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)

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in three patients with increased serum FDP, that were caused by various diseases. In the patient suffering from tuberculous constrictive pericarditis (case 1), the most part of the FDP fragments were DD and D. In the patient suffering from infection in addition to liver cirrhosis (case 2), the most part of the FDP fragments were high molecular weight (HMW) and D. In case 1 and 2, serum FDP levels were increased in parallel with the elevations of CRP levels. Although DD and HMW fragments were remarkably increased in case 1 and 2 with our immunoblotting analysis, DD levels assayed with LPIA system were much lower than FDP levels. The reason this discrepancy was explained by the observation that affinities of the monoclonal antibody used in LPIA system with DD and HMW fragment were markedly lower than that to DD-E fragment. In the patient suffering from deep vein thrombosis probably caused by steroid therapy of nephrotic syndrome (case 3), the most part of detected FDP fragments were DD and HMW in the period when APTT was shorter than normal, whereas D was mainly observed in the period when APTT was normal. In case 3, FDP and DD levels were increased in parallel with the shortening of APTT. In these non-DIC patients, increased serum FDP levels were induced by the presence of ascites and/or pleural effusion plus infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on the fragments of FDP in 3 non-DIC patients with increased FDP levels in the sera]. 836 Oct 25

The behavior of plasma von Willebrand factor (vWF) in patients with acute leukemia (n = 5), decompensated cirrhosis (n = 10), and acute pancreatitis (n = 5) was investigated to evaluate whether the systemic proteolytic states associated with these diseases had affected the structure and function of the molecule. vWF antigen and, to a lesser degree, ristocetin cofactor activity in patient plasma were high. Multimeric analysis of plasma vWF revealed loss of high molecular weight multimers. The subunit composition and proteolytic pattern of vWF immunopurified from patient plasmas and reduced were studied by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis followed by transblotting and probing with monoclonal antibodies that distinguish cleavages caused by plasmin from those caused by other proteases. There was marked reduction of the relative concentration of the native vWF subunit of 225 Kd in all patient groups, indicating heightened cleavage of the protein. The concentrations of 189- and 140-Kd vWF fragments, normally present in plasma, were increased in cirrhosis and pancreatitis but not in leukemia. Novel fragments, ranging in size from less than 225 to approximately 120 Kd were present in leukemia and cirrhosis, including plasmin-generated fragments of 176 and 145 Kd. These data indicate that in clinical conditions in which there is heightened proteolysis vWF is degraded in vivo by plasmin and other proteases. Degraded vWF may be less effective than native vWF in supporting primary hemostasis, thereby being a cofactor in the multifactorial bleeding diathesis accompanying systemic proteolytic states.
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PMID:Degradation of von Willebrand factor in patients with acquired clinical conditions in which there is heightened proteolysis. 842 64

The possibility of open tubular capillary electrophoresis for clinical diagnostic use is examined. Capillary electrophoresis was performed in an untreated 50 microns (i.d.) x 100 cm (65 cm to detector) capillary with detection of absorbance at 200 nm. Conditions for the separation of serum proteins without adsorption to the capillary surface were established. Quantitative analyses of serum samples from 38 patients with liver cirrhosis, nephrotic syndrome, or polyclonal gammopathy by capillary electrophoresis were done and the results were compared with those by conventional agarose gel electrophoresis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. All samples were analyzed in duplicate. We evaluated linearity of response, within-run CV, and the correlation between capillary electrophoresis and agarose gel electrophoresis.
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PMID:Quantitative analysis of serum proteins separated by capillary electrophoresis. 847 68

Bleeding from duodenal varices is a rare finding in patients with liver cirrhosis. We report a 43 year old male with alcoholic liver cirrhosis who presented with upper gastrointestinal bleeding. Panendoscopy identified, prominent tortuous varices over the second portion of duodenum with spurting of blood. At first, the varices were treated successfully with sodium tetradecyl sulfate and bleeding stopped. Consequent endoscopic sclerotherapy was done 1 week later. The varices almost disappeared 2 weeks after the second endoscopic sclerotherapy and the patient was in good condition following this.
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PMID:Endoscopic injection sclerotherapy of bleeding duodenal varices. 852 18

Oral administration of zinc (zinc tolerance test) was performed in 6 healthy adults, 11 patients with chronic hepatitis and 17 patients with liver cirrhosis to evaluate the ability of the digestive organs in patients with chronic hepatic diseases to absorb zinc. That is 300 mg of zinc sulfate powder (ZnSO4 7H2O)--equivalent to 68 mg of zinc--was dissolved in 200 ml of physiological saline solution, and the subjects received oral administration of the solution in a fasting condition during the early morning. The mean levels of serum Zn (ppm) at 0, 1, 2, and 3 hours after the test dose of ZnSO4 were 0.8 +/- 0.06, 1.66 +/- 0.21, 2.73 +/- 0.22 and 2.53 +/- 0.33 in cirrhotic patients, respectively. In most subjects, serum Zn levels peaked at 2 or 3 ours. The increase in serum Zn at 60 minutes during the base line Zn tolerance test was similar in patients and controls. The area under the curve was also significantly decreased in cirrhotic patients. These results will confirm the presence of diminished absorption by the intestinal tract in patients with liver cirrhosis.
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PMID:[Methods and clinical significance of an oral tolerance test of essential trace element, especially an oral zinc tolerance test]. 858 84

Zinc deficiency is common in cirrhosis and has been involved in the altered nitrogen metabolism. In this study, we measured the effects of zinc supplementation on the dynamics of amino acid-derived urea synthesis in cirrhosis with mild or latent encephalopathy. The hepatic conversion of amino acids into urea was studied in eight patients with advanced cirrhosis under controlled conditions of substrate availability (continuous alanine infusion), before and after 3-month oral zinc sulfate supplementation (600 mg/d). Eight more patients, matched for hepatocellular failure and encephalopathy, served as controls. Plasma zinc levels were reduced in all patients and returned to normal after oral zinc. The alanine-stimulated urea nitrogen synthesis rate in relation to alpha-amino-N concentration--the functional hepatic nitrogen clearance--increased by 25% after zinc supplementation, i.e., more urea was produced at any alpha-amino-N concentration. Basal and alanine-induced glucagon decreased by 50%, and the ammonia response to alanine decreased by 30%. Psychometric tests improved, as did routine and dynamic liver function tests and the Child-Pugh score. Also, the plasma concentration of lipid peroxides was reduced by zinc. No significant changes were observed in the control group. Our data indicate that long-term oral zinc speeds up the kinetics of urea formation from amino acids and ammonia. Changes in the hormonal drive and/or the antioxidant activity of zinc might be involved in the general improvement in liver function, whereas the beneficial effects on encephalopathy might stem from decreased ammonia.
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PMID:Zinc supplementation and amino acid-nitrogen metabolism in patients with advanced cirrhosis. 862 Nov 38

The present study was undertaken in order to investigate the influence of ursodeoxycholic acid (UDCA) on the composition of sulfate-conjugated bile acids in the serum and urine of patients with chronic active hepatitis and compensated liver cirrhosis. After a 12 week UDCA treatment (600 mg/day), total serum bile acid concentration increased two-fold in patients with compensated liver cirrhosis and increased slightly in patients with chronic active hepatitis. The percentage of sulfated bile acids significantly increased in patients with both compensated liver cirrhosis and chronic active hepatitis. UDCA made up 63% of the total serum bile acids in compensated liver cirrhosis and 61% in chronic active hepatitis after UDCA treatment. Of the serum bile acids after UDCA treatment, 35.2 and 53.9% of UDCA was sulfate conjugated in compensated liver cirrhosis and chronic active hepatitis, respectively. Urinary excretion of total bile acid and UDCA after UDCA treatment in compensated liver cirrhosis were higher than in chronic active hepatitis. UDCA made up 68% of the total urinary bile acids in compensated liver cirrhosis and 64% in chronic active hepatitis after UDCA treatment. Of the urinary bile acids after UDCA treatment, 51.8 and 54.8% of UDCA was sulfate conjugated in compensated liver cirrhosis and chronic active hepatitis, respectively. UDCA treatment for compensated liver cirrhosis was less effective than for chronic active hepatitis. We found that sulfate conjugation is one of the major metabolic pathways for UDCA after UDCA treatment in chronic liver diseases.
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PMID:Increase of sulfated ursodeoxycholic acid in the serum and urine of patients with chronic liver disease after ursodeoxycholic acid therapy. 871 7

Membrane-bound heparan sulfate proteoglycans act as coreceptors for cytokines and are involved in cell-matrix or cell-cell adhesion. We have determined the gene expression of all four members of the syndecan-like integral membrane proteoglycans and of betaglycan, the transforming growth factor-beta type III receptor, in various types of isolated hepatic cells of the rat. Fat-storing cells express syndecan-1, -2, -3, -4, and betaglycan. During the transformation of fat-storing cells into myofibroblasts (the key process in the development of liver cirrhosis), the levels of mRNA for syndecan-1, -3, and -4 remain constant, whereas the amount of syndecan-2 mRNA increases and that for betaglycan decreases. Liver macrophages express syndecan-3 and -4, but only small amounts of syndecan-1. Freshly isolated hepatocytes express only syndecan-1, -2, and -4, but fail to express betaglycan. During cultivation, hepatocytes start to express betaglycan. Syndecan-3, -4, and betaglycan are transcribed into one mRNA population, whereas syndecan-1 and -2 are expressed in different-sized mRNA populations. The data show that the genes of all tested membrane heparan sulfate proteoglycans are expressed by hepatic cells, but that each cell type is characterized by its specific heparan sulfate proteoglycan mRNA profile.
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PMID:Gene expression of syndecans and betaglycan in isolated rat liver cells. 876 53

Hepatosplenic schistosomal infection is a common parasitic liver disease in Egypt, resulting in the formation of granuloma followed by fibrosis which leads to the chronic liver disease. Plasma level of acetaminophen (AAP) and its glucuronide and sulfate metabolites after oral administration at a dose of 1 g was determined in liver-cirrhotic younger (9 - 25 years old) and elderly patients (45 - 65 years old) suffering from schistosomal infection. These levels of AAP and its metabolites in patient groups were compared with those in corresponding healthy subject groups. Examinations for participants in the present study by physicians indicated the more severe cirrhosis in elderly patients compared to younger patients and the formation of collateral circulation and the renal insufficiency in elderly patients. The elimination of AAP from plasma was significantly prolonged in both younger and elderly patient groups. In elderly patients plasma concentration of AAP in early stage (before the time to reach Cmax) was significantly higher, indicating the partial avoidance of first-pass metabolism due to the formation of hepatic shunt pathway. Plasma concentration of AAP-glucuronide was greatly decreased in both patient groups, whereas no significant difference in the plasma concentration of AAP-sulfate compared to those in corresponding healthy subject groups. These results will suggest that with repeated dosing of AAP special care must be taken in schistosomal patients since the elimination of AAP from plasma is remarkably reduced.
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PMID:Acetaminophen plasma level after oral administration in liver cirrhotic patients suffering from schistosomal infection. 883 6

A qualitative and quantitative analysis of silver-stained nuclear organizer regions (AgNOR) proteins was performed during hepatocarcinogenesis induced in rats initiated by diethylnitrosamine (DENA) using the resistant-hepatocyte model. Nuclear proteins from control hepatocytes, hyperplastic nodules, and hepatocellular carcinomas (HCC) separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were transferred to nitrocellulose membranes and specifically silver-stained for AgNOR proteins. No difference was observed in the distribution pattern of the silver-stained bands among control, hyperplastic, or cancer cells. The same was true if human cirrhosis and HCC were compared. The evaluation of individual AgNOR protein amounts by computerized densitometric analysis showed that 1) the integrated optical density value of the total AgNOR proteins was greatest in cancer cells, lesser in hyperplastic hepatocytes, and lowest in control hepatocytes, and 2) the amount of the two major silver-stained proteins, nucleolin (105 kd) and protein B23 (39 kd), was always a constant percentage of total AgNOR proteins. An experiment using bromodeoxyuridine incorporation showed that, during hepatocarcinogenesis, AgNOR protein quantity progressively increased and was significantly related to the increased hepatocyte labeling index. These results show that AgNOR protein distribution changes during hepatocarcinogenesis are caused neither by the synthesis of new AgNOR proteins nor by an unbalanced synthesis of individual AgNOR proteins, but to an increased synthesis of nucleolin and protein B23, which is associated with a progressive increased hepatocyte proliferation rate.
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PMID:Qualitative and quantitative analysis of AgNOR proteins in chemically induced rat liver carcinogenesis. 890 9


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