fibrin and Liver-Cirrhosis
fibrin has been researched along with Liver-Cirrhosis* in 72 studies
Reviews
5 review(s) available for fibrin and Liver-Cirrhosis
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Actions of thrombin in the interstitium.
Thrombin is a pleiotropic enzyme best known for its contribution to fibrin formation and platelet aggregation during vascular hemostasis. There is increasing evidence to suggest a role for thrombin in the development of interstitial fibrosis, but interstitial thrombin has not been demonstrated by the direct determination of activity. Rather its presence is inferred by products of thrombin action such as fibrin and activated fibroblasts. This review will focus on possible mechanisms of thrombin formation in the interstitial space, the possible actions of thrombin, processes regulating thrombin activity in the interstitial space, and evidence supporting a role for thrombin in fibrosis. Topics: Animals; Blood Coagulation; Extracellular Matrix; Extracellular Space; Fibrin; Fibrinogen; Fibroblasts; Fibrosis; Hemostasis; Humans; Liver Cirrhosis; Mice; Platelet Aggregation; Prothrombin; Pulmonary Fibrosis; Signal Transduction; Thrombin | 2016 |
Alterations in Fibrin Structure in Patients with Liver Diseases.
The hemostatic balance in patients with liver diseases is relatively well preserved due to concomitant alterations in pro- and antihemostatic pathways. Thrombin generation studies support the notion of hemostatic competence in liver diseases, but in such tests alterations in fibrinogen level and function are not taken into account. We have recently studied structural and functional properties of the fibrin clot in patients with liver diseases. Although we have confirmed previous findings that hypersialylation of the fibrinogen molecule in patients with liver diseases contributes to a defective fibrinogen-to-fibrin conversion, we have found that once the clot has been formed, it has a thrombogenic nature as assessed by permeability assays. These thrombogenic properties of the fibrin clot in cirrhosis relate to incompletely characterized intrinsic changes in the fibrinogen molecule, which may include oxidation and hypersialylation. In addition, in patients with nonalcoholic fatty liver disease thrombogenic properties of the fibrin clot are not only due to liver disease but also to obesity and the metabolic syndrome. During liver transplantation, the clot normalizes and becomes increasingly permeable, and the functional properties of the fibrin clot are markedly normalized by fibrinogen concentrate, when added to plasma samples in vitro. These new insights in the functional properties of the fibrin clot in patients with liver diseases facilitate a more rational approach to treatment and prevention of both bleeding and thrombotic complications. Topics: Fibrin; Fibrinogen; Hemorrhage; Humans; Liver Cirrhosis; Protein Processing, Post-Translational; Thrombosis | 2016 |
[Consumption coagulopathy and liver cirrhosis: etiopathogenesis and diagnosis].
Topics: Afibrinogenemia; Disseminated Intravascular Coagulation; Fibrin; Humans; Kallikreins; Liver; Liver Cirrhosis; Spleen; Thrombocytopenia | 1989 |
[Significance of thrombogenesis in the pathogenesis of arteriosclerosis (literature review)].
Topics: Animals; Aorta; Arteriosclerosis; Blood Coagulation; Blood Coagulation Disorders; Blood Vessels; Endocrine Glands; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Heparin; Heparin Antagonists; Hepatitis; Humans; Lipid Metabolism; Lipoprotein Lipase; Liver; Liver Cirrhosis; Stress, Physiological; Thrombin; Thrombosis; Triglycerides | 1967 |
[THE PHYSIOPATHOLOGY OF FIBRINOLYSIS AND ITS CLINICAL AND THERAPEUTIC APPLICATIONS].
Topics: Blood Transfusion; Enzyme Inhibitors; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemostatics; Humans; Leukemia; Liver Cirrhosis; Male; Pathology; Physiology; Polycythemia Vera; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Prostatectomy; Prostatic Neoplasms; Prothrombin; Thrombin; Thromboplastin | 1964 |
Other Studies
67 other study(ies) available for fibrin and Liver-Cirrhosis
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Fibrin clots from patients with acute-on-chronic liver failure are weaker than those from healthy individuals and patients with sepsis without underlying liver disease.
Previous studies identified decreased clot permeability, without differences in fibrin fiber density in clots, from patients with cirrhosis compared with those from healthy controls (HCs). Fibrinogen hypersialylation could be the reason for this discrepancy.. The aim of this work was to study mechanical properties of clots and reassess clot permeability in relation to hypersialylation in patients with stable cirrhosis, acute decompensation, and acute-on-chronic liver failure (ACLF). Sepsis patients without liver disease were included to distinguish between liver-specific and inflammation-driven phenotypes.. Pooled plasma was used for rheology and permeability experiments. Permeability was assessed with compression using a rheometer and by liquid permeation. Purified fibrinogen treated with neuraminidase was used to study the effects of fibrinogen hypersialylation on liquid permeation.. Mechanical properties of clots from patients with stable cirrhosis and acute decompensation were similar to those of clots from HCs, but clots from patients with ACLF were softer and ruptured at lower shear stress. Clots from sepsis patients without liver disease were stiffer than those from the other groups, but this effect disappeared after adjusting for increased plasma fibrinogen concentrations. Permeability was similar between clots under compression from HCs and clots under compression from patients but decreased with increasing disease severity in liquid permeation. Removal of fibrinogen sialic acid residues increased permeability more in patients than in controls.. Clots from patients with ACLF have weak mechanical properties despite unaltered fibrin fiber density. Previous liquid permeation experiments may have erroneously concluded that clots from patients with ACLF are prothrombotic as fibrinogen hypersialylation leads to underestimation of clot permeability in this setting, presumably due to enhanced water retention. Topics: Acute-On-Chronic Liver Failure; Fibrin; Fibrinogen; Fibrinolysis; Fibrosis; Hemostatics; Humans; Liver Cirrhosis; Sepsis; Thrombosis | 2023 |
Nonmalignant portal vein thrombi in patients with cirrhosis consist of intimal fibrosis with or without a fibrin-rich thrombus.
Portal vein thrombosis (PVT) is a common complication of cirrhosis. The exact pathophysiology remains largely unknown, and treatment with anticoagulants does not lead to recanalization of the portal vein in all patients. A better insight into the structure and composition of portal vein thrombi may assist in developing strategies for the prevention and treatment of PVT.. Sixteen prospectively and 63 retrospectively collected nonmalignant portal vein thrombi from patients with cirrhosis who underwent liver transplantation were included. Histology, immunohistochemistry, and scanning electron microscopy were used to assess structure and composition of the thrombi. Most recent CT scans were reanalyzed for thrombus characteristics. Clinical characteristics were related to histological and radiological findings. All samples showed a thickened, fibrotic tunica intima. Fibrin-rich thrombi were present on top of the fibrotic intima in 9/16 prospective cases and in 21/63 retrospective cases. A minority of the fibrotic areas stained focally positive for fibrin/fibrinogen (16% of cases), von Willebrand factor (VWF; 10%), and CD61 (platelets, 21%), while most of the fibrin-rich areas stained positive for those markers (fibrin/fibrinogen, 100%; VWF, 77%; CD61, 100%). No associations were found between clinical characteristics including estimated thrombus age and use of anticoagulants and presence of fibrin-rich thrombi.. We demonstrate that PVT in patients with cirrhosis consists of intimal fibrosis with an additional fibrin-rich thrombus in only one-third of cases. We hypothesize that our observations may explain why not all portal vein thrombi in patients with cirrhosis recanalize by anticoagulant therapy. Topics: Anticoagulants; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Portal Vein; Retrospective Studies; Thrombosis; Venous Thrombosis; von Willebrand Factor | 2022 |
Fibrin clot quality in acutely ill cirrhosis patients: Relation with outcome and improvement with coagulation factor concentrates.
Patients with liver disease may acquire substantial changes in their hemostatic system, which are most pronounced in patients who are critically ill. Changes in the quality of the fibrin clot in critically ill patients have not been studied in detail. Here we assessed markers of fibrin clot quality and effects of coagulation factor concentrates in patients with acutely decompensated (AD) cirrhosis and acute on chronic liver failure (ACLF).. We measured plasma levels of fibrinogen, factor XIII, prothrombin and performed thrombin generation assays in 52 AD patients, 58 ACLF patients and 40 controls. In addition, we examined the effects of coagulation factor concentrates on functional assays of fibrin quality.. We found increased thrombin generating capacity in both AD and ACLF in comparison with healthy controls. Plasma levels of prothrombin, fibrinogen, and factor XIII were lower in patients compared to controls, appeared lower in ACLF compared to AD patients, and were related to clinical outcomes. Fibrinogen concentrate, but not factor XIII or prothrombin complex concentrate, improved clot quality in vitro. Prothrombin complex concentrate increased the resistance of the clot to break down.. We have demonstrated elevated thrombin generation but decreased plasma levels of prothrombin, fibrinogen and FXIII in acutely ill patients with cirrhosis. In addition, we showed that fibrinogen concentrate and PCCs, but not factor XIII concentrate, improve clot properties in patient plasma. Whether there is true clinical benefit from coagulation factor concentrates in prevention or treatment of bleeding requires further study.. Patients with liver diseases are at risk of bleeding, but mechanisms involved in this bleeding risk are incompletely understood. We studied components that determine the stability of the blood clot and found that concentrations of certain proteins involved in clot stability are present in low levels in acutely ill patients with liver disease. We furthermore demonstrated that some clinically available drugs improve the stability of blood clots from these patients in a test tube. Topics: Blood Coagulation; Blood Coagulation Factors; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Thrombosis | 2022 |
Molecular Magnetic Resonance Imaging of Fibrin Deposition in the Liver as an Indicator of Tissue Injury and Inflammation.
Liver inflammation is associated with nonalcoholic steatohepatitis and other pathologies, but noninvasive methods to assess liver inflammation are limited. Inflammation causes endothelial disruption and leakage of plasma proteins into the interstitial space and can result in extravascular coagulation with fibrin deposition. Here we assess the feasibility of using the established fibrin-specific magnetic resonance probe EP-2104R for the noninvasive imaging of fibrin as a marker of liver inflammation.. Weekly 100 mg/kg diethylnitrosamine (DEN) dosing was used to generate liver fibrosis in male rats; control animals received vehicle. Magnetic resonance imaging at 1.5 T with EP-2104R, a matched non-fibrin-binding control linear peptide, or the collagen-specific probe EP-3533 was performed at 1 day or 7 days after the last DEN administration. Imaging data were compared with quantitative histological measures of fibrosis and inflammation.. After 4 or 5 DEN administrations, the liver becomes moderately fibrotic, and fibrosis is the same if the animal is killed 1 day (Ishak score, 3.62 ± 0.31) or 7 days (Ishak score, 3.82 ± 0.25) after the last DEN dose, but inflammation is significantly higher at 1 day compared with 7 days after the last DEN dose (histological activity index from 0-4, 3.54 ± 0.14 vs 1.61 ± 0.16, respectively; P < 0.0001). Peak EP-2104R signal enhancement was significantly higher in animals imaged at 1 day post-DEN compared with 7 days post-DEN or control rats (29.0% ± 3.2% vs 22.4% ± 2.0% vs 17.0% ± 0.2%, respectively; P = 0.017). Signal enhancement with EP-2104R was significantly higher than control linear peptide at 1 day post-DEN but not at 7 days post-DEN indicating specific fibrin binding during the inflammatory phase. Collagen molecular magnetic resonance with EP-3533 showed equivalent T1 change when imaging rats 1 day or 7 days post-DEN, consistent with equivalent fibrosis.. EP-2104R can specifically detect fibrin associated with inflammation in a rat model of liver inflammation and fibrosis. Topics: Animals; Disease Models, Animal; Fibrin; Gadolinium; Inflammation; Liver; Liver Cirrhosis; Magnetic Resonance Imaging; Male; Peptides; Rats; Rats, Wistar | 2020 |
Haemostatic Profiles are Similar across All Aetiologies of Cirrhosis.
Patients with cirrhosis may acquire profound changes in haemostasis. Although haemostatic changes in cirrhosis have been extensively studied, most studies were performed in groups of patients with mixed aetiology. As thrombotic events appear more common in some aetiologies of disease, notably non-alcoholic steatohepatitis (NASH) and cholestatic disease, we hypothesized that haemostatic changes might be different across aetiologies.. We studied 109 patients with cirrhosis (31 cholestatic liver disease, 23 NASH, 37 alcoholic liver disease [ALD], 18 viral hepatitis) and 44 healthy controls. Patients with malignancy were excluded. Routine diagnostic tests of haemostasis, thrombin generation assays, fibrin permeability assays and a plasma-based fibrinolytic assay were performed.. All patients had comparable severity of disease according to their Model for End-Stage Liver Disease score (9 [7-11]). Plasma levels of von Willebrand factor were substantially elevated across all aetiologies, with a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 levels comparable to controls. Thrombin generation capacity was elevated in all aetiologies, most profoundly in ALD. Fibrin permeability was decreased in all aetiologies, which was accompanied by elevated fibrinogen levels. Clot lysis times were prolonged in NASH and cholestatic disease. Plasma levels of individual proteins were similarly altered in all aetiologies.. Our in-depth haemostatic profiling of primary, secondary and tertiary haemostasis in a group of patients with Childs-Turcotte-Pugh A/B cirrhosis showed no large differences between aetiologies, and was consistent with a general hypercoagulable profile in patients with mild cirrhosis. These results suggest that patients with cirrhosis have an increased risk of thrombosis, irrespective of their aetiology. Topics: Aged; Blood Coagulation; Blood Coagulation Tests; Case-Control Studies; Cholestasis; Female; Fibrin; Fibrinolysis; Fibrosis; Hemostasis; Hemostatics; Hepatitis; Humans; Liver Cirrhosis; Liver Diseases, Alcoholic; Male; Middle Aged; Partial Thromboplastin Time; Thrombin | 2019 |
Portal Vein Thrombosis Repeatedly Observed in a Cirrhotic Patient with Antiphospholipid Antibody Syndrome.
Although portal vein thrombosis in cirrhotic patients is frequently observed, the\ detailed process remains to be clarified, and the role of anticardiolipin antibody in the development of\ portal vein thrombosis has been controversial.. A 52-year-old man, who had been diagnosed with alcoholic cirrhosis of the liver, was\ admitted to our hospital suffering from dyspnea and ascites. Just after being diagnosed as having\ antiphospholipid antibody syndrome with lung thrombosis and delivering a positive result for the β\ 2-glycoprotein I-dependent anticardiolipin antibody, he sustained rupture of the esophageal varices\ with rapid development of portal vein thrombosis, which resolved under anticoagulant therapy. Two\ years later, he was admitted again on suspicion of thrombosis because of an elevation in the serum\ D-dimer level, and computed tomography showed portal and upper mesenteric vein thrombosis.\ Although immediate anticoagulant therapy resulted in complete recanalization, he suffered the same\ episode 2 months later, which occurred with re-elevation of the serum D-dimer level.. A positive finding of an anticardiolipin antibody in cirrhotic patients has been considered\ to be nonspecific and not related to the development of thrombus in the portal vein. This case,\ however, seems to indicate that cirrhotic patients with the β2-glycoprotein I-dependent\ anticardiolipin antibody should be regarded as being at high risk for portal vein thrombosis. Monitoring\ with the serum D-dimer was useful in detecting portal vein thrombosis in its early stage. Topics: Antiphospholipid Syndrome; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Male; Middle Aged; Portal Vein; Tomography, X-Ray Computed; Venous Thrombosis | 2016 |
Phosphatidylserine on blood cells and endothelial cells contributes to the hypercoagulable state in cirrhosis.
The mechanism of thrombogenicity in cirrhosis is largely unknown. Our objective was to study the relationship between phosphatidylserine on blood cells and endothelial cells and the hypercoagulable state in cirrhotic patients.. Patients with cirrhosis and healthy controls were studied. Lactadherin was used to quantify phosphatidylserine exposure on blood cells and endothelial cells. Procoagulant activity of cells was evaluated using clotting time and purified coagulation complex assays. Fibrin production was determined by turbidity. Phosphatidylserine exposure, fibrin strands and FVa/Xa binding on cells were observed using confocal microscopy.. These results lead us to believe that exposed phosphatidylserine on activated or injured erythrocytes, platelets, leucocytes and endothelial cells plays an important role in the hypercoagulable state in cirrhotic patients. Thus, blocking phosphatidylserine binding sites might be a new therapeutic target for preventing thrombosis. Topics: Adult; Blood Cells; Blood Coagulation Tests; Blood Platelets; Case-Control Studies; Cell-Derived Microparticles; China; Endothelial Cells; Female; Fibrin; Humans; Liver Cirrhosis; Male; Middle Aged; Phosphatidylserines; Thrombin; Thrombophilia | 2016 |
Chronic passive venous congestion drives hepatic fibrogenesis via sinusoidal thrombosis and mechanical forces.
Chronic passive hepatic congestion (congestive hepatopathy) leads to hepatic fibrosis; however, the mechanisms involved in this process are not well understood. We developed a murine experimental model of congestive hepatopathy through partial ligation of the inferior vena cava (pIVCL). C57BL/6 and transgenic mice overexpressing tissue factor pathway inhibitor (SM22α-TFPI) were subjected to pIVCL or sham. Liver and blood samples were collected and analyzed in immunohistochemical, morphometric, real-time polymerase chain reaction, and western blot assays. Hepatic fibrosis and portal pressure were significantly increased after pIVCL concurrent with hepatic stellate cell (HSC) activation. Liver stiffness, as assessed by magnetic resonance elastography, correlated with portal pressure and preceded fibrosis in our model. Hepatic sinusoidal thrombosis as evidenced by fibrin deposition was demonstrated both in mice after pIVCL as well as in humans with congestive hepatopathy. Warfarin treatment and TFPI overexpression both had a protective effect on fibrosis development and HSC activation after pIVCL. In vitro studies show that congestion stimulates HSC fibronectin (FN) fibril assembly through direct effects of thrombi as well as by virtue of mechanical strain. Pretreatment with either Mab13 or Cytochalasin-D, to inhibit β-integrin or actin polymerization, respectively, significantly reduced fibrin and stretch-induced FN fibril assembly.. Chronic hepatic congestion leads to sinusoidal thrombosis and strain, which in turn promote hepatic fibrosis. These studies mechanistically link congestive hepatopathy to hepatic fibrosis. Topics: Actins; Adult; Aged; Animals; Anticoagulants; Case-Control Studies; Cells, Cultured; Disease Models, Animal; Female; Fibrin; Fibronectins; Hepatic Stellate Cells; Humans; Hyperemia; Ligation; Liver Circulation; Liver Cirrhosis; Male; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; Thrombosis; Vena Cava, Inferior; Young Adult | 2015 |
Hepatic congestion leads to fibrosis: findings in a newly developed murine model.
Topics: Actins; Animals; Female; Fibrin; Humans; Hyperemia; Liver Cirrhosis; Male; Thrombosis | 2015 |
Ruptured varix: tips to tackle the demon.
Topics: Abdomen, Acute; Blood Platelets; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Fibrin; Hematemesis; Humans; Hypertension, Portal; Ligation; Liver Cirrhosis; Male; Middle Aged; Pressure; Rupture, Spontaneous; Treatment Outcome; Varicose Veins | 2015 |
The antifibrinolytic drug tranexamic acid reduces liver injury and fibrosis in a mouse model of chronic bile duct injury.
Hepatic fibrin deposition has been shown to inhibit hepatocellular injury in mice exposed to the bile duct toxicant α-naphthylisothiocyanate (ANIT). Degradation of fibrin clots by fibrinolysis controls the duration and extent of tissue fibrin deposition. Thus, we sought to determine the effect of treatment with the antifibrinolytic drug tranexamic acid (TA) and plasminogen activator inhibitor-1 (PAI-1) deficiency on ANIT-induced liver injury and fibrosis in mice. Plasmin-dependent lysis of fibrin clots was impaired in plasma from mice treated with TA (1200 mg/kg i.p., administered twice daily). Prophylactic TA administration reduced hepatic inflammation and hepatocellular necrosis in mice fed a diet containing 0.025% ANIT for 2 weeks. Hepatic type 1 collagen mRNA expression and deposition increased markedly in livers of mice fed ANIT diet for 4 weeks. To determine whether TA treatment could inhibit this progression of liver fibrosis, mice were fed ANIT diet for 4 weeks and treated with TA for the last 2 weeks. Interestingly, TA treatment largely prevented increased deposition of type 1 collagen in livers of mice fed ANIT diet for 4 weeks. In contrast, biliary hyperplasia/inflammation and liver fibrosis were significantly increased in PAI-1(-/-) mice fed ANIT diet for 4 weeks. Overall, the results indicate that fibrinolytic activity contributes to ANIT diet-induced liver injury and fibrosis in mice. In addition, these proof-of-principle studies suggest the possibility that therapeutic intervention with an antifibrinolytic drug could form a novel strategy to prevent or reduce liver injury and fibrosis in patients with liver disease. Topics: 1-Naphthylisothiocyanate; Animals; Antifibrinolytic Agents; Bile Duct Diseases; Collagen Type I; Disease Models, Animal; Fibrin; Fibrinogen; Liver; Liver Cirrhosis; Mice; Mice, Inbred C57BL; Mice, Knockout; Plasminogen Activator Inhibitor 1; Tranexamic Acid | 2014 |
Higher prognostic value of soluble fibrin complexes than D-dimer and fibrin degradation product for disseminated intravascular coagulation in patients with liver cirrhosis.
Fibrin-related markers may help differentiate disseminated intravascular coagulation (DIC) from liver cirrhosis-associated dysfunctional coagulation. We investigated the significance of three fibrin-related markers [D-dimer, fibrin degradation product (FDP), and soluble fibrin complexes (sFC)] for the assessment of DIC status and prognosis. We classified 235 patients with suspected DIC into two groups according to their condition: the liver cirrhosis group (n = 47) and the no liver cirrhosis group (n = 188). Prothrombin time (PT), and fibrinogen, sFC, D-dimer, antithrombin, and protein C concentrations were measured and DIC scores were calculated using four parameters: platelet count, D-dimer, fibrinogen, and PT. In the liver cirrhosis group, the sFC concentration increased significantly in accordance with DIC score compared with the no liver cirrhosis group, and this increase was more prominent than D-dimer and FDP concentration increases. For the diagnosis of overt DIC in patients with liver cirrhosis, the area under the concentration curve (AUC) was larger for sFC (0.746) than for D-dimer (0.733) and FDP (0.687). Cox analysis also indicated that an elevated sFC concentration is a more significant prognostic factor of DIC than D-dimer or FDP (hazard ratio: 10.78; P = 0.036) in liver cirrhosis group; however, it was not a prognostic factor in the no liver cirrhosis group. sFC is a powerful diagnostic and prognostic marker of DIC in patient with liver cirrhosis. The use of sFC is expected to enhance the diagnosis and prognosis of DIC, particularly in patients with liver cirrhosis. Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Child; Disseminated Intravascular Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Liver Cirrhosis; Middle Aged; Prognosis; Young Adult | 2013 |
Fibrinogen deficiency increases liver injury and early growth response-1 (Egr-1) expression in a model of chronic xenobiotic-induced cholestasis.
Chronic cholestatic liver injury induced by cholestasis in rodents is associated with hepatic fibrin deposition, and we found evidence of fibrin deposition in livers of patients with cholestasis. Key components of the fibrinolytic pathway modulate cholestatic liver injury by regulating activation of hepatocyte growth factor. However, the exact role of hepatic fibrin deposition in chronic cholestasis is not known. We tested the hypothesis that fibrinogen (Fbg) deficiency worsens liver injury induced by cholestasis. Fbg-deficient mice (Fbgα(-/-) mice) and heterozygous control mice (Fbgα(+/-) mice) were fed either the control diet or a diet containing 0.025% α-naphthylisothiocyanate (ANIT), which selectively injures bile duct epithelial cells in the liver, for 2 weeks. Hepatic fibrin and collagen deposits were evident in livers of heterozygous control mice fed the ANIT diet. Complete Fbg deficiency was associated with elevated serum bile acids, periportal necrosis, and increased serum alanine aminotransferase activity in mice fed the ANIT diet. Fbg deficiency was associated with enhanced hepatic expression of the transcription factor early growth response-1 (Egr-1) and enhanced induction of genes encoding the Egr-1-regulated proinflammatory chemokines monocyte chemotactic protein-1, KC growth-regulated protein, and macrophage inflammatory protein-2. Interestingly, peribiliary collagen deposition was not evident near necrotic areas in Fbg-deficient mice. The results suggest that in this model of chronic cholestasis, fibrin constrains the release of bile constituents from injured intrahepatic bile ducts, thereby limiting the progression of hepatic inflammation and hepatocellular injury. Topics: 1-Naphthylisothiocyanate; Afibrinogenemia; Aged; Animals; Bile Ducts; Cholestasis; Chronic Disease; Collagen; Diet; Disease Models, Animal; Early Growth Response Protein 1; Feeding Behavior; Female; Fibrin; Fibrinogen; Gene Expression Regulation; Humans; Hyperplasia; Inflammation; Liver; Liver Cirrhosis; Male; Mice; Middle Aged; Neutrophils; Xenobiotics | 2011 |
Vascular invasion and herniation by hepatocellular carcinoma in cirrhosis: A wolf in sheep's clothing?
Vascular invasion is an important diagnostic and prognostic feature of hepatocellular carcinoma (HCC) in cirrhosis. Intravascular free-floating tumor clusters (IvCs) of HCC are found histologically in the vicinity of HCC. Thrombus formation is not seen morphologically in association with these IvCs, which are usually covered by endothelium.. Our hypothesis is that these IvCs are the result of a nondestructive form of vascular invasion by HCC, and we tried to define this aspect of microvascular invasion more accurately.. Tissue sections were stained with hematoxylin-eosin, and consecutive sections were stained for fibrin (Martius scarlet blue, fibrinogen), platelets (factor XIIIa), smooth muscle actin, and endothelium (CD34). We studied cirrhotic livers removed at transplantation between 1997 and 1999. Of the livers studied, 35 of 81 consecutive cirrhotic livers contained HCC, and 17 showed microscopic vascular invasion. Five of these 17 cases showed IvCs and were subjected to the study.. Presence or absence of thrombus formation in association with IvC.. Usually, IvCs were covered by endothelium, and no associated thrombus formation was seen. In 1 case of HCC, thrombus formation was seen focally in association with disruption of the endothelial coating.. We propose that the endothelial-lined trabecular structure of HCC everts, frondlike, via vascular structures within the tumor capsule into peritumoral vascular lumens without destruction of the endothelial coating. This may protect these HCC tumor projections from thrombus formation but may also act as a barrier to tumor extravasation, and this may be exploited from a therapeutic point of view. Topics: Actins; Adult; Biomarkers, Tumor; Carcinoma, Hepatocellular; Endothelium, Vascular; Factor XIIIa; Female; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Neoplasm Invasiveness; Neoplastic Cells, Circulating; Receptors, Complement 3b | 2005 |
[Alterations of hemostasis in liver cirrhosis of the dog].
In seven dogs with histologically proven liver cirrhosis the activity of the single coagulation factors with the exception of factor VIII:C, of the inhibitors antithrombin III and protein C as well as plasminogen and alpha 2-antiplasmin was distinctly lower than in the control group (p < 0.0001). The changes of the factors VII [median (x0.50) = 17 %] and X (x0.50 = 18 %) as well as of protein C (x0.50 = 15 %) were particularly pronounced. Diminution of activity certainly exceeded also in nearly all of the remaining haemostatic proteins the decrease of albumin concentration. Besides the shorter half life time, this reflected an increased consumption in consequence of intravascular coagulations and fibrinolysis. The latter could also be seen from the significantly increased concentrations of soluble fibrin and fibrin(ogen) degradation products. Therefore, the alterations of the haemostatic system measured in dogs in many details were in accordance with findings in human beings suffering from liver cirrhosis. Topics: Animals; Blood Coagulation Factors; Dog Diseases; Dogs; Fibrin; Fibrinogen; Hemostasis; Humans; Liver Cirrhosis; Reference Values | 1998 |
Measuring plasma fibrinogen levels in patients with liver cirrhosis. The occurrence of proteolytic fibrin(ogen) degradation products and their influence on several fibrinogen assays.
In patients with liver cirrhosis the fibrinogen molecule is under constant attack of various proteolytic enzymes, which might affect results of the different assay systems for fibrinogen. We therefore studied the measurement of fibrinogen in the plasma of patients with mild, moderate and severe cirrhosis of the liver. Fibrinogen levels were measured with the Clauss method (functional fibrinogen); an enzyme immuno assay (EIA) for HMW + L MW fibrinogen; and an assay that measures the total clottable fibrinogen. With all three methods we found normal or slightly increased fibrinogen levels in patients with mild or moderate cirrhosis, whereas patients with severe cirrhosis had decreased levels. No evidence was found for increased partial fibrinogen proteolysis, resulting in increases of LMW'-fibrinogen in cirrhotic patients. We further observed that fibrinogen degradation products levels increased slightly with the severity of the disease, but were still in the normal range in patients with severe cirrhosis. This indicates a very low level of primary fibrinolysis. Fibrin degradation products levels increased much stronger, which points to intravascular coagulation. The levels of the fibrin degradation products remained below the level where they are expected to influence the Clauss assay. In patients with liver cirrhosis the measurement of plasma fibrinogen levels with the three studied methods give comparable results. We suggest to apply the Clauss assay in cirrhotic patients because of this and because it has good reproducibility and because the test is cheap, quick and easy to perform. Topics: Child; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Liver Cirrhosis | 1995 |
Disordered hemostasis in extrahepatic portal hypertension.
To assess the contribution of naturally occurring portal-systemic shunts to the coagulopathy of patients with liver disease, we studied laboratory parameters of hemostasis in 20 adult patients with extrahepatic portal hypertension, secondary to portal vein thrombosis, that had resulted in variceal bleeding. All extrahepatic portal hypertension patients had normal liver function and histological appearance. None had any evidence of preexisting coagulation disorders, and none had bled or undergone sclerotherapy in the 6 mo before study. Age- and gender-matched groups of 20 healthy individuals and 20 stable patients with cirrhosis and portal hypertension who had a history of variceal bleeding served as controls. Both patient groups had thrombocytopenia consistent with hypersplenism and portal hypertension. Prothrombin international normalized ratio (extrahepatic portal hypertension, 1.3 +/- 0.12; cirrhosis, 1.7 +/- 0.2; control, 1.02 +/- 0.06; p < 0.05) and partial thromboplastin time ratios (extrahepatic portal hypertension, 1.12 +/- 0.1; cirrhosis, 1.26 +/- 0.2; controls, 1.01 +/- 0.03; p < 0.05) were significantly prolonged in both patient groups. Extrahepatic portal hypertension and cirrhotic patient groups had significantly increased levels of serum total fibrin(ogen)-related antigen (extrahepatic portal hypertension, 818 +/- 150 ng/ml; cirrhosis, 454 +/- 52 ng/ml; controls, 124 +/- 7.3 ng/ml; p < 0.05), fibrin monomer (extrahepatic portal hypertension, 168.8 +/- 16.9 ng/ml; cirrhosis, 115.6 +/- 11.1 ng/ml; controls, 19.7 +/- 0.4 ng/ml; p < 0.05) and D-dimer (extrahepatic portal hypertension, 118 +/- 9.6 ng/ml; cirrhosis, 129 +/- 10 ng/ml; controls, 53.2 +/- 1.6 ng/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Adult; Blood Coagulation; Blood Coagulation Factors; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemostasis; Humans; Hypertension, Portal; Liver Cirrhosis; Male; Middle Aged; Plasminogen Activator Inhibitor 1; Portal Vein; Thrombosis | 1993 |
Disseminated intravascular coagulation in liver cirrhosis.
We measured thrombin-antithrombin III complex (TAT), soluble fibrin (SF) and D-dimer levels in 51 patients with liver cirrhosis to determine whether these tests provide new evidence for the presence of disseminated intravascular coagulation (DIC) in liver cirrhosis. TAT levels (median, range) were increased in the patient group (4.2 micrograms/l, 1.8-60.0) compared to the reference group (2.0 micrograms/l, range 1.5-7.6 micrograms/l). SF levels (0 nmol/l, range 0-80 nmol/l) were also increased in the patients as compared to the controls (0 nmol/l, 0), but there was no correlation between TAT and SF levels (r = 0.23, p less than 0.98). TAT levels did not correlate with AT-III levels (r = -0.36, p less than 0.49), but there was an inverse correlation between SF and AT-III (r = 0.60, p less than 0.001). If AT-III levels were above 0.30 U/ml, SF levels remained low, whereas SF levels were increased in patients with AT-III levels below 0.30 U/ml. These findings suggest that if sufficient AT-III is present, thrombin formation is adequately controlled, whereas at low levels of AT-III, thrombin escapes inactivation by AT-III and may act upon fibrinogen, leading to the formation of SF and a low-grade DIC. SF levels correlated well with D-dimer levels (r = 0.55, p less than 0.001), which is consistent with DIC and secondary fibrinolysis.. (1) thrombin formation is increased in liver cirrhosis, as indicated by increased TAT levels in 21 of 51 patients; (2) the plasma concentration of AT-III appears to be of major importance for the development of DIC. The present study provides evidence for DIC in severe liver cirrhosis when AT-III levels are less than 0.30 U/ml. Topics: Adult; Aged; Antithrombin III; Disseminated Intravascular Coagulation; Female; Fibrin; Humans; Liver Cirrhosis; Male; Middle Aged; Peptide Hydrolases; Statistics as Topic | 1992 |
A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis.
The aim of this study was to assess the cause of enhanced fibrinolysis in cirrhosis by studying the balance between profibrinolytic and antifibrinolytic proteins in 24 patients with mild or severe cirrhosis. Antigen levels of both tissue-type plasminogen activator and plasminogen-activator inhibitor 1 were increased in mild and severe cirrhosis. Activity levels showed a very wide variability, but median activity levels of both proteins were normal. In most patients, the increase in tissue-type plasminogen activator was counterbalanced by the increased levels of plasminogen-activator inhibitor 1, but in a subgroup of patients the change in balance resulted in extremely high tissue-type plasminogen-activator levels. The specific activity of both proteins (activity/antigen quotient) was reduced in either mild or severe cirrhosis. This finding indicates either that more enzyme-inhibitor complexes circulate in the blood of patients with cirrhosis than in normal individuals or that dysfunctional molecules circulate. Plasminogen and alpha 2-antiplasmin antigen and activity levels were decreased in both mild and severe cirrhosis. The binding of alpha 2-antiplasmin to fibrin was decreased in severe cirrhosis, making fibrin clots more susceptible to lysis. Clot lysis experiments were performed to see if equal decreases in plasminogen and alpha 2-antiplasmin levels, as found in cirrhosis, result in a change in the rate of fibrinolysis. It was found that the proportionate decreases led to enhancement of fibrinolysis, indicating that the inhibitor depletion is more important than the proenzyme depletion. The authors conclude that enhanced fibrinolysis frequently found in cirrhosis may be attributed to an increased tissue-type plasminogen-activator activity relative to plasminogen-activator-inhibitor activity and decreased levels of alpha 2-antiplasmin, resulting in a reduced binding of alpha 2-antiplasmin to fibrin. Topics: alpha-2-Antiplasmin; alpha-Macroglobulins; Fibrin; Fibrinolysin; Fibrinolysis; Humans; Liver Cirrhosis; Plasminogen; Plasminogen Inactivators; Protein Binding; Tissue Plasminogen Activator | 1991 |
Incidence and clinical significance of elevated fibrin(ogen) degradation product and/or D-dimer levels in liver cirrhosis patients.
Fibrin(ogen) degradation product (FDP) and D-dimer levels were evaluated in 168 liver cirrhosis (LC) patients without evidence of bleeding. Eighty-two (48%) had FDP higher than 10 micrograms/ml; only 43 of them had a concomitant increase of D-dimer. These alterations were more frequent in older and decompensated patients and correlated to the Child-Turcotte score. In the patients with elevated FDP and/or D-dimer levels the mean values of platelets, prothrombin activity and fibrinogen were not significantly different from those of the other patients and remained fairly stable over the period of the study. Finally, an increase of FDP is frequent in LC and this may suggest a diagnosis of disseminated intravascular coagulation (DIC), but a concomitant increase of D-dimer is rarely detectable, thus excluding this diagnosis. Moreover, even in the cases with increased levels of D-dimer the presence of clinical or laboratory evidence of a consumption coagulopathy, expression of a manifest DIC, seems to be unusual. Topics: Adult; Aged; Aged, 80 and over; Analysis of Variance; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Liver Cirrhosis; Male; Middle Aged; Platelet Count; Prothrombin | 1990 |
[Fibrin glue injection--a hemostatic technic after laparoscopic liver biopsy].
Fibrin glue was injected into or near the site of needle biopsy puncture in 33 patients (38 laparoscopically guided liver biopsies), 21 with histologically confirmed liver cirrhosis, to arrest post-puncture bleeding. A special double-lumen needle was introduced, suitable for multiple injections. Fibrin-glue injection was successful in 37 instances, but in one case it failed because the injection needle could not be optimally placed. The method thus seems to be a reliable and sensible means of obtaining haemostasis if compression and electrocoagulation have failed. Topics: Adult; Aged; Aprotinin; Biopsy, Needle; Drug Combinations; Factor XIII; Female; Fibrin; Fibrin Tissue Adhesive; Fibrinogen; Hemostatic Techniques; Humans; Laparoscopy; Liver; Liver Cirrhosis; Male; Middle Aged; Thrombin; Tissue Adhesives | 1989 |
A DIC-like picture on plasma and ascitic fluid of cirrhotic patients.
Ascitic fluid reinfusion in severe cirrhosis has frequently been associated with intravascular coagulation (DIC). A low-grade DIC has been postulated to be present in liver cirrhosis. PT, APTT, fibrinogen, plasminogen, antiplasmin, fibrin degradation producers (FDP), euglobulin lysis time, tissue plasminogen activator, and fibrinopeptide A were investigated both in the plasma and ascitic fluid of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicate that increased thrombin formation associated with hyperfibrinolysis is present in the plasma of cirrhotic patients. In ascitic fluid very high levels of thrombin and fibrinolysis activation were found. We conclude that (1) a DIC-like picture exists in ascites and (2) after ascites reinfusion procedures, ascitic fluid is the principal factor in the pathogenesis of DIC. During ascitic fluid reinfusion heparin treatment could be used successfully. Topics: Aged; Ascites; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinopeptide A; Humans; Liver Cirrhosis; Male; Middle Aged; Partial Thromboplastin Time; Plasminogen; Prothrombin Time; Reference Values; Tissue Plasminogen Activator | 1988 |
Sensitive and rapid measurement of fibrin polymerisation by laser nephelometry.
Topics: Batroxobin; Biopolymers; Colorimetry; Fibrin; Humans; Kinetics; Liver Cirrhosis; Nephelometry and Turbidimetry | 1986 |
[Diagnostic significance of proteolytic breakdown products of fibrinogen and fibrin].
Topics: Disseminated Intravascular Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Fibrinolysis; Glomerulonephritis; Hemostasis; Humans; Liver Cirrhosis; Postoperative Complications; Pulmonary Embolism; Thrombin; Thromboembolism; Thrombophlebitis | 1984 |
[Changes in fibrin formation in liver cirrhosis].
Topics: Adult; Blood Coagulation Disorders; Fetal Blood; Fibrin; Fibrinogen; Humans; Infant, Newborn; Liver; Liver Cirrhosis | 1982 |
[Abnormal fibrin polymerization and its clinical usefulness in patients with chronic liver disease (author's transl)].
Topics: Adolescent; Adult; Blood Coagulation Tests; Child; Chronic Disease; Esophageal and Gastric Varices; Female; Fibrin; Humans; Liver Cirrhosis; Liver Diseases; Male; Middle Aged; Polymers; Portacaval Shunt, Surgical; Prognosis | 1981 |
Structure of fibrin and fibrinmonomer in renal and hepatic failure.
After reduction and splitting of disulfide linkages the fibrinmonomer and fibrin of 45 patients with histologically confirmed liver cirrhosis and 38 patients with chronic renal failure (serum creatinine greater than 5 mg%) were analysed by SDS-PAA electrophoresis. Furthermore the activity of factor XIII was measured immunologically. The results indicated no polymerization of alpha-chains of fibrin while gamma-dimers were formed regularly in 71% of patients with liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis the lack of alpha-polymerization correlated to the severity of the disease and to the decrease of factor XIII activity (no alpha-polymers formed when below 80% of normal). In renal failure this correlation was not demonstrable since in all cases the activity of factor XIII was within the normal range. After the addition of C14-labelled urea to normal plasma during clotting an incorporation of this tracer could be demonstrated by scintiscanner diamins like urea, forming in the course of renal failure, probably serve as the "wrong substrate" for the transaminidase factor XIII. Topics: Factor XIII; Fibrin; Fibrinogen; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Protein Conformation | 1980 |
Investigations on intravascular coagulation in liver disease: souble fibrin monomer complexes in liver cirrhosis.
Souble fibrin monomer complexes (SFMC) have been quantitated in 18 patients with liver cirrhosis by means of plasma gel filtration on an agarose column. The concentration of SFMC (as related to total fibrinogen) was increased in cirrhotic patients. The difference between controls and patients, as well as the difference between compensated and decompensated cirrhotic subjects, was statisically significant. Although these data, together with the results of heparin administration in one reported case, suggest intravascular coagulation, some alternative explanations should also be considered. Topics: Bacteriological Techniques; Blood Coagulation; Blood Coagulation Tests; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Heparin; Humans; Injections, Subcutaneous; Liver Cirrhosis; Liver Diseases; Solubility; Staphylococcus | 1979 |
[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)].
The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices. Topics: Blood Coagulation Disorders; Blood Platelets; Cell Count; Electrophoresis, Polyacrylamide Gel; Factor XIII; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Hemostasis; Humans; Liver Cirrhosis; Sodium Dodecyl Sulfate | 1978 |
Quantitative abnormality of an Aalpha chain molecular weight form in the fibrinogen of cirrhotic patients.
The molecular weight heterogeneity of fibrinogen from the whole plasma of 12 normal and seven cirrhotic individuals was examined by means of a novel two-dimensional sodium dodecyl suphate (SDS) gel electrophoretic technique. Fibrinogen was first separated from other plasma proteins on a large pore gel, cut out of the gel, reduced, and separated into its component Aalpha, Bbeta and gamma chains on a second gel. Fibrinogen was resolved into two major bands, I and II, on the first gel. The ratio of fibrinogen II to fibrinogens I plus II was approximately 0.3 (range 0.2-0.35) for both normals and cirrhotic patients. Two major molecular weight (mol wt) forms of Aalpha chain were present in normal fibrinogen I: Aalpha/I and/or Aalpha/2, mol wt 7 X 10(4) and 6.7 X 10(4) respectively. Normal fibrinogen II contained either one of these Aalpha chains plus one of the smaller Aalpha chains, Aalpha/6--10, accounting for the 3--4 X 10(4) mol wt difference between bands I and II. Aalpha/2 comprised 33% of the total Aalpha chains (range 27--41%) in normal fibrinogen I and approximately 25% of the Aalpha chains in normal fibrinogen II. In contrast, fibrinogen I from six out of the seven patients contained a lower percentage of Aalpha/2 (range 10--25%). Similarly fibrinogen II from these patients was deficient in Aalpha/2, although the protein contained normal levels of lower mol wt Aalpha derivatives. No correlation was found between per cent fibrinogen II and per cent Aalpha/2 in either normal or cirrhotic subjects. These results suggest that at least two independent processes are responsible for the observed levels of Aalpha heterogeneity in normals and cirrhotics and that the process controlling Aalpha/2 production is a abnormal in cirrhotic individuals. This decrease in Aalpha/2 does not affect the coagulability of fibrinogen. Fibrin monomer aggregation studies indicate that a serum component is, in part, responsible for the abnormally transparent clot formed from the plasma of cirrhotics. Topics: Blood Coagulation Tests; Densitometry; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Male; Molecular Weight; Thrombin | 1978 |
Association of abnormal fibrin polymerisation with severe liver disease.
The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices. Topics: Aspartate Aminotransferases; Bilirubin; Blood Coagulation Disorders; Chronic Disease; Factor VII; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Liver Diseases; Prothrombin Time; Serum Albumin; Serum Globulins | 1977 |
[The detection of soluble fibrin complexes by a haemagglutination test. Clinical applications (author's transl)].
Testing for soluble fibrin complexes was performed using a sensitive and reliable haemagglutination assay, with red cells sensitized by fibrin monomers. The principle is based on the fact that the monomers linked to red cells and induce their agglutination. This test, used in clinical trials, has revealed the presence of soluble complexes in every confirmed case of acute DIC, but also in Chronic DIC where diagnosis is difficult to establish (negative ethanol gelation test, normal or sub-normal levels of fibrin breakdown products). In Cirrhosis of the liver, the test gives positive results in a non negligible number of cases. Several hypotheses are made to explain why in certain confirmed cases of DIC, low fibrin breakdown products levels are found. Topics: Aged; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Hemagglutination Tests; Humans; Liver Cirrhosis; Male; Prostatic Neoplasms; Solubility; Surgical Procedures, Operative; Thromboembolism | 1977 |
Impaired fibrin formation in advanced cirrhosis.
The process of fibrin formation was systematically in 25 patients with severe alcoholic cirrhosis. Results of functional tests are reported. A significant lengthening of the thrombin time was found which could not be completely attributed either to hypofibrinogenaemia or to an increase in physiological anticoagulants or to the presence of pathological antithrombins. A defect in fibrin polymerization was seen in the absence of significant levels of antipolymerizing agents. Indirect evidence pointed to an abnormal fibrinogen function. This was mainly suggested by the "polymerization curves" of mixtures of normal and pathological plasmas and the changes in physico-chemical properties of the clot (optical and elastic properties; tensile strength). Altered synthesis in hepatocytes may lead to an "acquired dysfibrinogenaemia" in the late stages of liver cirrhosis, although alteration of a normal fibrinogen molecule after secretion cannot be definitely excluded. Topics: Adult; Aged; Blood Coagulation Tests; Fibrin; Fibrinogen; Fibrinolysis; Humans; Liver Cirrhosis; Middle Aged; Polymers; Thrombin; Time Factors | 1977 |
Dysfibrinogenemia associated with liver disease.
To test the possibility that a functionally abnormal fibrinogen may exist in some patients with liver disease, we studied the plasma and purified fibrinogens of five patients whose plasma thrombin times were prolonged at least 40% over normal controls. In no patient was there evidence of disseminated intravascular coagulation and/or fibrinolysis. No abnormalities were detected by immunoelectrophoresis of plasmas or purified fibrinogens. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of reduced patient fibrinogens showed normal mobility and amount of Aalpha, Bbeta, and gamma chains. Alkaline polyacrylamide gel electrophoresis and gradient elution, DEAE-cellulose chromatography of admixtures of radio-iodinated patient (125)I-fibrinogen and normal (131)I-fibrinogen showed identical mobility in the gel and simultaneous elution from the column, respectively. Thrombin and Reptilase (Abbott Scientific Products Div., Abbott Laboratories, South Pasadena, Calif.) times of purified patient fibrinogens were prolonged, and calcium ions improved but did not completely correct these defects. Increasing amounts of thrombin progressively shortened the clotting times of patient fibrinogens but not to the level of normal. Addition of equal amounts of patient fibrinogen to normal fibrinogen resulted in a prolongation of the thrombin time of the normal protein. Thrombin-induced fibrinopeptide release was normal. Fibrin monomers prepared from patient plasmas and purified fibrinogens demonstrated impaired aggregation at low (0.12) and high (0.24) ionic strength. These studies demonstrate that some patients with liver disease and prolonged plasma thrombin times have a dysfibrinogenemia functionally characterized by an abnormality of fibrin monomer polymerization. Topics: Alcoholism; Batroxobin; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Chemical and Drug Induced Liver Injury; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Liver Diseases; Prothrombin Time; Thrombin | 1977 |
[Localization of HBsAg, immunoglobulins, fibrin and C3 in the liver by direct immunoflourescence].
Liver biopsies of sixty patients with different forms of hepatitis and ten control subjects without hepatic disorders were examined by means of direct immunofluorescent methods for the HBsAg, immunoglobulins, fibrin and C3. The presence of fluorescent particles of HBsAg in the cytoplasm of hepatocytes were correlated with the presence of HBsAg in the serum. The fluorescence did not seem specific of histological stage of hepatitis. Immunoglobulins and fibrin were often demonstrated in hepatic sinusoids, especially in chronic aggressive hepatitis. In contrast, C3 is rarely observed. Topics: Biopsy; Complement C3; Complement System Proteins; Cytoplasm; Epitopes; Fatty Liver; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Hepatitis; Hepatitis B Antigens; Humans; Immunoglobulins; Liver; Liver Cirrhosis; Liver Diseases; Renal Dialysis | 1976 |
Abnormal fibrin polymerization in liver disease.
Although there have been isolated reports of an acquired abnormal fibrinogen in patients with liver disease, its frequency and clinical significance is not known. In this study 121 consecutive patients with a wide spectrum of hepatic disorders were screened for abnormal fibrin polymerization. A simple colorimetric method using Reptilase was employed. Of 32 patients with proven cirrhosis, 16 (50%) showed abnormal fibrin polymerization. The incidence in decompensated alcoholic cirrhosis was particularly high. The abnormality was also detected in all patients with acute liver failure and seven of 15 with chronic active liver disease. Clinical improvement often correlated with its disappearance. Two patients with primary liver cell tumours demonstrated the abnormal polymerization. In patients with bleeding oesophageal varices the detection of abnormal fibrin polymerization was associated with a poor prognosis. None of the patients with surgical obstructive jaundice (26) or miscellaneous liver disorders (37) had abnormal fibrin polymerization. The occurrence of abnormal fibrin polymerization in liver disease is more frequent than previously suspected and usually signifies severe primary hepatocellular dysfunction. Evidence is presented to support the presence of a primary abnormality of fibrinogen as the cause of impaired fibrin monomer polymerization. Topics: Batroxobin; Blood Coagulation Tests; Carcinoma, Hepatocellular; Cholestasis; Chronic Disease; Fibrin; Fibrinogen; Hepatic Encephalopathy; Humans; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Polymers; Thrombin; Time Factors | 1976 |
[Fibrin structure in hepatitis and liver cirrhosis].
Topics: Blood Protein Electrophoresis; Fibrin; Hepatitis; Humans; Liver Cirrhosis; Platelet Aggregation | 1976 |
Heparin cofactor activity measured with an amidolytic method.
Topics: Acute Disease; Alpha-Globulins; Antithrombin III; Antithrombins; Biological Assay; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Heparin; Hexadimethrine Bromide; Humans; Liver Cirrhosis; Methods; Myocardial Infarction; Spectrophotometry; Thrombin | 1975 |
[Letter: Coagulation and common viral hepatitis].
Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Fibrin; Hepatitis A; Humans; Liver Cirrhosis; Prothrombin; Time Factors | 1975 |
Proceedings: Abnormal fibrin monomer polymerization in liver disease.
Topics: Fibrin; Fibrinogen; Hemorrhage; Humans; Liver Cirrhosis; Liver Diseases | 1975 |
[Disseminated intravascular coagulation in blastic leukemia and certain other disorders].
Topics: Acute Disease; Antithrombins; Blood Cell Count; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Humans; Leukemia; Leukemia, Monocytic, Acute; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Liver Cirrhosis; Lymphatic Diseases; Platelet Adhesiveness; Prothrombin Time; Retinal Detachment; Thrombin; Thrombophlebitis | 1974 |
The fibrinolytic enzyme system in acute and chronic liver injury.
Topics: Acute Disease; Adult; Aged; Alcoholism; alpha 1-Antitrypsin; Alpha-Globulins; Chronic Disease; Fatty Liver; Female; Fibrin; Fibrinogen; Fibrinolysis; Hepatitis; Humans; Liver Cirrhosis; Liver Cirrhosis, Biliary; Macroglobulins; Male; Middle Aged; Plasminogen | 1974 |
[Case of hypofibrinogenemia with disorders of fibrin polymerization during hepatic cirrhosis].
Topics: Afibrinogenemia; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Male; Middle Aged; Polymers | 1974 |
Hyperfibrinolysis in cirrhosis.
Topics: Adult; Alpha-Globulins; Aminocaproates; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Esophageal and Gastric Varices; Factor V; Factor VII; Factor X; Female; Fibrin; Fibrinolysin; Fibrinolysis; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Macroglobulins; Male; Middle Aged; Plasminogen; Protamines | 1973 |
Disseminated intravascular coagulation.
Topics: Blood Cell Count; Blood Platelets; Chronic Disease; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Heparin; Humans; Liver Cirrhosis; Pregnancy; Pregnancy Complications, Hematologic; Prothrombin Time; Thrombin; Thromboplastin | 1973 |
[Measurement of fibrinogen degradation products: its usefulness in consumption coagulopathies].
Topics: Agglutination Tests; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Hemagglutination Inhibition Tests; Humans; Liver Cirrhosis; Neoplasms; Staphylococcus | 1973 |
Antihaemophilic factor A (F VIII) and serum fibrin-fibrinogen degradation products in hepatic cirrhosis.
Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Factor VIII; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Inhibition Tests; Humans; Liver Cirrhosis; Male; Plasminogen; Thromboplastin | 1973 |
[Decomposition products of fibrin(ogen) and collateral circulation in liver cirrhosis].
Topics: Blood Protein Electrophoresis; Collateral Circulation; Fibrin; Fibrinogen; Humans; Immunoelectrophoresis; Immunoglobulin G; Liver Circulation; Liver Cirrhosis; Microcirculation; Thrombocytopenia | 1973 |
F.D.P.
Topics: Ascitic Fluid; Female; Fibrin; Fibrinogen; Humans; Liver Cirrhosis; Ovarian Neoplasms | 1972 |
Hyperalimentation in cirrhotic patients.
Topics: Acid-Base Equilibrium; Acidosis; Alanine Transaminase; Alkaline Phosphatase; Amino Acids; Ammonia; Arginine; Carbon Dioxide; Caseins; Catheterization; Cysteine; Diet Therapy; Fibrin; Glutamine; Glycine; Histidine; Humans; Isoleucine; Leucine; Liver; Liver Cirrhosis; Lysine; Methionine; Parenteral Nutrition; Phenylalanine; Potassium; Sodium; Threonine; Tryptophan | 1972 |
[Fibrinogen and fibrin degradation products (FDP) in hepatic cirrhosis].
Topics: Blood Coagulation Disorders; Fibrin; Fibrinogen; Humans; Liver Cirrhosis | 1972 |
Detection of fibrinogen-fibrin degradation products by counterelectrophoresis.
Counterelectrophoresis using a discontinuous buffer system permits detection of fibrinogen-fibrin degradation products (FDP) under a variety of clinical circumstances. The method is sensitive, reliable, and is easily performed using conventional equipment in any clinical laboratory assuming the responsibility for assaying fibrinogen-fibrin degradation products. Topics: Blood Coagulation Tests; Contraceptives, Oral; Female; Fibrin; Fibrinogen; Humans; Immunoelectrophoresis; Liver Cirrhosis; Methods; Neoplasms; Postoperative Complications; Precipitin Tests; Sepsis; Thrombin | 1972 |
The clinical significance of fibrinogen-fibrin-related antigen in serum.
Topics: Abruptio Placentae; Antigens; Blood Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Liver Cirrhosis; Neoplasms; Pregnancy | 1971 |
Detection of intravascular coagulation by a serial-dilution protamine sulfate test.
Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Agglutination Tests; Arteries; Arteriosclerosis Obliterans; Blood Coagulation Tests; Contraceptives, Oral; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Humans; Liver Cirrhosis; Male; Methods; Middle Aged; Neoplasm Metastasis; Protamines; Pulmonary Embolism; Staphylococcus; Sulfates; Thrombosis; Veins | 1971 |
[The alcohol plasma gelation test in the diagnosis of disseminated intravascular coagulation].
Topics: Abortion, Septic; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Ethanol; Female; Fibrin; Hematoma; Humans; Leukemia; Liver Cirrhosis; Methods; Neoplasms; Phlebitis; Postpartum Hemorrhage; Pregnancy; Pregnancy Complications, Hematologic; Sepsis | 1971 |
Measurement of fibrinogen and fibrin degradation products in serum by staphylococcal clumping test.
Topics: Animals; Arthritis, Rheumatoid; Blood Coagulation Tests; Cats; Cattle; Chromatography, Gel; Electrophoresis; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Liver Cirrhosis; Methods; Prothrombin Time; Rabbits; Staphylococcus; Streptokinase; Thrombin; Thrombosis; Time Factors | 1970 |
A comparative study of four methods for detecting fibrinogen degradation products in patients with various diseases.
Topics: Adult; Agglutination Tests; Arthritis, Rheumatoid; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Contraceptives, Oral; Erythrocytes; False Negative Reactions; False Positive Reactions; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemagglutination Inhibition Tests; Hodgkin Disease; Humans; Immunoassay; Immunodiffusion; Kidney Diseases; Liver Cirrhosis; Lymphoma, Non-Hodgkin; Male; Methods; Middle Aged; Myocardial Infarction; Neoplasms; Plasminogen; Staphylococcus | 1970 |
Fibrinolytic activity and haemagglutination inhibition immunoassays.
Topics: Adult; Aged; Biguanides; Clofibrate; Coronary Disease; Ethylestrenol; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Inhibition Tests; Hemostasis; Humans; Immunoassay; Immunodiffusion; Immunoelectrophoresis; Liver Cirrhosis; Male; Metformin; Middle Aged; Neoplasm Metastasis; Nicotinic Acids; Physical Exertion; Plasminogen; Prostatic Neoplasms; Stimulation, Chemical; Time Factors; Tolazamide | 1970 |
[Influence of anticoagulant therapy on the development of liver cirrhosis following injury with CCl4 in rats].
Topics: Animals; Anticoagulants; Blood Coagulation; Blood Coagulation Factors; Carbon Tetrachloride Poisoning; Collagen; Fibrin; Hydroxyproline; Liver Cirrhosis; Rats | 1970 |
[Endogenous and exogenous fibrinolysis].
Topics: Antifibrinolytic Agents; Blood Coagulation; Fibrin; Fibrinolysin; Fibrinolysis; Humans; Liver Cirrhosis; Plasminogen; Streptokinase | 1969 |
Fibrinolysis at rest and after exercise in hepatic cirrhosis.
Topics: Adult; Aged; Female; Fibrin; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Humans; Liver Cirrhosis; Male; Middle Aged; Physical Exertion; Plasminogen; Serum Globulins | 1969 |
Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 21-1969.
Topics: Acute Kidney Injury; Aged; Bronchopneumonia; Diagnosis, Differential; Fibrin; Humans; Hypertension, Portal; Kidney Cortex Necrosis; Kidney Glomerulus; Liver Cirrhosis; Male; Mesenteric Veins; Portal Vein; Sclerosis; Shwartzman Phenomenon; Splenic Vein; Thrombosis | 1969 |
Pathophysiology, clinical manifestations and therapy of consumption-coagulopathy ("Verbrauchskoagulopathie").
Topics: Adolescent; Adult; Blood Coagulation Disorders; Blood Coagulation Factors; Extraembryonic Membranes; Female; Fibrin; Fibrinolysis; Heparin; Humans; Kidney; Liver Cirrhosis; Middle Aged; Mononuclear Phagocyte System; Obstetric Labor, Premature; Pituitary Gland; Pregnancy; Sepsis; Shwartzman Phenomenon; Thrombin | 1967 |
[Current problems of arteriosclerosis].
Topics: Aging; Animals; Aorta; Arteriosclerosis; Cholesterol; Diet, Atherogenic; Fatty Acids; Fibrin; Fibrinolysis; Glucuronidase; Heparin; Humans; Lipid Metabolism; Liver; Liver Cirrhosis; Pituitary Hormones, Posterior; Protein Biosynthesis; Stress, Psychological; Thrombin | 1967 |
[CLINICAL STUDIES ON ANTITHROMBIN-I].
Topics: Anemia; Anemia, Hypochromic; Biomedical Research; Blood Chemical Analysis; Collagen Diseases; Enzyme Inhibitors; Fibrin; Hemophilia A; Hepatitis; Hepatitis A; Jaundice; Jaundice, Obstructive; Leukemia; Liver Cirrhosis; Multiple Myeloma; Nephritis; Nephrotic Syndrome; Physiology; Purpura; Thrombin; Uremia | 1963 |
Plasma fibrinolytic activity in cirrhosis of the liver.
Topics: Blood; Fibrin; Humans; Liver Cirrhosis; Thrombolytic Therapy | 1956 |
Plasma fibrinolytic activity in cirrhosis of the liver.
Topics: Fibrin; Humans; Liver Cirrhosis; Thrombolytic Therapy | 1956 |