fibrin and Hemorrhagic-Disorders

fibrin has been researched along with Hemorrhagic-Disorders* in 96 studies

Reviews

15 review(s) available for fibrin and Hemorrhagic-Disorders

ArticleYear
Acquired factor XIII inhibitor: clinical features, treatment, fibrin structure and epitope determination.
    Haemophilia : the official journal of the World Federation of Hemophilia, 2011, Volume: 17, Issue:3

    Acquired factor XIII (FXIII) deficiency, arising from an autoantibody against factor XIII, is a rare bleeding disorder. This autoimmune disorder most commonly occurs in the elderly. Patients who develop such acquired FXIII inhibitors may present with catastrophic bleeding events and are hard to be diagnosed with the normal general coagulation tests. Though the disease is relatively rare, it is known to cause significant mortality. In this article we briefly describe a patient who presented with extensive bleeding and a normal activated partial thromboplastin time and prothrombin time (PT), but had an acquired inhibitor to FXIII; her primary disease was systemic lupus erythematosus (SLE). Also, we will focus on the clinical features, treatment modalities, fibrin structure and epitope identification for acquired factor XIII inhibitor with a review of the literature.

    Topics: Adult; Blood Coagulation Disorders; Blood Coagulation Factor Inhibitors; Epitopes; Factor VIII; Factor XIII Deficiency; Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Immunosuppressive Agents; Lupus Erythematosus, Systemic

2011
Coagulopathies associated with lymphoproliferative disorders.
    Current hematology reports, 2004, Volume: 3, Issue:1

    Topics: Adult; Aged; Aged, 80 and over; Autoantibodies; Autoantigens; Autoimmune Diseases; Biopolymers; Blood Coagulation Disorders; Blood Coagulation Factors; Female; Fibrin; Hemorrhagic Disorders; Humans; Lymphoproliferative Disorders; Male; Middle Aged; Paraproteins; Thrombophilia

2004
[Cross-linked fibrin polymer and degradation products by plasmin (XDP)].
    Nihon rinsho. Japanese journal of clinical medicine, 2004, Volume: 62 Suppl 12

    Topics: Biomarkers; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Fibrinolysis; Hemorrhagic Disorders; Humans; Immunoenzyme Techniques; Latex Fixation Tests; Nephelometry and Turbidimetry; Polymers; Reference Standards; Specimen Handling; Thrombophilia

2004
[Blind spots of the diagnostic hemostasis screen].
    Nederlands tijdschrift voor geneeskunde, 2000, Mar-04, Volume: 144, Issue:10

    The most powerful instrument to establish the presence or absence of a coagulation disorder is the history of the patient. In addition, screening laboratory tests (consisting of the platelet count, bleeding time and global clotting assays, such as the prothrombin time and the activated partial thromboplastin time) may be helpful to support the diagnosis. In two patients, a 21-year-old man and a 10-year-old girl, with a marked history of enhanced bleeding normal screening laboratory tests were found. The male patient had a congenital alpha 2-antiplasmin deficiency and the girl had a homozygous deficiency of factor XIII. Some defects in the coagulation system (such as defects in fibrin network formation and fibrinolysis, but also mild Von Willebrand disease) are indeed not detected by screening laboratory tests. In patients with a strong suspicion of a coagulation disorder such defects should be specifically tested for.

    Topics: Adult; alpha-2-Antiplasmin; Antifibrinolytic Agents; Blood Coagulation Tests; Child; Diagnosis, Differential; Factor XIII; Factor XIII Deficiency; Female; Fibrin; Fibrinolysis; Hemorrhagic Disorders; Humans; Male; Medical History Taking; Tranexamic Acid

2000
[Rational diagnosis in blood coagulation disorders].
    Der Internist, 1994, Volume: 35, Issue:7

    Topics: Blood Coagulation Tests; Diagnosis, Differential; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Thrombosis

1994
Factor XIII: inherited and acquired deficiency.
    Blood reviews, 1993, Volume: 7, Issue:4

    Factor XIII (XIII), an enzyme found in plasma (present as a pro-enzyme), platelets and monocytes, is essential for normal haemostasis. It may also have a role to play in the processes of wound healing and tissue repair. Inherited XIII deficiency results in a life-long, severe bleeding diathesis which, if untreated, carries a very high risk of death in early life from intracranial bleeding. XIII is a zymogen requiring thrombin and calcium for activation. In plasma, XIII has two subunits: the 'a' subunit, which is the active enzyme, and the 'b' subunit which is a carrier protein. Activated XIII modifies the structure of clot by covalently crosslinking fibrin through an epsilon (gamma-glutamyl)lysine link. It also crosslinks other proteins, including fibronectin and alpha-2-plasmin inhibitor (alpha-2PI), into the clot through the same link. Clot modified by XIII is physically stronger, relatively more resistant to fibrinolysis and may be a more suitable medium for the ingrowth of fibroblasts. Inheritance of factor XIII is autosomal recessive. The majority of patients with the inherited defect show no XIII activity and absence of 'a' subunit protein in plasma, platelets and monocytes. At the molecular level, the defect is not a major gene rearrangement or deletion, but most likely a single point mutation which may be different in each family. Because of the severity of the bleeding diathesis, prophylaxis is desirable and has been shown to be very effective as the in vivo half-life of plasma XIII is long, and low plasma levels are sufficient for haemostasis. Acquired inhibitors have been reported in only two cases with inherited XIII deficiency. Acquired XIII deficiency has been described in a variety of diseases and bleeding has been controlled by therapy with large doses of XIII in such conditions as Henoch-Schönlein purpura, various forms of colitis, erosive gastritis and some forms of leukaemia. Large dose XIII therapy has also been used in an endeavour to promote wound healing after surgery and bone union in non-healing fractures. The use of XIII in these conditions remains controversial. Very rarely a bleeding diathesis results from the development of a specific inhibitor to XIII arising de novo, often as a complication in the course of a disease or in association with long-term drug therapy. The bleeding diathesis in these patients is difficult to treat.

    Topics: Amino Acid Sequence; Enzyme Activation; Factor XIII; Factor XIII Deficiency; Fibrin; Hemorrhagic Disorders; Hemostasis; Humans; Molecular Sequence Data; Protein Conformation; Wound Healing

1993
Fibrinogen anomalies and disease. A clinical update.
    Hematology/oncology clinics of North America, 1992, Volume: 6, Issue:5

    The precipitous increase in the number of structurally defined fibrinogen defects in recent years has resulted from application of high performance liquid chromatography in combination with peptide mapping and sequencing procedures. More recently, application of DNA sequence of polymerase chain reaction products has accelerated the pace of identification of mutations. Highly frequent defects are Arg substitutions, accounting for eight mutation sites substituted by Cys or His and less frequently by Ser. Amino acid substitutions at different positions on all three chains have pointed to possible structures with polymerization-related functions. Also, substitutions yielding consensus sequences resulted in extra glycosylations of the appropriate Asn in four different mutation sites; the impaired polymerization was reported associated with undue bleeding in two of these. Among informative defects have been those of homozygous probands with A alpha 16Arg----His and A alpha 16Arg----Cys in that failure of release of peptide A (but not of B), as shown with A alpha 16Arg----Cys, resulted in markedly delayed polymerization of such fibrin monomers, in general agreement with conclusions reached in studies of normal fibrin. This dysfunction, as well as the slow rate of release of A shown with A alpha 16Arg----His, was associated with clinically significant hemorrhagic diathesis (in the homozygous probands), consistent with the known physiologic importance of peptide A cleavage in normal hemostasis. Also, defects on the A alpha 17-19 sequence resulting in impaired polymerization are consistent with the known role of this segment in polymerization. Of similar interest have been defects within a B beta chain span encoded its exon 2. Two defects resulting in impaired polymerization and thrombin binding were associated with clinical thrombosis commencing in early life, and this lends strong support to other evidence suggesting a role in polymerization and in noncatalytic thrombin binding by this B beta chain segment. Thrombosis associated with A alpha 554Arg----Cys in a heterozygous proband with impaired tPA interaction is unique and may shed light on this poorly understood but important interaction among fibrin, plasminogen, and tPA. A group of different defects within the gamma 275-375 sequence have pointed to a polymerization role, evidenced by delayed gelation and impaired binding of mutant D to normal fibrin E. An unusual example is a 15 residue insertion between gamm

    Topics: Afibrinogenemia; Blood Coagulation Tests; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Mutation; Protein Conformation; Protein Processing, Post-Translational; Protein Structure, Tertiary

1992
Normal and abnormal haemostasis.
    British medical bulletin, 1977, Volume: 33, Issue:3

    Topics: Animals; Blood Coagulation; Blood Vessels; Endothelium; Fibrin; Hemorrhagic Disorders; Hemostasis; Humans; Platelet Adhesiveness; Platelet Aggregation; Thrombocytopenia

1977
[Blood coagulation factor XIII and fibrin stabilization (author's transl)].
    Klinische Wochenschrift, 1975, Dec-15, Volume: 53, Issue:24

    Coagulation factor XIII (fibrin stabilizing factor, FSF) is detectable in plasma, platelets, placenta and various tissues. In the activated form FSF has the enzymatic properties of a transglutaminase and is capable of stabilizing fibrin by inducing covalent bondings between fibrin monomers. In patients with congenital factor XIII deficiency or acquired immune inhibitors of fibrin stabilization a severe bleeding tendency is evident. There is not yet enough information available concerning the significance of reduced FSF-activity as cofactor in hemorrhagic diathesis and wound healing disturbances in various disease states. There are some indications from experimental studies that there might be an influence of FSF on tumor growth and metastasis as well as arteriosclerosis. The quantitation of the enzyme by radiological and immunological techniques yield reproducible results. Fibrin in its stabilized or non stabilized form can be discriminated in polyacrylamide gel electrophoresis after reduction of fibrin clots.

    Topics: Adult; Blood Coagulation Disorders; Electrophoresis, Polyacrylamide Gel; Factor XIII; Factor XIII Deficiency; Female; Fibrin; Hemorrhagic Disorders; Humans; Infant, Newborn; Pregnancy; Pregnancy Complications, Hematologic

1975
[Factor XIII, its physiological significance (a review of the literature)].
    Problemy gematologii i perelivaniia krovi, 1973, Volume: 18, Issue:2

    Topics: Animals; Blood Coagulation; Blood Protein Electrophoresis; Calcium; Enzyme Activation; Factor XII; Factor XIII; Factor XIII Deficiency; Fibrin; Fibrinogen; Fibrinolysin; Half-Life; Hemorrhage; Hemorrhagic Disorders; Hemostasis; Heparin; Humans; Molecular Weight; Rats; Sulfhydryl Compounds; Thrombin

1973
The fibrin stabilizing factor, factor XIII.
    Blut, 1973, Volume: 26, Issue:3

    Topics: Abortion, Spontaneous; Blood; Blood Coagulation Tests; Blood Platelets; Cerebral Hemorrhage; Ecchymosis; Factor XIII; Factor XIII Deficiency; Female; Fetal Death; Fibrin; Hematoma; Hemorrhage; Hemorrhagic Disorders; Humans; Infant, Newborn; Placenta; Pregnancy; Pregnancy Complications, Hematologic; Umbilical Cord

1973
Blood clotting abnormalitis in relation to pre-eclampsia: a review.
    Canadian Medical Association journal, 1969, Jan-18, Volume: 100, Issue:3

    Topics: Abruptio Placentae; Adrenal Glands; Aminocaproates; Animals; Basement Membrane; Biopsy; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Brain; Female; Fibrin; Fibrinogen; Fibrinolysis; Fluorescent Antibody Technique; Hemorrhage; Hemorrhagic Disorders; Heparin; Humans; Hypertension, Malignant; Kidney Cortex Necrosis; Kidney Failure, Chronic; Kidney Glomerulus; Liver; Maternal Mortality; Microscopy, Electron; Myocardium; Placental Extracts; Pre-Eclampsia; Pregnancy; Rabbits; Shwartzman Phenomenon; Thromboplastin; Thrombosis

1969
Infection and the spleen: association between hyposplenism, pneumococcal sepsis and disseminated intravascular coagulation.
    The Medical journal of Australia, 1969, Jun-14, Volume: 1, Issue:24

    Topics: Adolescent; Adrenal Glands; Adult; Aged; Blood Coagulation Disorders; Child; Female; Fibrin; Hemorrhagic Disorders; Heparin; Humans; Kidney; Male; Meningitis; Middle Aged; Pneumococcal Infections; Sepsis; Splenectomy; Splenic Diseases; Thrombosis; Waterhouse-Friderichsen Syndrome

1969
[Hemorrhagic diathesis].
    Saishin igaku. Modern medicine, 1969, Volume: 24, Issue:4

    Topics: Anticoagulants; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Diagnosis, Differential; Fibrin; Fibrinogen; Hemorrhage; Hemorrhagic Disorders; Humans; Prothrombin; Prothrombin Time; Thromboplastin; Vascular Resistance

1969
[SOME BASIC PROBLEMS OF ANTICOAGULANT THERAPY].
    Orvosi hetilap, 1964, Jul-19, Volume: 105

    Topics: Anticoagulants; Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Coumarins; Drug Therapy; Fibrin; Hemorrhagic Disorders; Hemostasis; Heparin; Humans

1964

Trials

1 trial(s) available for fibrin and Hemorrhagic-Disorders

ArticleYear
[Application possibilities of fibrin glue in dentistry and maxillofacial surgery].
    Zahn-, Mund-, und Kieferheilkunde mit Zentralblatt, 1980, Volume: 68, Issue:6

    Topics: Adult; Clinical Trials as Topic; Dentistry, Operative; Fibrin; Hemorrhagic Disorders; Humans; Mouth Mucosa; Oroantral Fistula; Surgery, Oral; Tissue Adhesives; Tooth Extraction

1980

Other Studies

80 other study(ies) available for fibrin and Hemorrhagic-Disorders

ArticleYear
A novel simultaneous clot-fibrinolysis waveform analysis for assessing fibrin formation and clot lysis in haemorrhagic disorders.
    British journal of haematology, 2019, Volume: 187, Issue:4

    Simultaneous evaluation of coagulation and fibrinolysis facilitates an overall understanding of normal and pathological haemostasis. We established an assay for assessing clot formation and fibrinolysis simultaneously using clot waveform analysis by the trigger of a mixture of activated partial thromboplastin time reagent and an optimized concentration of tissue-type plasminogen activator (0·63 μg/ml) to examine the temporal reactions in a short monitoring time (<500 s). The interplay between clot formation and fibrinolysis was confirmed by analysing the effects of argatroban, tranexamic acid and thrombomodulin. Fibrinogen levels positively correlated with coagulation and fibrinolytic potential and initial fibrin clot formation was independent of plasminogen concentration. Plasminogen activator inhibitor-1-deficient (-def) and α2-antiplasmin-def plasmas demonstrated different characteristic hyper-fibrinolytic patterns. For the specificity of individual clotting factor-def plasmas, factor (F)VIII-def and FIX-def plasmas in particular demonstrated shortened fibrinolysis lag-times (FLT) and enhanced endogenous fibrinolysis potential in addition to decreased maximum coagulation velocity, possibly reflecting the fragile formation of fibrin clots. Tranexamic acid depressed fibrinolysis to a similar extent in FVIII-def and FIX-def plasmas. We concluded that the clot-fibrinolysis waveform analysis technique could sensitively monitor both sides of fibrin clot formation and fibrinolysis, and could provide an easy-to-use assay to help clarify the underlying pathogenesis of bleeding disorders in routine clinical practice.

    Topics: Arginine; Fibrin; Fibrin Clot Lysis Time; Fibrinolysis; Hemorrhagic Disorders; Humans; Kinetics; Pipecolic Acids; Sulfonamides; Thrombomodulin; Tranexamic Acid

2019
Teaching an old dog new tricks?
    British journal of haematology, 2019, Volume: 187, Issue:4

    Topics: Fibrin; Fibrin Clot Lysis Time; Fibrinolysis; Hemorrhagic Disorders; Humans; Thrombosis

2019
Plasminogen activator inhibitor-1 deficiency augments visceral mesothelial organization, intrapleural coagulation, and lung restriction in mice with carbon black/bleomycin-induced pleural injury.
    American journal of respiratory cell and molecular biology, 2014, Volume: 50, Issue:2

    Local derangements of fibrin turnover and plasminogen activator inhibitor (PAI)-1 have been implicated in the pathogenesis of pleural injury. However, their role in the control of pleural organization has been unclear. We found that a C57Bl/6j mouse model of carbon black/bleomycin (CBB) injury demonstrates pleural organization resulting in pleural rind formation (14 d). In transgenic mice overexpressing human PAI-1, intrapleural fibrin deposition was increased, but visceral pleural thickness, lung volumes, and compliance were comparable to wild type. CBB injury in PAI-1(-/-) mice significantly increased visceral pleural thickness (P < 0.001), elastance (P < 0.05), and total lung resistance (P < 0.05), while decreasing lung compliance (P < 0.01) and lung volumes (P < 0.05). Collagen, α-smooth muscle actin, and tissue factor were increased in the thickened visceral pleura of PAI-1(-/-) mice. Colocalization of α-smooth muscle actin and calretinin within pleural mesothelial cells was increased in CBB-injured PAI-1(-/-) mice. Thrombin, factor Xa, plasmin, and urokinase induced mesothelial-mesenchymal transition, tissue factor expression, and activity in primary human pleural mesothelial cells. In PAI-1(-/-) mice, D-dimer and thrombin-antithrombin complex concentrations were increased in pleural lavage fluids. The results demonstrate that PAI-1 regulates CBB-induced pleural injury severity via unrestricted fibrinolysis and cross-talk with coagulation proteases. Whereas overexpression of PAI-1 augments intrapleural fibrin deposition, PAI-1 deficiency promotes profibrogenic alterations of the mesothelium that exacerbate pleural organization and lung restriction.

    Topics: Animals; Bleomycin; Blood Coagulation; Epithelium; Fibrin; Hemorrhagic Disorders; Humans; Lung; Lung Injury; Mice; Mice, Inbred C57BL; Mice, Knockout; Plasminogen Activator Inhibitor 1; Pleura; Soot; Thrombin

2014
Fibrinogen Šumperk II: dysfibrinogenemia in an individual with two coding mutations.
    American journal of hematology, 2012, Volume: 87, Issue:5

    Fibrinogen—a 340-kDa glycoprotein—plays a crucial role in blood coagulation, platelet aggregation, wound healing, and other physiological processes. A mutation in fibrinogen may lead to congenital dysfibrinogenemia,a rare disease characterized by the functional deficiency of fibrinogen. About 580 cases of abnormal fibrinogens have been reported worldwide; thereof 335 cases in the fibrinogen Aa chain[1]. To our knowledge, only five cases of abnormal fibrinogens with two mutations [2–6] and one case of two different mutations in the same family [7] have been described earlier. A 52-year-old female was examined for bleeding. Routine hemostasis screening resulted in a diagnosis of dysfibrinogenemia. Functional testing revealed prolonged fibrin polymerization, prolonged lysis of the clot, abnormal fibrin morphology,and fibrinopeptides release. Genetic analysis showed two heterozygous nonsense mutations—previously described mutation AaGly13Glu and a novel mutation Aa Ser314Cys. The mutation Aa Gly13-Glu was found in her brother and niece, but there was no evidence in either of the mutation Aa Ser314Cys. While mutation Aa Gly13Glu is responsible for abnormal fibrinopeptide release and prolonged thrombin time, the novel mutation Aa Ser314Cys seems to affect fibrin morphology and fibrinolysis.

    Topics: Adult; Afibrinogenemia; Blood Protein Electrophoresis; Child; Codon, Nonsense; Female; Fibrin; Fibrinogens, Abnormal; Fibrinopeptide A; Hemorrhagic Disorders; Heterozygote; Humans; Male; Microscopy, Electron, Scanning; Middle Aged; Point Mutation; Protein Processing, Post-Translational

2012
The ex vivo reversibility of dabigatran-induced whole-blood coagulopathy as monitored by thromboelastography: mechanistic implications for clinical medicine.
    Thrombosis and haemostasis, 2012, Volume: 108, Issue:3

    Topics: Antithrombins; Benzimidazoles; Blood Coagulation; Blood Coagulation Factors; Dabigatran; Drug Evaluation, Preclinical; Drug Monitoring; Factor VIIa; Fibrin; Hemorrhagic Disorders; Humans; In Vitro Techniques; Point-of-Care Systems; Pyridines; Recombinant Proteins; Thrombelastography; Thrombin; Whole Blood Coagulation Time

2012
Bacterial endotoxin as inhibitor of the enzymatic activity of human thrombin.
    European journal of haematology, 2006, Volume: 76, Issue:6

    Endotoxemia caused by bacterial lipopolysaccharides (LPS) deleteriously affects many aspects of hemostasis. Much of this effect is well characterized as being secondary to the LPS-mediated inflammatory response, but direct effects of LPS on coagulation factors may also contribute to disregulation of the hemostatic process. Spectrophotometric assays were used to investigate the effects of LPS from different bacteria on thrombin and plasmin activities. We found that enzymatic activity of purified thrombin, but not plasmin, decreases in the presence of endotoxin. LPS-mediated inhibition of thrombin activity can be reversed by plasma gelsolin and recombinant endotoxin-neutralizing protein. Preincubation of thrombin with LPS before platelet activation results in inhibition of aggregation and secretion. Additionally, a decrease of elastic shear moduli of fibrin gels was observed when their formation was induced with thrombin preincubated with LPS or when LPS was present in fibrinogen solutions during fibrin gel formation. When added to platelet-rich plasma, after activation with collagen, LPS-inhibited thrombin activity. LPS-mediated inhibition of thrombin activity may contribute to the hemostasis dysfunctions observed during endotoxemia.

    Topics: Calcium; Collagen; Endotoxemia; Escherichia coli; Fibrin; Gels; Gelsolin; Hemorrhagic Disorders; Humans; Klebsiella pneumoniae; Lipopolysaccharides; Platelet Aggregation; Pseudomonas aeruginosa; Recombinant Proteins; Salmonella enteritidis; Shear Strength; Species Specificity; Thrombin

2006
[Increased thrombin time in a patient with multiple myeloma].
    Therapeutische Umschau. Revue therapeutique, 1999, Volume: 56, Issue:9

    We describe a 56-year-old patient with multiple myeloma and very high paraprotein concentration (IgG kappa). Coagulation studies showed unclottable thrombin and reptilase times caused by impaired fibrin polymerization presumably due to the paraproteinemia. There was no obvious bleeding tendency. The differential diagnosis of thrombin time prolongation includes inhibition of the added thrombin by exogenous heparin, hirudin or seldom by endogenous heparin-like anticoagulants or by acquired (bovine) thrombin antibodies, qualitative fibrinogen disorders (congenital and acquired dysfibrinogenemia), quantitative fibrinogen disorders (severe hypo- and afibrinogenemia) and delayed fibrin polymerization due to fibrin/fibrinogen degradation products, paraproteins and antibodies against fibrin(ogen). In multiple myeloma, thrombin time prolongation may seldom be due to endogenous heparin-like anticoagulants or antibodies to thrombin and more frequently to impaired fibrin polymerization by paraproteins. Simultaneous reptilase time prolongation as present in this case hints to this latter possibility.

    Topics: Diagnosis, Differential; Fibrin; Hemorrhagic Disorders; Humans; Immunoglobulin kappa-Chains; Male; Middle Aged; Multiple Myeloma; Thrombin Time

1999
Autopsy study of patients dying of bleeding diathesis.
    Indian journal of pathology & microbiology, 1998, Volume: 41, Issue:1

    Ten thousand & thirty seven autopsies performed from the year 1982 to 1992 were studied retrospectively, to find out the number of deaths due to bleeding diathesis. Eighty-seven (0.87%) patients died due to bleeding diathesis, out of which haemolytic uraemic syndrome (HUS) was seen in 9 cases (10.34%), disseminated intravascular coagulation (DIC) in 67 cases (77.01%) & 11 cases were grouped as miscellaneous. Martius scarlet blue stain was carried out to demonstrate fibrin & depending on the number of thrombi in the glomerulus & blood vessels, the lesions were graded as mild, moderate or severe. Kidney was the most common organ involved in all groups of bleeding diathesis. In DIC kidney & lung involvement was almost equal.

    Topics: Autopsy; Disseminated Intravascular Coagulation; Female; Fibrin; Hemolytic-Uremic Syndrome; Hemorrhagic Disorders; Humans; Kidney; Lung; Male; Necrosis; Retrospective Studies; Staining and Labeling; Thrombosis

1998
Fibrinogen Guarenas I: partial characterization of a new dysfibrinogenemia with an altered rate of fibrinopeptide release and an impaired polymerization.
    Thrombosis research, 1995, Apr-15, Volume: 78, Issue:2

    A congenitally abnormal fibrinogen was isolated from the blood of a young woman with a severe bleeding diathesis. Coagulation tests showed a prolonged Thrombin and Reptilase time partially corrected by Ca2+. Polymerization of thrombin induced preformed fibrin monomers was severely impaired. Thrombin caused the release of fibrinopeptides with normal retention times on HPLC. However, the rate of release was abnormally slow and the total amount of fibrinopeptide A (FpA) released reached only approximately 50% of the theoretical maximum. The rate and quantity of FpA release was normal when Reptilase was used. Transmission Electron Microscopy (TEM) of Thrombin induced clots showed an altered clot structure characterized by a reduced mean fiber diameter. The mother has a polymerization defect similar to the propositus, her fibrinopeptide release is unaffected however. The father has a minor fibrinopeptide release defect suggesting the presence of two populations of fibrinogen. This study supports the idea that the fibrinogen isolated from the propositus has two defects inherited as separate genetic traits. This fibrinogen has been named Fibrinogen Guarenas I.

    Topics: Adolescent; Afibrinogenemia; Biopolymers; Female; Fibrin; Fibrinogens, Abnormal; Fibrinopeptide A; Fibrinopeptide B; Hemorrhagic Disorders; Humans; Kinetics; Male; Metrorrhagia; Microscopy, Electron; Thrombin; Thrombin Time

1995
[Experience with the human fibrin adhesive, Tissucol, in operative intervention in the jaw and face region in patients with haemostasis problems].
    Stomatologie der DDR, 1988, Volume: 38, Issue:8

    Topics: Adolescent; Adult; Aged; Aprotinin; Drug Combinations; Face; Factor XIII; Female; Fibrin; Fibrin Tissue Adhesive; Fibrinogen; Hemorrhagic Disorders; Humans; Male; Maxilla; Middle Aged; Thrombin; Tissue Adhesives

1988
alpha 2-Antiplasmin Enschede: dysfunctional alpha 2-antiplasmin molecule associated with an autosomal recessive hemorrhagic disorder.
    The Journal of clinical investigation, 1987, Volume: 80, Issue:5

    alpha 2-Antiplasmin (alpha 2-AP) is a major fibrinolysis inhibitor, whose complete, congenital absence has been found to be associated with a distinct hemorrhagic diathesis. We studied a 15-yr-old male with a hemorrhagic diathesis after trauma from early childhood on. This bleeding tendency was associated with a minimal alpha 2-AP level recorded functionally in the immediate plasmin inhibition test: less than or equal to 4% of normal. However, a normal plasma concentration of alpha 2-AP antigen (83%) was found. His sister (5 yr old) showed similar results (2 and 92%). In their family, eight heterozygotes could be identified by half-normal activity results and normal antigen concentrations. The inheritance pattern is autosomal recessive. On analysis, the alpha 2-AP of the propositus was homogeneous in all respects tested, suggesting a homozygous defect. We designated the abnormal alpha 2-AP as alpha 2-AP Enschede. alpha 2-AP Enschede showed the following characteristics: (a) complete immunological identity with normal alpha 2-AP; (b) normal molecular weight (sodium dodecyl sulfate-polyacrylamide gel electrophoresis); (c) normal alpha-electrophoretic mobility; (d) presence in plasma of both molecular forms excluding an excessive conversion to the less reactive non-plasminogen-binding form; (e) quantitatively normal binding to lys-plasminogen and to immobilized plasminogen kringle 1-3; and (f) normal Factor XIII-mediated binding to fibrin. Functional abnormalities were found in: (i) no inhibition of amidolytic activities of plasmin and trypsin, even on prolonged incubation; (ii) no formation of plasmin-antiplasmin complexes in plasma with plasmin added in excess; and (iii) no inhibition of fibrinolysis by fibrin-bound alpha 2-AP. In the heterozygotes, the presence of abnormal alpha 2-AP did not interfere with several functions of the residual normal alpha 2-AP. One-dimensional peptide mapping showed an abnormal pattern of papain digestion. We conclude that in this family, abnormal antiplasmin molecules, defective in plasmin inhibition but with normal plasminogen-binding properties, have been inherited. The residual plasminogen-binding properties do not protect against a hemorrhagic diathesis.

    Topics: Adolescent; alpha-2-Antiplasmin; Fibrin; Fibrinolysin; Fibrinolysis; Hemorrhagic Disorders; Humans; Immunodiffusion; Immunoelectrophoresis, Two-Dimensional; Male; Mutation; Papain; Pedigree; Plasminogen

1987
An acquired inhibitor of factor XIII with a qualitative abnormality of fibrin cross-linking.
    Acta haematologica, 1984, Volume: 71, Issue:5

    A patient with an acquired inhibitor to factor XIII is reported. The patient's plasma produced a profound inhibition of factor XIII activity in normal plasma measured by a dansylcadaverine casein assay and stimulated a very abnormal pattern of fibrin cross-linking, not normally seen with factor XIII. Partial characterisation of the inhibitor suggests that it is heat stable and not an immunoglobulin.

    Topics: Acetates; Blood Coagulation Disorders; Blood Coagulation Tests; Electrophoresis, Polyacrylamide Gel; Factor XIII; Female; Fibrin; Hemorrhagic Disorders; Humans; Urea

1984
Preoperative disseminated intravascular coagulation associated with aortic aneurysms. A prospective study of 76 cases.
    Archives of surgery (Chicago, Ill. : 1960), 1983, Volume: 118, Issue:11

    A prospective study of 76 preoperative patients with aortic aneurysms was undertaken to determine the true incidence of associated disseminated intravascular coagulation (DIC). Although 39% of the patients showed a notable elevation of the fibrin split products level, only three had thrombocytopenia and a clinical bleeding diathesis, as well. Thus, clinically overt DIC occurred preoperatively in only 4% of the patients. All three patients had extensive aneurysms that involved the thoracoabdominal aorta. Preoperative fibrinogen levels in this series tended to be high-normal or elevated and were not good indicators of underlying excessive fibrinolysis. Hemostatic abnormalities, such as ecchymoses and petechiae, may be the key to the clinical diagnosis of DIC in preoperative patients with aortic aneurysms.

    Topics: Aged; Aorta, Abdominal; Aorta, Thoracic; Aortic Aneurysm; Blood Platelet Disorders; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Prospective Studies

1983
[Treatment of patients at risk of hemorrhage with the aid of fibrin adhesion].
    Schweizerische Monatsschrift fur Zahnheilkunde = Revue mensuelle suisse d'odonto-stomatologie, 1980, Volume: 90, Issue:3

    341 cases of surgery on patients with difficulties in hemostasis are reported. Therapy was the use of fibrine fixation technique, a simple and riskless method. Tooth extractions and other surgical interventions oin anticoagulated patients may be performed without interruption of the anticoagulant therapy, also patients with hemorrhages and other complications need not be expected, if the material is properly handled.

    Topics: Fibrin; Gingivectomy; Gingivoplasty; Hemorrhagic Disorders; Hemostasis, Surgical; Humans; Oral Hemorrhage; Tooth Extraction

1980
[Oral-surgical management of the hemorrhage-prone patient with risk-free fibrin adhesive].
    Zahnarztliche Praxis, 1979, Apr-13, Volume: 30, Issue:4

    Topics: Dental Care; Fibrin; Hemorrhagic Disorders; Hemostasis, Surgical; Hemostatics; Humans; Oral Hemorrhage; Tissue Adhesives

1979
[Fibrinogen Quebec I and Quebec II: two new families of dysfibrinogenemia (author's transl)].
    Acta haematologica, 1978, Volume: 59, Issue:2

    Two new families of congenital dysfibrinogenemia originating from French Canada are reported. The dysfibrinogenemia in the first family is characterized by an abnormal aggregation of the fibrin monomers; the defect in the second family is due to a faulty release of fibrinopeptides during the proteolytic phase of the thrombin-fibrinogen reaction.

    Topics: Blood Coagulation Disorders; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Male

1978
Diathesis haemorrhagica in children suffering from rheumatoid arthritis complicates with amyloidosis.
    Verhandlungen der Deutschen Gesellschaft fur Rheumatologie, 1978, Volume: 5

    Topics: Amyloidosis; Arthritis, Juvenile; Blood Platelets; Child; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans

1978
[Disorders of fibrin polymerization in paraproteinemia].
    Verhandlungen der Deutschen Gesellschaft fur Innere Medizin, 1978, Issue:84

    Topics: Fibrin; Hemorrhagic Disorders; Humans; Paraproteinemias; Polymers

1978
[Tonsillectomy in patients with bleeding disorders].
    Fortschritte der Medizin, 1977, May-19, Volume: 95, Issue:19

    When injury of a major vessel can be ruled out as the cause of bleeding after tonsillectomy, a discrete disturbance of hemostasis must be considered. These are mainly slight thrombopathies or a pathologically increased fibrinolysis, which were not detected by routine tests and the past history. In former times severe bleeding disorders were a strict contra-indication for tonsillectomy. Under the supposition of an exact coagulogram and the substitution of highly purified factor concentrates the risk of severe post-tonsillectomy hemorrhages in such patients today is nearly the same as in patients with a normal hemostase.

    Topics: Antifibrinolytic Agents; Blood Coagulation Factors; Blood Platelet Disorders; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Postoperative Complications; Tissue Adhesives; Tonsillectomy

1977
[Structure of the fibrin clot in a patient with macroglobulinemia (author's transl)].
    Przeglad lekarski, 1976, Volume: 33, Issue:3

    Topics: Fibrin; Hemorrhagic Disorders; Humans; Male; Microscopy, Electron; Middle Aged; Waldenstrom Macroglobulinemia

1976
Disseminated intravascular coagulation.
    Haematologia, 1976, Volume: 10, Issue:3-4

    Topics: Adolescent; Adult; Blood Platelets; Blood Transfusion; Diagnosis, Differential; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Hematuria; Hemolytic-Uremic Syndrome; Hemorrhagic Disorders; Heparin; Humans; Male; Melena; Middle Aged; Neurologic Manifestations; Prednisolone; Pregnancy; Pregnancy Complications, Hematologic; Thrombocytopenia

1976
[Disseminated intravasal coagulation as an important pathogenetic principle].
    Monatsschrift fur Kinderheilkunde, 1975, Volume: 123, Issue:7

    Topics: Blood Coagulation Factors; Collagen; Disseminated Intravascular Coagulation; Fibrin; Hemorrhagic Disorders; Hemostasis; Humans; Microcirculation; Mononuclear Phagocyte System; Platelet Adhesiveness; Polymers; Thrombin

1975
[Hypodysfibrinogenemia: fibrinogen giessen II (author's transl)].
    Klinische Wochenschrift, 1975, Aug-15, Volume: 53, Issue:16

    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

1975
[Goodpasture's syndrome: progressive glomerulonephritis - disturbance of coagulation - ferritin-induced alveolar inhibition of fibrin polymerisation (author's transl)].
    Klinische Wochenschrift, 1974, Nov-15, Volume: 52, Issue:22

    Topics: Adult; Anti-Glomerular Basement Membrane Disease; Blood Coagulation Disorders; Female; Ferritins; Fibrin; Glomerulonephritis; Hemorrhagic Disorders; Humans

1974
A new haemorrhagic disorder with defective fibrin stabilization and cryofibrinogenaemia.
    British journal of haematology, 1974, Volume: 26, Issue:2

    Topics: Abdomen; Antibodies; Blood Coagulation Tests; Blood Protein Disorders; Chromatography; Cold Temperature; Diagnosis, Differential; Ecchymosis; Electrophoresis; Factor XIII; Female; Fibrin; Fibrinogen; Hematuria; Hemorrhagic Disorders; Humans; Immunoglobulin G; Isoniazid; Middle Aged; Pain; Sarcoidosis

1974
Fibrinogen 'Leuven', another genetic variant.
    British journal of haematology, 1974, Volume: 26, Issue:3

    Topics: Adult; Blood Coagulation Disorders; Blood Coagulation Factors; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Hysterectomy; Molecular Conformation; Plasma; Prothrombin Time; Thrombin

1974
Fibrinogen Cleveland II. An abnormal fibrinogen with defective release of fibrinopeptide A.
    The Journal of clinical investigation, 1974, Volume: 53, Issue:5

    An abnormal fibrinogen (fibrinogen Cleveland II) was detected in the plasma of a 23-yr-old white man with a mild bleeding diathesis. The one-stage prothrombin time, thrombin time, and Reptilase time were all prolonged. 16 of 24 tested relatives had the defect, which appeared to be transmitted as an autosomal dominant characteristic. The thrombin time of normal plasma was slightly inhibited by the proband's plasma. The abnormally long thrombin time of fibrinogen Cleveland II was partially corrected by addition of calcium ions. Fibrinogen Cleveland II was indistinguishable from normal fibrinogen by immunoelectrophoresis, DEAE-cellulose column chromatography, or polyacrylamide gel electrophoresis of reduced fibrinogen in sodium dodecyl sulfate. The major defect detected appeared to be impaired release of fibrinopeptide A when fibrinogen Cleveland II was incubated with thrombin. This defect was localized to the NH(2)-terminal disulfide knot portion of the molecule. An abnormality of polymerization of fibrin monomers was also present, but the abnormal fibrin demonstrated relatively normal crosslinking. Despite these defects, fibrinogen Cleveland II achieved a degree of coagulability similar to normal fibrinogen and appeared to incorporate some molecules of fibrin with intact fibrinopeptide A into the clot. The fibrin clot that was formed appeared to be abnormal by electron microscopy. These functional defects and other descriptive characteristics appear to distinguish fibrinogen Cleveland II from other inherited abnormal fibrinogens.

    Topics: Adult; Animals; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Hydrogen-Ion Concentration; Immunoelectrophoresis; Male; Microscopy, Electron; Pedigree; Peptide Hydrolases; Peptides; Prothrombin Time; Snakes; Thrombin; Time Factors; Venoms

1974
[Studies on hemorrhagic diathesis in fulminant hepatitis (author's transl)].
    [Rinsho ketsueki] The Japanese journal of clinical hematology, 1974, Volume: 15, Issue:2

    Topics: Adolescent; Adult; Child; Female; Fibrin; Hemorrhagic Disorders; Hepatitis; Humans; Male; Middle Aged

1974
[Electrophoretic studies on fibrinogen subunits and factor-XIII+-stabilized fibrin, from normal and cobalt-treated rabbits].
    Folia haematologica (Leipzig, Germany : 1928), 1973, Volume: 100, Issue:3

    Topics: Animals; Blood Protein Electrophoresis; Cobalt; Electrophoresis, Polyacrylamide Gel; Factor XIII; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Male; Methods; Molecular Conformation; Molecular Weight; Rabbits

1973
[Efficiency and limits of fibrinolytic system function tests].
    Der Internist, 1973, Volume: 14, Issue:4

    Topics: Afibrinogenemia; Blood Coagulation Tests; Diagnosis, Differential; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Hemorrhagic Disorders; Humans; Methods; Prothrombin Time; Time Factors

1973
Coagulation studies in acute hepatic failure.
    Gut, 1973, Volume: 14, Issue:5

    Topics: Acute Disease; Disseminated Intravascular Coagulation; Fibrin; Hemorrhagic Disorders; Humans; Liver Diseases; Prothrombin Time

1973
[Dysproteinemic diseases and hemorrhagic tendency].
    Rinsho byori. The Japanese journal of clinical pathology, 1971, Volume: 19, Issue:8

    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

1971
Care of the critically ill child: the problem of disseminated intravascular coagulation.
    Pediatrics, 1970, Volume: 46, Issue:5

    Topics: Anemia, Hemolytic; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Blood Transfusion; Child; Diagnosis, Differential; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Fibrin; Fibrinolysis; Hemorrhagic Disorders; Heparin; Hepatitis; Humans; Infections; Pediatrics; Uremia

1970
[Clinical aspects and therapy of disseminated intravascular coagulation].
    Hamatologie und Bluttransfusion, 1970, Volume: 9

    Topics: Abortion, Septic; Adolescent; Adult; Anticoagulants; Antithrombins; Blood; Blood Coagulation Disorders; Blood Coagulation Factors; Child; Disseminated Intravascular Coagulation; Encephalitis; Encephalitis Viruses; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Liver; Male; Necrosis; Pituitary Gland; Pregnancy; Prostatic Neoplasms; Prothrombin; Sepsis; Shock, Septic; Spleen; Streptokinase

1970
Fibrinolysis produced by contact with a caterpillar.
    Lancet (London, England), 1969, Apr-19, Volume: 1, Issue:7599

    Topics: Aminocaproates; Animals; Antifibrinolytic Agents; Aprotinin; Cattle; Fibrin; Fibrinolysis; Fibrinolytic Agents; Hemorrhagic Disorders; Humans; In Vitro Techniques; Insecta; Venezuela

1969
[Natural inhibitors of fibrinolysis and thrombohemorrhagic phenomena].
    Pathologia Europaea, 1969, Volume: 4

    Topics: Adolescent; Adult; Age Factors; Aged; Animals; Anticoagulants; Arthritis, Rheumatoid; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Cardiovascular Diseases; Cattle; Child; Child, Preschool; Dogs; Electrophoresis; Female; Fibrin; Fibrinolysin; Fibrinolysis; Fibrinolytic Agents; Hemorrhage; Hemorrhagic Disorders; Humans; Infant; Male; Menstruation; Methods; Middle Aged; Neoplasms; Plasminogen; Pregnancy; Rabbits; Sex Factors; Thromboembolism; Thrombosis; Uremia

1969
[The problem of hemostatic disorders following extracorporeal circulation].
    Thoraxchirurgie, vaskulare Chirurgie, 1969, Volume: 17, Issue:5

    Topics: Autopsy; Blood Cell Count; Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Blood Preservation; Extracorporeal Circulation; Fibrin; Fibrinolysin; Hemorrhagic Disorders; Heparin; Humans; Kidney; Lung; Methods; Plasminogen; Plastics; Postoperative Complications; Silicon; Thrombosis; Time Factors

1969
[Fibrinolysis in surgical intervention].
    Arkhiv patologii, 1969, Volume: 31, Issue:9

    Topics: Acute Kidney Injury; Esophagus; Extracorporeal Circulation; Fibrin; Fibrinolysis; Hemorrhage; Hemorrhagic Disorders; Humans; Kidney; Lung; Pleura; Pneumonectomy; Postoperative Complications; Splenectomy; Thrombosis

1969
Bleeding syndrome in a patient with IgA myeloma: interaction of protein and connective tissue.
    Blood, 1967, Volume: 29, Issue:6

    Topics: Aged; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Blood Protein Disorders; Calcium; Collagen; Connective Tissue; Fibrin; Fibrinogen; gamma-Globulins; Hemorrhagic Disorders; Humans; Male; Multiple Myeloma; Nitrogen Mustard Compounds; Plasmapheresis; Prothrombin Time; Thromboplastin; Tryptophan

1967
Hypofibrinogenaemia in acute leukaemia with extensive fibrinous pericarditis.
    Australasian annals of medicine, 1967, Volume: 16, Issue:4

    Topics: Adolescent; Afibrinogenemia; Blood Coagulation Disorders; Bone Marrow Cells; Cardiac Tamponade; Factor V Deficiency; Factor VIII; Fibrin; Hemorrhagic Disorders; Humans; Leukemia, Myeloid, Acute; Male; Pericarditis; Pericardium; Staining and Labeling

1967
[Hemorrhagic diathesis with dominant heredity, caused by an abnormal fibrinogen (fibrinogen Baltimore)].
    Schweizerische medizinische Wochenschrift, 1966, Sep-17, Volume: 96, Issue:37

    Topics: Adult; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Neuraminic Acids; Thrombin

1966
DEFECTIVE FIBRINASE ACTIVITY IN TWO BROTHERS.
    The Journal of laboratory and clinical medicine, 1965, Volume: 65

    Topics: Blood Coagulation Factors; Blood Coagulation Tests; Factor XIII; Fibrin; Fibrinolysin; Genetics, Medical; Hemorrhagic Disorders; Humans; Immunoelectrophoresis; Male; Siblings

1965
CONGENITAL DEFICIENCY OF FIBRIN-STABILIZING FACTOR. OBSERVATION OF A NEW CASE.
    The New England journal of medicine, 1965, May-06, Volume: 272

    Topics: Blood Coagulation Disorders; Blood Coagulation Tests; Cerebral Hemorrhage; Child; Diagnosis; Enzymes; Factor XIII; Fibrin; Genetics, Medical; Hemarthrosis; Hematoma; Hematoma, Subdural; Hemorrhagic Disorders; Humans; Knee Joint

1965
[ON THE FIBRIN STABILIZING FACTOR DURING DIFFERENT AGE PERIODS].
    Monatsschrift fur Kinderheilkunde, 1965, Volume: 113

    Topics: Child; Erythroblastosis, Fetal; Factor XIII; Fibrin; Hematologic Diseases; Hemorrhagic Disorders; Humans; Infant; Infant, Newborn; Infant, Premature

1965
CONGENITAL DEFICIENCY OF FIBRIN-STABILISING FACTOR; A REPORT OF THREE UNRELATED CASES.
    Lancet (London, England), 1965, Jul-24, Volume: 2, Issue:7404

    Topics: Blood Transfusion; Child; Factor XIII; Fibrin; Genetics, Medical; Hemorrhagic Disorders; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases

1965
Fibrinase deficiency.
    Israel journal of medical sciences, 1965, Volume: 1, Issue:4

    Topics: Adult; Blood Coagulation; Female; Fibrin; Hemorrhagic Disorders; Humans; Metabolism, Inborn Errors; Plasma

1965
PLASMA FIBRIN STABILIZING FACTOR ACTIVITY IN VARIOUS DISEASES.
    Blood, 1964, Volume: 23

    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

1964
CLINICAL ANESTHESIA CONFERENCE.
    New York state journal of medicine, 1964, Jul-15, Volume: 64

    Topics: Anesthesia; Blood Protein Disorders; Coagulants; Fibrin; Fibrinogen; Hemorrhagic Disorders; Hemostatics; Humans; Postoperative Complications

1964
CURRENT STATUS OF THROMBOLYTIC THERAPY.
    Geriatrics, 1964, Volume: 19

    Topics: Antibodies; Deoxyribonuclease I; Drug Therapy; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemorrhagic Disorders; Niacin; Physiology; Plasminogen; Pyrogens; Streptodornase and Streptokinase; Streptokinase; Thrombolytic Therapy; Thrombosis; Toxicology

1964
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization.
    The Journal of clinical investigation, 1962, Volume: 41

    Topics: Blood Coagulation Disorders; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Plasma; Polymerization; Thrombolytic Therapy

1962
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. III. Demonstration of abnormal clot structure by electron microscopy.
    The Journal of clinical investigation, 1962, Volume: 41

    Topics: Blood Coagulation Disorders; Electrons; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Microscopy; Microscopy, Electron; Thrombolytic Therapy

1962
[The influence of the fibrin-stabilizing factor on the function and morphology of fibroblasts in vitro].
    Zeitschrift fur Zellforschung und mikroskopische Anatomie (Vienna, Austria : 1948), 1962, Volume: 57

    Topics: Connective Tissue; Factor XIII; Fibrin; Fibroblasts; Hemorrhagic Disorders; Humans; In Vitro Techniques; Wound Healing

1962
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. I. The significance of fibrinogen proteolysis and circulating fibrinogen breakdown products.
    The Journal of clinical investigation, 1962, Volume: 41

    Topics: Blood Coagulation Disorders; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Plasma; Proteolysis; Thrombolytic Therapy

1962
[Generalized hemorrhagic diathesis and vascular fibrin precipitations in the secondary stages of experimental fat embolism].
    Die Medizinische Welt, 1962, Oct-06, Volume: 40

    Topics: Embolism; Embolism, Fat; Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Postpartum Hemorrhage; Postpartum Period; Pulmonary Embolism

1962
[Coagulation physiology research in a new coagulation disorder. Deficiency of a fibrin-stabilizing factor].
    Schweizerische medizinische Wochenschrift, 1961, Sep-30, Volume: 91

    Topics: Blood Coagulation; Blood Coagulation Disorders; Factor XIII; Fibrin; Hemorrhagic Disorders; Humans; Vascular Diseases

1961
[A new familial coagulation disorder due to a deficiency of a fibrinstabilizing factor].
    Schweizerische medizinische Wochenschrift, 1961, Sep-30, Volume: 91

    Topics: Blood Coagulation; Blood Coagulation Disorders; Fibrin; Hemorrhagic Disorders; Humans

1961
A haemorrhagic disorder in pregnancy due to an "anticoagulant" preventing the conversion of fibrinogen to fibrin.
    Journal of clinical pathology, 1960, Volume: 13

    A bleeding disorder occurring during labour and affecting mother and foetus is described. All stages of coagulation were normal until the reaction fibrinogen-->fibrin. Either there was some abnormality present in the fibrinogen molecule, or there was an "anticoagulant" acting at this stage. The abnormality was reversible by protamine sulphate and toluidine blue, but in other respects did not resemble hyperheparinaemia. Reversibility of a clotting defect by protamine or toluidine blue is not sufficient evidence on which to make a diagnosis of hyperheparinaemia. Demonstration of a prolonged clotting time occurring in late pregnancy does not necessarily justify the diagnosis of "afibrinogenaemia."

    Topics: Anticoagulants; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Tests; Female; Fibrin; Fibrinogen; Hemorrhagic Disorders; Humans; Pregnancy

1960
[Studies on fibrinolysis in hemorrhagic diathesis].
    Arztliche Forschung, 1958, Mar-10, Volume: 12, Issue:3

    Topics: Fibrin; Fibrinolysis; Hemorrhagic Disorders; Humans; Vascular Diseases

1958
[Defibrination hemorrhage during delivery].
    Munchener medizinische Wochenschrift (1950), 1957, Mar-01, Volume: 99, Issue:9

    Topics: Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Labor, Obstetric; Pregnancy

1957
[Indications for blood derivatives in hemorrhagic syndromes (excluding thrombopenia)].
    Le Sang, 1956, Volume: 27, Issue:1

    Topics: Blood Transfusion; Fibrin; Hemophilia A; Hemorrhagic Disorders; Humans; Hypoprothrombinemias; Prothrombin; Syndrome; Thrombocytopenia

1956
Fibrinogen-fibrin conversion syndrome.
    Western journal of surgery, obstetrics, and gynecology, 1956, Volume: 64, Issue:12

    Topics: Coagulants; Extracellular Space; Fibrin; Fibrinogen; Hemorrhagic Disorders; Hemostatics; Humans

1956
[Fibrinolysis].
    Revista brasileira de cirurgia, 1955, Volume: 29, Issue:6

    Topics: Fibrin; Fibrinolysis; Hemorrhagic Disorders; Humans

1955
[hemorrhage caused by afibrinogenemia and fibrinolysis after delivery; case report].
    Srpski arhiv za celokupno lekarstvo, 1955, Volume: 83, Issue:4

    Topics: Afibrinogenemia; Delivery, Obstetric; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Hemorrhagic Disorders; Humans; Pregnancy

1955
Fibrinolytic activity in the circulating blood following amniotic fluid infusion.
    Acta haematologica, 1955, Volume: 14, Issue:5

    Topics: Amniotic Fluid; Fibrin; Hemorrhage; Hemorrhagic Disorders; Obstetric Labor Complications

1955
[Hemorrhage caused by afibrinemia during a premature abruption of placenta].
    Bulletin de la Federation des societes de gynecologie et dobstetrique de langue francaise, 1955, Volume: 7, Issue:3

    Topics: Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Placenta; Pregnancy

1955
[Hemorrhagic syndrome caused by defibrination during prolonged retention of a dead fetus].
    Bulletin de la Federation des societes de gynecologie et dobstetrique de langue francaise, 1955, Volume: 7, Issue:4

    Topics: Abortion, Induced; Female; Fetus; Fibrin; Hemorrhagic Disorders; Humans; Pregnancy; Stillbirth; Syndrome

1955
[Four new observations on the incoagulability of the blood in afibrinemia].
    Bulletin de la Federation des societes de gynecologie et dobstetrique de langue francaise, 1955, Volume: 7, Issue:5

    Topics: Fibrin; Hemorrhagic Disorders; Humans

1955
Coagulation defects in obstetric shock: meconium embolism and heparin; fibrin embolism and defibrination.
    American journal of obstetrics and gynecology, 1955, Volume: 69, Issue:4

    Topics: Blood Coagulation; Blood Coagulation Disorders; Embolism; Female; Fibrin; Hemorrhagic Disorders; Heparin; Humans; Infant, Newborn; Meconium; Placenta; Pregnancy; Shock

1955
[Complex hemorrhagic diathesis with fibrinolysis in cancer of prostate].
    Lyon medical, 1955, Apr-24, Volume: 87, Issue:17

    Topics: Fibrin; Fibrinolysis; Hemorrhagic Disorders; Humans; Male; Neoplasms; Prostatic Neoplasms

1955
[Case of congenital afibrinemia].
    Orvosi hetilap, 1955, Mar-06, Volume: 96, Issue:10

    Topics: Fibrin; Hemorrhagic Disorders; Humans

1955
[Study of two groups of hemorrhage with afibrinemia; 4 observations].
    Bulletin de la Federation des societes de gynecologie et dobstetrique de langue francaise, 1954, Volume: 6, Issue:1

    Topics: Blood Coagulation; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans

1954
[Bleeding by afibrinemia obstetrics].
    Gynecologie et obstetrique, 1954, Volume: 53, Issue:2

    Topics: Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Obstetric Labor Complications; Obstetrics; Pregnancy

1954
Abnormal plasma proteolytic activity; diagnosis and treatment.
    Surgery, gynecology & obstetrics, 1954, Volume: 99, Issue:6

    Topics: Fibrin; Fibrinolysin; Hemorrhagic Disorders; Plasma

1954
[Hemorrhagic syndrome: the problem of fibrin].
    Laval medical, 1954, Volume: 19, Issue:9

    Topics: Fibrin; Hemorrhagic Disorders

1954
[Fibrinolysis and fibrinolytic syndrome causing mortal hemorrhages due to blood incoagulability].
    Revista brasileira de cirurgia, 1954, Volume: 28, Issue:6

    Topics: Fibrin; Fibrinolysis; Hemorrhage; Hemorrhagic Disorders; Humans; Syndrome; Thrombolytic Therapy

1954
[Haemorrhagic diathesis associated with fibrinogenopenia and fibrinolysis; a report of two cases].
    Acta haematologica, 1952, Volume: 8, Issue:3

    Topics: Afibrinogenemia; Fibrin; Fibrinolysis; Hemorrhagic Disorders

1952
[Hemorrhagic fibrinolysis in hepatics].
    Montpellier medical, 1952, Volume: 41-42, Issue:9

    Topics: Fibrin; Fibrinolysis; Hemorrhagic Disorders; Hepatophyta; Liver Diseases

1952
[Incoagulability of blood due to afibrinogenemia].
    La Presse medicale, 1952, Apr-02, Volume: 60, Issue:22

    Topics: Afibrinogenemia; Blood Coagulation; Fibrin; Hemorrhagic Disorders

1952
[Polycythemia vera with hemorrhagic diathesis and fibrinopenia].
    Ugeskrift for laeger, 1950, Sep-28, Volume: 112, Issue:39

    Topics: Blood Coagulation Disorders; Fibrin; Hemorrhagic Disorders; Humans; Polycythemia Vera

1950
The fibrinopenic diathesis; the great pseudo-hemophilic afibrinemia and hypofibrinemia; the dosage of fibrinogen in hemorrhagic states.
    Le Sang, 1948, Volume: 19, Issue:1

    Topics: Blood; Disease Susceptibility; Fibrin; Hemorrhagic Disorders; Humans

1948