming that the abnormal haemostasis in haemophilia A results in a severe imbalance between coagulation and fibrinolysis. The findings demonstrate that global haemostasis depends on a sensitive balance between coagulation and fibrinolysis, and that the modified T/P-G assay could provide an enhanced understanding of haemorrhage and thrombosis in clinical practice.

Topics: Afibrinogenemia; Blood Coagulation; Blood Coagulation Tests; Conjunctivitis; Factor V Deficiency; Factor X Deficiency; Feedback, Physiological; Fibrinolysin; Fibrinolysis; Hemophilia A; Hemostasis; Humans; Plasminogen; Protein C Inhibitor; Skin Diseases, Genetic; Thrombin; Thrombomodulin; Thromboplastin; Tissue Plasminogen Activator

The relationship between platelet and leukocyte activation, coagulation, and neointima development was investigated in noninjured murine blood vessels subjected to blood stasis. The left common carotid artery of C57BL/6J mice was ligated proximal to the bifurcation. Tissue-factor expression in luminal leukocytes progressively increased over 2 weeks. On day 3 after ligation, in addition to infiltrated granulocytes, platelet microthrombi and platelet-covered leukocytes as well as tissue-factor-positive fibrin deposits lined the endothelium. Maximal neointima formation in carotid artery cross sections of control mice equaled 28+/-3.7% (n=11) and 42+/-5.1% (n=8) of the internal elastic lamina cross-sectional area 1 and 2 weeks after ligation. In FVIII(-/-) mice, stenosis was significantly lower 1 (11+/-3.6%, n=8) and 2 (21+/-4.7%, n=7) weeks after ligation (both P:<0.01 versus background-matched controls). In u-PA(-/-) mice, luminal stenosis was significantly higher 1 (38+/-7.0%, n=7) and 2 (77+/-5.6%, n=6) weeks after ligation (P:<0.05 and P:<0.01, respectively, versus matched controls). In alpha(2)-AP(-/-) mice, stenosis was lower at 1 week (14+/-2.6%, n=7, P:<0.01) but not at 2 weeks. Responses in tissue-type plasminogen activator or plasminogen activator inhibitor-1 gene-deficient mice equaled that in controls. Reducing plasma fibrinogen levels in controls with ancrod or inducing partial thrombocytopenia with busulfan resulted in significantly less neointima, but inflammation was inhibited only in busulfan-treated mice. We conclude that stasis induces platelet activation, leading to microthrombosis and platelet-leukocyte conjugate formation, triggering inflammation and tissue-factor accumulation on the carotid artery endothelium. Delayed coagulation then results in formation of a fibrin matrix, which is used by smooth muscle cells to migrate into the lumen.

Topics: Afibrinogenemia; Animals; Blood Coagulation; Blood Platelets; Carotid Arteries; Cell Division; Disease Models, Animal; Endothelium, Vascular; Fibrin; Hemostatic Disorders; Inflammation; Leukocytes; Ligation; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Smooth, Vascular; Platelet Activation; Thrombocytopenia; Thromboplastin; Thrombosis; Tunica Intima

The purpose of the present study was to compare the results obtained with a human recombinant thromboplastin (Innovin, Baxter) (IN) and a high-sensitivity rabbit brain reagent (Thromboplastin IS, Baxter) (IS), on the performance of prothrombin time (PT) test and the functional assay of factors included in the extrinsic coagulation system, in order to establish possible differences on imprecision, diagnostic accuracy and sensitivity to the oral anticoagulant defect, between the two products.. Six Spanish hospital took part in the study. Plasma samples from 221 healthy subjects, 100 patients with severe liver disease, 27 with dysfibrinogenaemia, 10 with lupus anticoagulant and from 13 individuals propositus and their relatives with congenital deficiencies of the extrinsic coagulation pathway, and their relatives were studied; 188 patients stabilized on oral anticoagulant therapy and 82 on heparin therapy were also included. The in vitro effect of heparin was tested by addition of increasing amounts of heparin (0.3 to 10.0 IU/mL) to aliquots of normal plasma.. Both in the intra-assay and in the inter-assay imprecision study, a better coefficient of variation was obtained with IN when the PT was performed on abnormal samples. Prothrombin time ratio from patients with liver disease had significantly higher values with IS. On the contrary, IN had a higher sensitivity in samples from patients with dysfibrinogenaemia or from those stabilized on oral anticoagulant therapy. In showed a very low sensitivity to heparin at concentrations corresponding to the therapeutic range.. The results of this field study indicate that IN, compared with a high-sensitivity rabbit brain thromboplastin, is a suitable reagent for PT determination in normal subjects, patients with liver disease or with congenital deficiencies of clotting factors. It shows a higher sensitivity in cases of dysfibrinogenaemia and in patients on oral anticoagulant therapy. In addition, the recombinant reagent had better reproducibility when the PT was performed on abnormal samples, and it was hardly affected by heparin within the therapeutic range.

Topics: Afibrinogenemia; Animals; Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Factors; Heparin; Humans; Indicators and Reagents; Liver Diseases; Lupus Coagulation Inhibitor; Phospholipids; Prothrombin Time; Rabbits; Recombinant Fusion Proteins; Reproducibility of Results; Sensitivity and Specificity; Thromboplastin

A case is described of acute defibrination following blunt head injury in a patient with a Spitz-Holter drain. The cause of the disseminated intravascular coagulation is thought to be due to brain thromboplastins entering the systemic circulation through the Spitz-Holter drain, thus bypassing the blood-brain barrier.

Topics: Accidents, Traffic; Adolescent; Afibrinogenemia; Brain Injuries; Cerebrospinal Fluid Shunts; Disseminated Intravascular Coagulation; Female; Humans; Thromboplastin; Wounds, Nonpenetrating

Topics: Afibrinogenemia; Blood Coagulation Disorders; Blood Coagulation Tests; Factor V Deficiency; Factor VII Deficiency; Factor X Deficiency; Factor XI Deficiency; Factor XII Deficiency; Factor XIII Deficiency; Hemophilia A; Hemophilia B; Humans; Hypoprothrombinemias; Kaolin; Phosphatidylethanolamines; Prekallikrein; Prothrombin Time; Thrombin; Thromboplastin; von Willebrand Diseases

When 125I-labeled canine prothrombin was given to normal adult dogs intravenously, it was calculated that 240% of the plasma prothrombin crossed the capillary barrier per day, 410% of the interstitial prothrombin returned to the blood stream daily, and 79% of the plasmatic prothrombin was catabolized per day. These data are in close agreement with those observed for bovine prothrombin in calves by Takeda (1970). When derived from normal dog prothrombin, prethrombin-1 is a mixture of 2 polypeptides, one larger than the other, and both present in about equal amounts. The longer peptide, "prethrombin-1-long," was catabolized twice as fast as prothrombin, and the shorter, "prethrombin-1-short," 4 times faster. Prothrombin fragment-1 was catabolized by the normal dog still more rapidly. The catabolism of prothrombin was not accelerated in 3 dogs receiving continuous infusions of a thromboplastic emulsion of dog brain. Nor was the level of prothrombin in their plasma remarkably altered.

Topics: Afibrinogenemia; Animals; Chromatography, Gel; Disseminated Intravascular Coagulation; Dogs; Iodine Radioisotopes; Kinetics; Prothrombin; Thrombocytopenia; Thromboplastin; Trichloroacetic Acid

Auto-Fi Dade has been used for thromboplastin time, activated partial thromboplastin time, fibrinogen determination and a few determinations of factors V, VII + X, II and VIII. The results of the thromboplastin time, using Dade Tromboplastin or thromboplastins from two other commerical firms, show a coefficient of variation (CV) ranging from 1.11 to 3.43% for short times and 1.97 to 2.64% for longer times.

Topics: Afibrinogenemia; Autoanalysis; Blood Coagulation Tests; Factor VIII; Fibrinogen; Humans; Phosphatidylethanolamines; Thromboplastin

A new case of facultative hemorrhagic diathesis is described in a 19 year old female and the coagulatory anomaly examined. The experiments show that the coagulatory disturbance should be ascribed to a defective aggregation of fibrin monomers associated with hypofibrinogenemia. Some of its characteristics are the markedly prolonged thrombin-, reptilase-time as well prolonged prothrombin and partial thromboplastin time. The plasma fibrinogen concentration measured by the immunologic method is reduced. The streptokinase induced digestion of fibrinogen Giessen II plasma occurred at a slower rate than normal plasma with persistence of the large fibrinogen degradation products. Fibrinogen Giessen II appears to be a congenital hypodysfibrinogenemia with abnormality of fibrinogen resulting in delayed coagulation and a retarded fibrinogenolysis rate.

Topics: Adult; Afibrinogenemia; Batroxobin; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Streptokinase; Thrombin; Thromboplastin

When mice are injected intravenously with a large dose of vaccinia virus, prepared in the Ehrlich ascites carcinoma of the mouse, there is a precipitous loss of plasma fibrinogen and blood platelets. Death occurs usually within 24 hours. A specific role of the virus in this toxic syndrome can be demonstrated when heparin is employed to circumvent intravascular coagulation and fibrinogen loss. Heparin does not prevent a profound thrombocytopenia from occurring, but it modifies the rate of platelet loss. Toxicity is prevented when heparinized virus preparations are pretreated with beta-propiolactone or specific antibody, although a mild thrombocytopenia occurs. Thrombocytopenia does not occur in mice injected with heparinized material prepared from uninfected tumors. These studies indicate that the basic mechanism of vaccinia virus toxicity is an early interaction between infectious virus and blood platelets, with marked thrombocytopenia and consequential pathophysiologic changes.

Topics: Afibrinogenemia; Animals; Antibodies, Viral; Antiviral Agents; Ascitic Fluid; Blood Platelets; Erythrocyte Aggregation; Fibrinogen; Heparin; Lung; Mice; Propiolactone; Rabbits; Thrombocytopenia; Thromboplastin; Thrombosis; Trypsin Inhibitor, Bowman-Birk Soybean; Vaccinia virus

Topics: Adult; Afibrinogenemia; Animals; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Cattle; Citrates; Collagen; Crystallization; Dogs; Edetic Acid; Factor VII Deficiency; Factor X Deficiency; Factor XII; Female; Fibrinogen; Hemophilia A; Hemostasis; Heparin; Humans; Male; Platelet Adhesiveness; Platelet Aggregation; Purpura, Thrombocytopenic; Thrombin; Thromboplastin; von Willebrand Diseases

Topics: Afibrinogenemia; Aneurysm; Bacteria; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Diagnosis, Differential; Disseminated Intravascular Coagulation; Enzyme Activation; Fibrin; Fibrinogen; Fibrinolysis; Hemostasis; Heparin; Models, Biological; Prothrombin; Sepsis; Shwartzman Phenomenon; Thrombin; Thromboplastin

Topics: Adolescent; Adult; Afibrinogenemia; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Child; Child, Preschool; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Female; Fibrinogen; Humans; Infant; Liver; Liver Diseases; Male; Middle Aged; Prothrombin; Prothrombin Time; Serum Globulins; Solubility; Thromboplastin

Topics: Adult; Afibrinogenemia; Blood Coagulation Factors; Blood Coagulation Tests; Female; Fibrinogen; Humans; Immunodiffusion; Immunoelectrophoresis; Pedigree; Phosphatidylethanolamines; Plasminogen; Platelet Adhesiveness; Prothrombin Time; Thrombelastography; Thromboplastin

Topics: Adenosine Diphosphate; Afibrinogenemia; Anti-Inflammatory Agents; Aspirin; Blood Platelets; Citrates; Densitometry; Dose-Response Relationship, Drug; Drug Stability; Drug Storage; Epinephrine; Factor V Deficiency; Factor VII Deficiency; Factor XIII Deficiency; Fatty Acids, Nonesterified; Heparin; Humans; Platelet Adhesiveness; Serum Albumin; Temperature; Thromboplastin; Time Factors

Topics: Adult; Afibrinogenemia; Blood Cell Count; Blood Coagulation Tests; Fibrinolysis; Hemorrhage; Humans; Leukemia, Myeloid, Acute; Male; Prothrombin Time; Thromboplastin

Topics: Afibrinogenemia; Aged; Blood Coagulation Tests; Blood Platelets; Blood Protein Disorders; Factor VIII; Female; Fibrin; Hemorrhagic Disorders; Humans; Immunoglobulin G; Japan; Male; Middle Aged; Multiple Myeloma; Thromboplastin; Waldenstrom Macroglobulinemia

Topics: Afibrinogenemia; Amniotic Fluid; Animals; Antifibrinolytic Agents; Brain Chemistry; Disseminated Intravascular Coagulation; Female; Heparin; Humans; Lethal Dose 50; Placenta; Placental Extracts; Pregnancy; Protease Inhibitors; Rats; Thromboplastin

Topics: Afibrinogenemia; Amniotic Fluid; Animals; Aprotinin; Blood Coagulation; Calcium; Caseins; Female; Fibrin; Fibrinogen; Humans; Peptide Hydrolases; Pregnancy; Pregnancy Complications, Hematologic; Prothrombin; Rabbits; Thromboplastin

Topics: Abruptio Placentae; Afibrinogenemia; Blood Coagulation Disorders; Embolism, Amniotic Fluid; Female; Humans; Obstetric Labor Complications; Postpartum Hemorrhage; Pregnancy; Pregnancy Complications; Shock; Thromboplastin; Tissue Extracts

Topics: Afibrinogenemia; Animals; Aprotinin; Blood Coagulation; Blood Coagulation Factors; Cyclohexanecarboxylic Acids; Female; Fibrinolysis; Guinea Pigs; Hemostasis; Humans; Pregnancy; Pregnancy Complications, Hematologic; Thromboplastin

Topics: Abruptio Placentae; Adult; Afibrinogenemia; Blood Coagulation Tests; Blood Transfusion; Female; Fibrinogen; Humans; Infant, Newborn; Pregnancy; Thromboplastin

Topics: Abortion, Spontaneous; Adult; Afibrinogenemia; Blood Coagulation Tests; Female; Fetal Death; Fibrinogen; Heparin; Humans; Pregnancy; Thromboplastin

Topics: Afibrinogenemia; Amniotic Fluid; Animals; Embolism; Female; Fibrinolysis; Haplorhini; Meconium; Pregnancy; Pregnancy, Animal; Thromboplastin

Topics: Afibrinogenemia; Blood Coagulation; Blood Coagulation Factors; Blood Platelets; Blood Vessels; Calcium; Female; Hemorrhagic Disorders; Hemostasis; Humans; Postoperative Complications; Pregnancy; Pregnancy Complications, Hematologic; Serotonin; Thromboplastin

Topics: Afibrinogenemia; Animals; Blood Coagulation Disorders; Blood Coagulation Factors; Caseins; Fibrinolysis; Humans; Peptide Hydrolases; Streptokinase; Thrombin; Thromboplastin

Topics: Afibrinogenemia; Ammonium Compounds; Animals; Anti-Infective Agents, Local; Blood Coagulation Disorders; Deoxyribonuclease I; Disseminated Intravascular Coagulation; Dogs; Fibrinolysis; Liver Circulation; Pathology; Pulmonary Circulation; Quaternary Ammonium Compounds; Research; Shock; Shock, Hemorrhagic; Streptodornase and Streptokinase; Streptokinase; Thrombin; Thromboplastin

Topics: Abruptio Placentae; Afibrinogenemia; Aminocaproates; Aminocaproic Acid; Blood Coagulation Tests; Blood Transfusion; Calcium; Dexamethasone; Drug Therapy; Female; Fetal Death; Fibrinogen; Fibrinolysin; Hemorrhagic Disorders; Humans; Pregnancy; Pregnancy Complications, Hematologic; Thrombin; Thromboplastin; Tolonium Chloride; Uterine Hemorrhage

Topics: Abruptio Placentae; Afibrinogenemia; Blood Coagulation Tests; Blood Platelets; Female; Fibrinolysis; Hematocrit; Pharmacology; Placenta; Pregnancy; Rabbits; Research; Thromboplastin

Topics: Afibrinogenemia; Amniotic Fluid; Blood Coagulation Disorders; Embolism; Embolism, Amniotic Fluid; Female; Humans; Hyaluronoglucosaminidase; Pregnancy; Thrombocytopenia; Thromboplastin

Topics: Afibrinogenemia; Anticoagulants; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Calcium; Factor IX; Factor V; Factor VII; Factor VIII; Factor X; Female; Fibrinogen; Fibrinolysis; Hemophilia B; Humans; Hypoprothrombinemias; Physiology; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Prothrombin; Thromboplastin

Topics: Abruptio Placentae; Afibrinogenemia; Blood Coagulation; Female; Fetal Blood; Humans; Placenta; Pregnancy; Thromboplastin; Umbilical Cord

Topics: Afibrinogenemia; Female; Fibrin; Hemorrhage; Humans; Postpartum Hemorrhage; Postpartum Period; Pregnancy; Pregnancy Complications; Thromboplastin

Topics: Afibrinogenemia; Amniotic Fluid; Factor Xa; Female; Fibrinogen; Hemorrhage; Hemorrhagic Disorders; Humans; Labor, Obstetric; Pregnancy; Thromboplastin; Work