scholarly journals Severe hepatocellular disease in mice lacking one or bothCaaXprenyltransferases

2011 ◽  
Vol 53 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Shao H. Yang ◽  
Sandy Y. Chang ◽  
Yiping Tu ◽  
Gregory W. Lawson ◽  
Martin O. Bergo ◽  
...  
Keyword(s):  
Hepatocellular Disease

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 Markedly Elevated Liver Enzymes in Choledocholithiasis in the absence of Hepatocellular Disease

2016 ◽  
Vol 4 (2) ◽  
pp. 232470961665109 ◽  
Author(s):  
Eula Plana Tetangco ◽  
Natasha Shah ◽  
Hafiz Muhammad Sharjeel Arshad ◽  
Hareth Raddawi
Keyword(s):  
Liver Enzymes ◽  
Elevated Liver Enzymes ◽  
Hepatocellular Disease

Hepatocellular necrosis associated with the subcutaneous injection of an intranasal Bordetella bronchiseptica-canine parainfluenza vaccine

1997 ◽  
Vol 33 (2) ◽  
pp. 126-128 ◽  
Author(s):  
K Toshach ◽  
MW Jackson ◽  
RR Dubielzig
Keyword(s):  
Bile Acid ◽  
Inflammatory Reaction ◽  
Subcutaneous Injection ◽  
Bordetella Bronchiseptica ◽  
Intravenous Fluids ◽  
Serum Bile Acid ◽  
Hepatocellular Necrosis ◽  
Local Inflammatory Reaction ◽  
Hepatocellular Disease ◽  
Hepatic Histopathology

A three-year-old wire fox terrier inadvertently was given an intranasal Bordetella bronchiseptica and canine parainfluenza vaccine subcutaneously. The dog subsequently developed both a local inflammatory reaction at the injection site and acute, nonseptic hepatocellular degeneration and necrosis. The patient was treated successfully with intravenous fluids and amikacin. Two months after the injection, the serum bile acid concentrations and hepatic histopathology indicated the presence of continued hepatocellular disease.

scholarly journals Human plasma extrinsic pathway inhibitor activity: II. Plasma levels in disseminated intravascular coagulation and hepatocellular disease

Blood ◽  
1989 ◽  
Vol 74 (3) ◽  
pp. 994-998 ◽  
Author(s):  
TA Warr ◽  
LV Rao ◽  
SI Rapaport
Keyword(s):  
Liver Disease ◽  
Tissue Factor ◽  
Disseminated Intravascular Coagulation ◽  
Factor Viia ◽  
Test Sample ◽  
Factor Ix ◽  
Factor X ◽  
Extrinsic Pathway ◽  
Intravascular Coagulation ◽  
Hepatocellular Disease

Abstract Plasma or serum extrinsic pathway inhibitor (EPI) activity was measured in 24 patients with disseminated intravascular coagulation (DIC) and in 23 patients with severe hepatocellular disease. EPI was measured as activity in a test sample that inhibited factor VIIa/tissue factor (TF)- catalyzed activation of 3H-factor IX (activation peptide release) in the presence of factor X. Of the 24 patients with DIC, 13 had sepsis and five had metastatic carcinoma, disorders in which tissue factor is believed to initiate DIC. EPI activity ranged from 68% to 300% (mean 134% +/- 50%). Serial measurements in nine patients failed to show depletion of EPI activity coincident with worsening DIC. DIC induced by tissue factor or other activating materials may progress despite normal EPI levels. In the patients with liver disease, of whom 15 had decompensated chronic hepatocellular disease (two fatal cases) and eight had acute fulminant liver failure (seven fatal cases), plasma or serum EPI activity varied from less than 20% to 194%. Values were distributed in a bimodal fashion. EPI activity could not be correlated with either the etiology of the liver disease or the degree of prolongation of the prothrombin time. Patients with chronic hepatocellular disease who survived had normal or elevated EPI activity. Patients with fatal hepatic dysfunction had low, normal, or high values for EPI activity. This must mean that secretion of EPI from cells other than hepatocytes can maintain normal plasma EPI levels.

Plasma Clotting Factors in Chronic Hepatocellular Disease

1960 ◽  
Vol 263 (6) ◽  
pp. 278-282 ◽  
Author(s):  
Samuel I. Rapaport ◽  
Sara B. Ames ◽  
Solveig Mikkelsen ◽  
Joseph R. Goodman
Keyword(s):  
Clotting Factors ◽  
Hepatocellular Disease
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