Fibrin Monomer Polymerization in Liver Disease

1975 ◽  
Author(s):  
G. Green ◽  
I. W. Dymock ◽  
Jean M. Thomson ◽  
L. Poller
Keyword(s):  
Liver Disease ◽  
Normal Liver ◽  
Acute Liver Damage ◽  
Normal Liver Function ◽  
Primary Hepatoma ◽  
True Incidence ◽  
Coagulation Defect ◽  
Fibrin Monomer ◽  
Hepatocellular Disease ◽  
Normal Controls

Despite a few reports of abnormal fibrin monomer polymerization in liver disease, particularly primary hepatoma, the true incidence of this phenomenon remains to be determined. The unexplained frequency of prolongation of the thrombin-fibrinogen and reptilase times in such patients suggest it is more common than previously suspected.Over a hundred patients with hepatocellular dysfunction or jaundice have been screened for evidence of abnormal fibrinogen polymerization by a calorimetric method utilizing reptilase. The results have been compared with normal controls and patients with diverse diseases but normal liver function.Of the patients with primary hepatocellular disease such as cirrhosis and acute liver damage over a quarter exhibited abnormal fibrinogen polymerization. In addition these same patients had prolonged thrombin-fibrinogen and reptilase times, this latter test being the most reliable single index of the presence of abnormal polymerization.In patients with jaundice due to extra-hepatic biliary obstruction abnormal fibrin monomer polymerization was not observed.These findings may have important implications in the aetiology of the coagulation defect of liver disease.

scholarly journals Pharmacokinetics of Amphotericin B Colloidal Dispersion in Critically Ill Patients with Cholestatic Liver Disease

2012 ◽  
Vol 56 (10) ◽  
pp. 5414-5418 ◽  
Author(s):  
Stefan Weiler ◽  
Elisabeth Überlacher ◽  
Julia Schöfmann ◽  
Eva Stienecke ◽  
Stefan Dunzendorfer ◽  
...  
Keyword(s):  
Steady State ◽  
Liver Disease ◽  
Amphotericin B ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Normal Liver ◽  
Colloidal Dispersion ◽  
Cholestatic Liver Disease ◽  
Normal Liver Function ◽  
Standard Dosage

ABSTRACTThe pharmacokinetics of lipid-bound and liberated amphotericin B (AMB) was assessed in 11 critically ill patients with cholestatic liver disease (CSLD) and in 9 subjects with normal liver function treated with AMB colloidal dispersion (ABCD). Exposure to lipid-bound AMB was higher in patients with CSLD. Levels of liberated AMB were elevated by CSLD only after the first dose, whereas its pharmacokinetics was unaffected at steady state. The standard dosage of ABCD is probably adequate for patients with CSLD.

scholarly journals Fibrinogen-Fibrin Monomer Complexes in Cirrhosis of The Liver

1977 ◽  
Author(s):  
S. Coccheri ◽  
G. Palareti ◽  
M. Poggi ◽  
G. Oca
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Liver Biopsy ◽  
Plasma Samples ◽  
Severe Liver ◽  
Decompensated Liver Cirrhosis ◽  
Chronic Active Liver Disease ◽  
Fibrin Monomer ◽  
Cirrhotic Patients ◽  
Normal Controls

Positivity of paracoagulation tests in a previously studied group of 80 patients with chronic active liver disease did not exceed 5-10% of the cases. In the present study, plasma samples from 20 cases of decompensated liver cirrhosis, assessed by liver biopsy, were investigated by means of agarose cromatography. Fibrinogen related materials were measured immunologically and by Staphylococcal Clumping Test.First appearance of fibrinogen-like materials occurred at earlier fractions in cirrhotic patients in comparison with normal controls. The relative amount of soluble fibrin monomer complexes (SFMC) as referred to total fibrinogen was significantly increased. No correlation was found between the amount of SFMC and the severity of fibrinogen polymerisation defect.Circulating SFMC are therefore present in severe liver cirrhosis. However, DIC may not be the only proposed explanation for this finding.

Parallel Reduction of Plasma Levels of High and Low Molecular Weight Kininogen in Patients with Cirrhosis

1999 ◽  
Vol 82 (11) ◽  
pp. 1428-1432 ◽  
Author(s):  
Cheryl Scott ◽  
Francesco Salerno ◽  
Elettra Lorenzano ◽  
Werner Müller-Esterl ◽  
Angelo Agostoni ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Liver Disease ◽  
Liver Function ◽  
Plasma Levels ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Low Molecular Weight ◽  
Major Band ◽  
Sds Page ◽  
Normal Controls

SummaryLittle is known about the regulation of high-molecular-weight-kininogen (HK) and low-molecular-weight-kininogen (LK) or the relationship of each to the degree of liver function impairment in patients with cirrhosis. In this study, we evaluated HK and LK quantitatively by a recently described particle concentration fluorescence immunoassay (PCFIA) and qualitatively by SDS PAGE and immunoblotting analyses in plasma from 33 patients with cirrhosis presenting various degrees of impairment of liver function. Thirty-three healthy subjects served as normal controls. Patients with cirrhosis had significantly lower plasma levels of HK (median 49 μg/ml [range 22-99 μg/ml]) and LK (58 μg/ml [15-100 μg/ml]) than normal subjects (HK 83 μg/ml [65-115 μg/ml]; LK 80 μg/ml [45-120 μg/ml]) (p < 0.0001). The plasma concentrations of HK and LK were directly related to plasma levels of cholinesterase (P < 0.0001) and albumin (P < 0.0001 and P < 0.001) and inversely to the Child-Pugh score (P < 0.0001) and to prothrombin time ratio (P < 0.0001) (reflecting the clinical and laboratory abnormalities in liver disease). Similar to normal individuals, in patients with cirrhosis, plasma HK and LK levels paralleled one another, suggesting that a coordinate regulation of those proteins persists in liver disease. SDS PAGE and immunoblotting analyses of kininogens in cirrhotic plasma showed a pattern similar to that observed in normal controls for LK (a single band at 66 kDa) with some lower molecular weight forms noted in cirrhotic plasma. A slight increase of cleavage of HK (a major band at 130 kDa and a faint but increased band at 107 kDa) was evident. The increased cleavage of HK was confirmed by the lower cleaved kininogen index (CKI), as compared to normal controls. These data suggest a defect in hepatic synthesis as well as increased destructive cleavage of both kininogens in plasma from patients with cirrhosis. The decrease of important regulatory proteins like kininogens may contribute to the imbalance in coagulation and fibrinolytic systems, which frequently occurs in cirrhotic patients.

Heparin Response and Clearance in Acute and Chronic Liver Disease

1985 ◽  
Vol 54 (03) ◽  
pp. 591-594 ◽  
Author(s):  
H Sette ◽  
R D Hughes ◽  
P G Langley ◽  
A E S Gimson ◽  
R Williams
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Peak Level ◽  
Chronic Liver ◽  
Clotting System ◽  
Activated Clotting Time ◽  
At Iii ◽  
Increased Sensitivity ◽  
Low Levels ◽  
Normal Controls

SummaryPatients with liver disease are at risk of bleeding due to abnormalities of the clotting system although they must be anticoagulated if they require haemodialysis or haemoperfusion. The anticoagulant of choice is heparin.In this study we have investigated heparin kinetics in patients with fulminant hepatic failure (FHF) after a single intravenous dose of heparin (2,500 units) and found there was an increased clearance of heparin whether measured by its anti-Xa effect (t1/2 = 27.8 ± 2.9 min compared to t1/2 = 50.2 ± 2.7 min in normal controls p <0.001) or by the whole blood activated clotting time (t1/2 = 23.7 ± 2.2 min compared to t1/2 = 37.0 ± 2.0 min p <0.001). There was a decreased peak level of heparin measured by anti-Xa effect (peak level in FHF = 0.48 ± 0.05 u/ml and in controls = 0.69 ± 0.04 u/ml, p <0.02), but an increased sensitivity to heparin (sensitivity in FHF = 0.072 ± 0.011 sec/unit, in controls 0.033 ± 0.003 sec/unit, p <0.001). Patients with FHF had very low levels of antithrombin III (AT III), but there was no correlation between this and any parameters of heparin effect or clearance. In a group of patients with chronic liver disease heparin kinetics did not differ from controls despite low levels of AT III.The changes in heparin kinetics in FHF are likely to be complex with the balance between the proteins that act as cofactors, (e.g. AT III) and the proteins that have heparin neutralising activity, controlling the response of added heparin.

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