thromboplastin and Hematoma

Coagulation factor (F) V deficiency is associated with a bleeding tendency of variable severity, but phenotype determinants are largely unknown. Recently, we have shown that three patients with undetectable plasma FV and mild bleeding symptoms had sufficient residual platelet FV to support thrombin generation in platelet-rich plasma (PRP). Therefore, we hypothesized that FV-deficient patients with severe bleeding manifestations may lack platelet FV.. To characterize a FV-deficient patient with a severe bleeding diathesis.. We performed FV mutation screening and functional studies in a 31-year-old male (FV:C < 1%) with umbilical bleeding at birth, recurrent hemarthrosis and muscle hematomas, and a recent intracranial hemorrhage.. The proband was homozygous for a deep-intronic mutation (F5 IVS8 +268A→G) causing the inclusion of a pseudo-exon with an in-frame stop codon in the mature F5 mRNA. Although platelet FV antigen was detectable by immunoprecipitation followed by Western blotting, no FV activity could be demonstrated in the proband's plasma or platelets with a prothrombinase-based assay. Moreover, no thrombin generation was observed in PRP triggered with 1-50 pm tissue factor (even in the presence of platelet agonists), whereas an acquired FV inhibitor was excluded. Clot formation in the proband's whole blood, as assessed by thromboelastometry, was markedly delayed but not abolished.. This is the first report of a pathogenic deep-intronic mutation in the F5 gene. Our findings indicate that the minimal FV requirement for viability is extremely low and suggest that thrombin generation in PRP may predict bleeding tendency in patients with undetectable plasma FV.

Topics: Adult; Alternative Splicing; Blood Coagulation; Factor V; Factor V Deficiency; Hemarthrosis; Hematoma; Homozygote; Humans; Immunoprecipitation; Introns; Male; Mutation; Platelet-Rich Plasma; Thrombin; Thromboplastin

To clarify factors that may contribute to the development of intratumoral hemorrhage, we analyzed the expression of tissue factor (TF), an initiator of the extrinsic coagulation pathway, and of tissue factor pathway inhibitor (TFPI) in glioblastomas with or without massive intratumoral hematoma. Among 196 glioma cases reviewed, there were 13 with macroscopic intratumoral hemorrhage. We focused on the glioblastomas and used immunoblot- and immunohistochemical methods to compare the expression of TF and TFPI in 9 glioblastomas with macroscopic hematoma and 30 glioblastomas without macroscopic hemorrhage. Although TF was expressed in most glioblastomas irrespective of the presence or absence of macroscopic hemorrhage, the staining patterns differed significantly: TF-positive glioma cells were diffusely present in the non-hemorrhage group; in the group with hemorrhage, positive cells, primarily macrophages, were scattered throughout the tissue examined. The expression of TFPI was significantly higher in the group with than in the group without hemorrhage. Our results suggest that local suppression of the TF-dependent coagulation cascade is a contributing factor that permits the occurrence of intratumoral hemorrhage.

Topics: Adult; Aged; Brain Neoplasms; Child, Preschool; Female; Glioblastoma; Glioma; Hematoma; Hemorrhage; Humans; Immunoblotting; Immunohistochemistry; Lipoproteins; Macrophages; Magnetic Resonance Imaging; Male; Middle Aged; Thromboplastin; Tomography, X-Ray Computed

Tissue factor (TF) was initially identified as an important factor in the initiation of coagulation. TF has recently been found to be expressed highly in certain types of malignant tumors. It has also been reported to be involved in systemic coagulopathy in cancer patients and in the proliferative and invasive activities of tumor cells. Tissue factor pathway inhibitor (TFPI) is a strong biologic inhibitor of TF. To the authors' knowledge, this is the first study of the expression of TF and TFPI in human pituitary adenoma.. The expression of TF and TFPI were analyzed by immunohistochemical methods in human pituitary adenoma samples. To examine whether TF and TFPI expression influence the proliferative and/or invasive character of pituitary adenomas, the authors determined the MIB-1 labeling indices and invasiveness of all the pituitary adenomas they examined. Furthermore, to determine whether TF contributes to coagulation inside adenoma tissues, the incidence of cysts or hematomas in adenomas was analyzed.. In cells from 29 of 83 pituitary adenomas, overexpression of TF was observed. This was not the case for normal pituitary gland cells. TFPI was not expressed in either the adenomas or the normal pituitary glands from adenoma-bearing individuals. The expression of TF was significantly correlated with the formation of cysts or hematomas in pituitary adenomas. However, no such correlation with either the proliferative activity or the invasive character of the adenomas was observed.. Locally overexpressed TF in adenoma cells may contribute to the development of vascular events, such as infarction and/or hemorrhagic infarction, in pituitary adenomas.

Topics: Adenoma; Adult; Aged; Cysts; Female; Hematoma; Humans; Infarction; Lipoproteins; Male; Middle Aged; Pituitary Gland; Pituitary Neoplasms; Thromboplastin

The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.

Topics: Animals; Basal Ganglia; Blood Cells; Blood Coagulation; Blood Physiological Phenomena; Brain Edema; Cerebral Hemorrhage; Hematoma; Injections; Male; Plasma; Rats; Rats, Sprague-Dawley; Stereotaxic Techniques; Thrombin; Thromboplastin

Topics: Adolescent; Adult; Blood Coagulation Tests; Child; Child, Preschool; Factor VIII; Female; Hemarthrosis; Hematoma; Hemophilia A; Hemophilia B; Humans; Infant; Male; Oral Hemorrhage; Thromboplastin; von Willebrand Diseases

An otherwise healthy elderly man developed massive, life-threatening, sublingual bleeding associated with an idiopathic factor VIII inhibitor. The patient was treated wtih cyclophosphamide, steroids, factor VIII concentrates, and repeated plasmapheresis (including three times with NCI-IBM blood-cell separator). Rapid clinical and laboratory improvement occurred, with complete disappearance of the inhibitor. The patient has remained well, without evidence of an inhibitor, for 8 mo. The possible role of each of the therapeutic measures in the disappearance of the inhibitor and the possible pathogenetic mechanism of this disorder are discussed. A high mortality rate and a striking incidence of sublingual hematoma have been observed in cases in the literature.

Topics: Aged; Antibodies; Cyclophosphamide; Factor VIII; Hematoma; Humans; Male; Oral Hemorrhage; Plasmapheresis; Prednisone; Thromboplastin

Four basic coagulation tests, the prothrombin time, thrombin time, partial thromboplastin time, and prothrombin consumption time, were used, with relatively simple modifications, to demonstrate the presence of two circulating anticoagulants in the blood of a patient with IgG myeloma and a severe bleeding tendency.

Topics: Antithrombins; Blood Coagulation Tests; Ear Diseases; Factor IX; Factor V; Factor VIII; Hemagglutination Inhibition Tests; Hematoma; Hemorrhage; Hot Temperature; Humans; Immunoelectrophoresis; Immunoglobulin G; Male; Melphalan; Middle Aged; Multiple Myeloma; Plasmapheresis; Prednisone; Prothrombin Time; Thromboplastin

Topics: Aged; Autopsy; Chronic Disease; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrosarcoma; Hematoma; Hematuria; Humans; Leiomyosarcoma; Pulmonary Artery; Sarcoma; Thromboplastin

Topics: Blood Coagulation Factors; Blood Coagulation Tests; Blood Specimen Collection; Factor IX; Factor V; Factor VII; Factor VIII; Factor X; Factor XI; Factor XII; Hematoma; Humans; Methods; Prothrombin Time; Punctures; Thrombin; Thromboplastin; Veins

Topics: Adenoma; Antithyroid Agents; Drug Synergism; Fibrinolysis; Goiter; Hematoma; Hemorrhage; Humans; Plasminogen; Postoperative Complications; Preoperative Care; Thromboplastin; Thyroid Gland; Thyroid Neoplasms

Topics: Blood Coagulation Tests; Blood Transfusion; Cerebral Hemorrhage; Factor X; Female; Hematoma; Humans; Hypoprothrombinemias; Infant; Infant, Newborn; Male; Melena; Pedigree; Pregnancy; Thrombelastography; Thromboplastin

Topics: Blood Coagulation Disorders; Blood Specimen Collection; Blood Transfusion; Factor VIII; Female; Hematoma; Humans; Immunoglobulin G; Middle Aged; Thromboplastin

Topics: Adipose Tissue; Adolescent; Adult; Aged; Blood Coagulation; Bone Marrow; Brain Chemistry; Factor VIII; Female; Fracture Fixation; Fractures, Bone; Fractures, Spontaneous; Hematoma; Hemophilia A; Hemophilia B; Hemorrhage; Humans; Male; Middle Aged; Muscles; Plasma; Radiography; Thromboplastin

Topics: Child; Child, Preschool; Factor VIII; Female; Hematoma; Hemophilia A; Hemophilia B; Hemorrhage; Humans; Infant; Infant, Newborn; Italy; Male; Thromboplastin; von Willebrand Diseases

Topics: Abortion, Missed; Abruptio Placentae; Adolescent; Adult; Aprotinin; Blood Coagulation Tests; Female; Hematoma; Hemorrhagic Disorders; Humans; Pregnancy; Pregnancy Complications, Hematologic; Thromboplastin; Uterine Hemorrhage