Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

20 coagulation parameters were investigated in 144 patients with different liver diseases. The groups of acute hepatitis, chronic active hepatitis and liver cirrhosis were compared and the prognostic value of the coagulation analyses investigated. It is clear that the determination of the factor V activity is a good and easy test for detection of actual liver function. Repeated controls over several weeks revealed with a statistical significance (p less than 0.0005) that all patients with a factor XIII below 35% and a plasminogen below 19% will die in liver coma, if they have not died beforehand from acute gastrointestinal haemorrhage, acute infection or cardiac arrest. Plasminogen is also lower in the group of non-survivors but the values of the two groups are overlapping and of no prognostic help in a single case. The possible causes of the diminution of factor XIII activity are discussed.
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PMID:Quantitative estimation of coagulation factors in liver disease. The diagnostic and prognostic value of factor XIII, factor V and plasminogen. 70 94

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.
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PMID:A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis. 171 9

Plasminogen and plasmin have been determined in the same plasma samples in normal subjects and in various physiological and pathological conditions (pregnancy, liver cirrhosis, untreated cancer, and myocardial infarction during treatment with streptokinase) by means of two different methods. These were an enzymatic assay and a new immunochemical assay based on radial immunodiffusion employing cellulose acetate strips.A significant correlation was found in normal subjects. However, in the other conditions marked discrepancies were observed in the results by the two methods. These findings might be related to variations in the functional activity of plasminogen and plasmin in disease.
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PMID:Enzymatic and immunochemical determination of plasminogen and plasmin in different physiological and pathological states. 425 95

We studied extrinsic and intrinsic fibrinolysis in 20 patients with cirrhosis (nine mild/moderate, group 1; 11 severe, group 2) and 19 normal controls to define the role of intrinsic (contact factor medaited) fibrinolysis in cirrhosis. Global plasma fibrinolytic activity (fibrin plate lysis) was similar in all groups. Dextran sulphate activated contact factor mediated fibrinolysis was decreased in group 2 (median 95.2%) compared with group 1 (121.0%) and controls (131.7%). Tissue plasminogen activator antigen (t-PA Ag) levels were increased in group 2 (28.2 ng/ml) compared both with group 1 (8.5 ng/ml) and controls (5.9 ng/ml). Plasma t-PA activity was raised in group 2 (5.50 IU/ml) and group 1 (5.25 IU/ml) versus controls (0.82 IU/ml). Plasminogen activator inhibitor-1 (PAI-1 Ag) levels were raised in group 2 (28.0 IU/ml) versus controls (8.5 IU/ml) but PAI activity was similar in all groups. Factor XII activity was decreased in group 2 (48.76 u/dl), but not group 1, versus controls (89.1 u/dl). Prekallikrein activity was decreased both in group 2 (27.27 u/dl) and group 1 (33.01 u/dl) versus controls (108.59 u/dl) and was lower in group 2 than group 1. C1-esterase inhibitor chromogenic activity was decreased in group 1 (102.30 u/dl) and group 2 (58.76 u/dl) versus controls (116.24 u/dl). The normal global fibrinolytic activity despite increased t-PA activity may be due to a concomitant increase in PAI. The decreased intrinsic fibrinolysis in severe cirrhosis, unaccompanied by a rise in C1-esterase inhibitor, may be explained by the decreased factor XII and prekallikrein activity. These changes are probably due to reduced liver cell mass.
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PMID:Decreased contact factor mediated fibrinolysis in cirrhosis. 813 76

Cirrhosis is associated with compromised hemostasis and coagulopathy during orthotopic liver transplantation (OLT). It has been suggested that hemostasis is better preserved during OLT in primary biliary cirrhosis (PBC) than other cirrhotic states. The aim of this study was to compare coagulation and fibrinolysis in 15 patients with PBC with 31 patients with other liver disease before and during OLT. Preoperatively, both groups had subnormal mean levels of prekallikrein, factor XIIa, antithrombin III (ATIII), plasminogen, and alpha2-antiplasmin. C1 esterase inhibitor and kallikrein inhibition in PBC was higher than the normal range (P < .01), but not in non-PBC. Non-PBC had lower median fibrinogen levels and shorter euglobulin clot lysis times (ECLT) (P < .05). Tissue plasminogen activator (tPA) antigen levels did not differ between groups but were elevated from the normal range, as were median thrombin-antithrombin complexes (TAT). Plasminogen activator inhibitor (PAI) activity was significantly higher in PBC (0.0041). Perioperatively in the PBC group during the early anhepatic phase of OLT, there was more thrombin generation, as evidenced by higher TAT levels (P = .0455) and less hyperfibrinolysis with longer ECLTs. We hypothesize that there is a preserved capacity to generate thrombin and less fibrinolytic activation during the anhepatic phase of OLT, and we suggest that, in PBC, the use of antifibrinolytic agents may have an adverse effect.
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PMID:Coagulation and fibrinolysis in primary biliary cirrhosis compared with other liver disease and during orthotopic liver transplantation. 904 19