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)

Systematic screening of forty-seven haemophiliacs in Sheffield revealed abnormal liver-function tests in thirty-six (77%), with a tendency for these abnormalities to persist. To assess the importance of these abnormalities, percutaneous liver biopsy was carried out on eight symptom-free patients under factor-VIII cover. A wide spectrum of chronic liver disease was demonstrated, including chronic aggressive hepatitis and cirrhosis. The liver pathology bore no relation to clinical history or to biochemical findings. Hepatitis-B-virus markers were common, but evidence suggests that this is not the only factor contributing to the development of liver disease. The high incidence of chronic liver disease seems to be a recent development and is probably related to factor-concentrate replacement therapy.
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PMID:Percutaneous liver biopsy and chronic liver disease in haemophiliacs. 8 May 24

F VIII activity, F VIII-related antigen and von Willebrand factor were measured in 46 patients with hepatic cirrhosis and in 30 normal individuals. These parameters were significantly higher in hepatic cirrhosis than in the controls. Linear relationships between F VIII activity and F VIII-related antigen and between F VIII-related antigen and von Willebrand factor were found in patients with hepatic cirrhosis as well as in normal individuals. However, in both groups no relationship between F VIII activity and von Willebrand factor was present. The existence of a low-grade intravascular coagulation in hepatic cirrhosis may be postulated but more information about the metabolism of F VIII protein is needed before such a statement can be proven.
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PMID:Antihaemophilic factor A activity, F VIII-related antigen and von Wilebrand factor in hepatic cirrhosis. 40 32

For the evaluation of certain differences in the diminution of export proteins of the liver we examined some exactly defined groups of liver diseases with the aim of further differentiation of the pathogenetic mechanisms. We measured the activity of glutamate-oxalacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, lactate dehydrogenase, alkaline phosphatase, cholinesterase and lecithin-cholesterol acyltransferase, the Quick value, the coagulation factors I, II, V, VII, VIII, IX and X. Clotting factors were determined by a Schnitger-Gross Coagulometer. Prothrombin, antithrombin III, plasminogen, factor VIII associated antigen and activated factor XIII were measured by immunoelectrophoresis according to Laurell. Lipoprotein electrophoresis in agarose gel was performed to evaluate changes in lecithin-cholesterol acyltransferase activity. Except of the rising diminution of export proteins in the course of liver disease from acute hepatitis to cirrhosis we found also specific changes of the patterns of the plasma specific enzymes. These proteins were diminished dependent on their half life time and the inflammatory activity--measured as the height of the transaminases. Lecithin cholesterol acyltransferase and factor VIII did not participate in the general diminution of the most export proteins; some details were found to explain this differing behaviour. Results are critically discussed with regard to new aspects in the biochemistry of the damaged liver cell.
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PMID:[Correlations between the diminished secretion of export proteins from the liver and the plasmatic activity of liver cell enzymes (author's transl)]. 42 91

A prothrombin complex concentrate was used in attempts to control life-threatening hemorrhage in 4 patients with chronic liver disease. The population manifested profuse bleeding from varices and/or hemorrhagic gastritis; 3 had Laennec's cirrhosis and 1 had postnecrotic cirrhosis from childhood hepatitis. In all patients the complex was given in amounts needed to raise the prothrombin (factor II) level to approximately 100% of normal. In all 4 cases the prothrombin time and prothrombin complex factors approached normal within 1-2 hr after beginning the infusion. In all patients bleeding ceased with correction of the clotting status. One patient rebled several hours after completing the infusion. In several patients, increases in factors V and VIII were noted following infusion of the concentrate. A further unexpected finding was a spontaneous increase in factors II and IX at 3 days postinfusion. Prothrombin complex concentrate appears to be useful in controlling the hemorrhage of chronic liver disease when used alone or in combination with other modalities to correct specific hemostatic defects; however, patients may be expected to rebleed when the effect of the concentrate wears off. Its use, therefore, should probably be restricted to those patients who are to undergo corrective surgery of the bleeding point once hemostasis is achieved.
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PMID:Prothrombin complex concentrate: use in controlling the hemorrhagic diathesis of chronic liver disease. 108 Mar 55

The authors have analysed the development of various coagulation factors in 104 cases of common virus hepatitis in young adults. Total plasma coagulability, the prothrombin complex, factors VIII and IX, fibrination and fibrinolysis were followed up during this evolution and compared, using the usual statistical methods, with the results of the same investigations carried out on 100 healthy subjects belonging to the same age-group and on 31 patients suffering from cirrhosis of the liver. Statistical methods showed up the slightest disturbances of any significance which would have been overlooked if individual results only had been examined. As it was, there was total plasma hypercoagulability which was at its maximum at the onset of development but which persisted until the 7th week. It was mainly connected with an abnormality at the second stage of fibrination, that is : polymerisation of the fibrin monomers. The results obtained do not allow a conclusion to be drawn as to whether there exists an antipolymerase or dysfibrinogenaemia. Later research dealing specifically with the chemical structure of fibrinogen in hepatitis should provide further information. In practice, assessment of total plasma coagulability, using cephalinkaolin time, and analysis of fibrination by thrombin time are of definite value on account of their sensitivity.
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PMID:[Coagulation factors during the development of common viral hepatitis]. 121 72

This study was conducted to determine the role of a relatively new tumor marker, CA-195, in the diagnosis of hepatocellular carcinoma and metastatic hepatic carcinoma, and in distinguishing between these two conditions. CA-195 levels were measured using a commercially available immunoradiometric assay (Tandem-R CA-195) in 30 black inpatients with hepatocellular carcinoma, 15 metastatic carcinoma, 10 with amoebic liver abscess, 10 with cirrhosis and 10 normal individuals at King Edward VIII Hospital, Durban. A cutt-off value of 10 u/ml was used. The sensitivity and specificity of CA-195 in hepatocellular carcinoma and metastatic carcinoma was 60% and 22%, and 87% and 42% respectively. False positive results occurred in 5 (50%) patients with amoebic liver abscess, 10 (100%) with cirrhosis and 2 (20%) normal individuals. These results indicate this tumor marker as of limited value in the diagnosis of hepatocellular carcinoma and metastatic carcinoma, and in distinguishing between these conditions.
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PMID:Circulating CA-195 in hepatocellular carcinoma and metastatic hepatic carcinoma. 166 31

There is increasing interest in the changes of the endothelial lining of the hepatic sinusoids during the development of chronic liver disease. In this study we looked for evidence of hepatic sinusoidal endothelial cell transformation and basement membrane production in patients with primary biliary cirrhosis. Morphological transformation to vascular-type endothelial cells, as evidenced by the development VIII-related antigen, was seen at the interface between portal tracts or fibrous septae and hepatic parenchyma; the most marked changes were observed in patients with established cirrhosis. Increased immunohistochemical staining for the basement membrane components type IV collagen and laminin was also found in a similar distribution. Raised serum levels of hyaluronic acid, a glycosaminoglycan metabolized by normal hepatic endothelial cells, were found in most patients and correlated strongly with advancing histological stage. Furthermore, significant positive correlations were found between serum hyaluronic acid and serum levels of laminin and type IV collagen. The unique structure of the normal endothelial lining of the hepatic sinusoids is important in the maintenance of hepatic function. Our data show that significant changes in endothelial cell structure and function occur in primary biliary cirrhosis and appear to be a contributing factor to the progression of the disease. Further studies are needed to determine the extent and importance of these changes in other forms of chronic liver disease.
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PMID:Endothelial cell transformation in primary biliary cirrhosis: a morphological and biochemical study. 234 45

The sinusoidal endothelial cells of human liver can be identified by light and electron microscopy, but there appear to be no specific immunocytochemical markers of these cells. Among specific markers available for vascular endothelial cells in general, Ulex europaeus I lectin (UEA I) is the most sensitive. In the present study, 37 liver biopsies were examined for UEA I binding and for Factor VIII related antigen (F VIII RAg) to determine if sinusoidal endothelial cells were positive. The material included normal liver, biopsies from patients with cirrhosis and biopsies in a variety of other liver diseases. Three embryonal human livers were also included in the immunocytochemical analysis. Eleven oesophageal rings obtained at mechanical transection for variceal bleeding in cirrhotic patients were used as control tissue. Sinusoidal endothelial cells of normal liver did not stain with UEA I, but six of seven with alcoholic cirrhosis and only one of 25 non-cirrhotic liver specimens (a case of acute hepatitis with bridging necrosis) were positive. In two of the six cirrhoses the sinusoidal endothelial cells were stained for F VIII RAg as well. Embryonal sinusoidal endothelial cells were stained with UEA I but were negative for F VIII RAg. The results of the study confirm that sinusoidal endothelial cells of normal adult human liver are phenotypically different from those lining blood vessels in other sites. In cirrhosis, positive staining may be related to the transformation of hepatic sinusoids into true capillaries and thus be a marker of the severity of physiological disturbance in the liver.
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PMID:Hepatic sinusoidal endothelium: Ulex lectin binding. 249 24

The case of a 17-year-old female with a rare form of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor is reported. Laparoscopy showed a tumor 50 mm in diameter in the lower portion of the right lobe of the liver. The tumor was biopsied under ultrasonic guidance, and tentatively diagnosed as adenomatous hyperplasia. The patient was also diagnosed as having type VIII glycogenosis (phosphorylase kinase deficiency).
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PMID:A female case of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor. 255 39

A limited liver resection was performed in two patients with cirrhosis and a hepatocellular carcinoma situated in segment VIII (anterosuperior subsegment of the right lobe). One of the patient had previously bled from esophageal varices. Resection of segment VIII was performed following the anatomical planes of section after complete mobilization of the right lobe of the liver. Both patients were alive and free of recurrence 14 and 30 months after surgery. Hepatocellular carcinomas are thus treatable by limited anatomic liver resection even when they are situated in the vicinity of the major hepatic veins and the vena cava.
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PMID:Surgical resection of segment VIII (anterosuperior subsegment of the right lobe) in patients with liver cirrhosis and hepatocellular carcinoma. 299 45


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