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)

Serum alpha-fetoprotein (AFP) subfraction profile is a predictive indicator for the discrimination of hepatic malignancies, benign liver diseases and yolk sac tumor in adults. In the present study, AFP subfractions were examined in AFP-positive sera from 59 patients of less than 15 years of age. Fractionation of AFP was carried out by lectin affinity crossed-line immunoelectrophoresis. Concanavalin A, Lens culinaris hemagglutinin and phytohemagglutinin E were used as lectins. Fifty-four of 59 (91.5%) AFP subfraction profiles in patients with pediatric diseases were classified into three common types: (1) benign liver disorder, (2) hepatic malignancy and (3) yolk sac tumor. An atypical AFP subfraction profile resembling hepatic malignancy type was found in 5 of 59 (8.5%) infants. It was concluded that estimation of serum AFP subfraction profiles facilitates differential diagnosis of various AFP-positive pediatric diseases, such as hepatoblastoma, hepatoma, hepatic cirrhosis, hepatitis or germ cell tumors.
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PMID:Clinical significance of serum alpha-fetoprotein subfractionation in pediatric diseases. 752 30

Lens culimaris agglutinin A-reactive alpha-fetoprotein (AFP L3) and erythroagglutinating phytohemagglutin-reactive alpha-fetoprotein (AFP P4 + P5) were determined by a sensitive method using lectin-affinity electrophoresis coupled with antibody-affinity blotting, and the usefulness of this method for early detection of hepatocellular carcinoma (HCC) was examined. For 72 operated cases of the HCC group including 28 cases of small liver cancer, the AFP value was 124 +/- 198ng/ml (Mean +/- SD); the lectin fraction values for L3 and P4 + P5 were 12.2 +/- 17.9 and 17.9 +/- 17.9%, respectively, which were significantly higher compared with the chronic hepatitis (CH).cirrhosis (LC) group and showed an increasing tendency with an increase in tumor diameter. The cut-off values for distinguishing HCC from CH.LC, determined with the receiver-operating characteristic (ROC) plots, were 10.0 and 15.0% for the L3 and P4 + P5 fractions, respectively, and the positive rates in the patient with HCC were 33.3 and 48.6% for AFP L3 and AFP P4 + P5, respectively, and 59.7% with a combination assay. For small liver cancer, the positive rate was 17.9% with protein induced by vitamin K absence-II (PIVKA-II) and 46.4% with combination assay of AFP L3 and AFP P4 + P5. Also, for HCC below AFP 50ng/ml, a positive rate of 45.0% was obtained. In the CH.LC group, all cases were negative for AFP L3 and 2 of 44 cases (4.5%) were false-positive for AFP P4 + P5.
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PMID:[Early detection of hepatocellular carcinoma with lectin reactive alpha-fetoprotein]. 752 71

Levels of two types of lectin-reactive alpha-fetoprotein (AFP), designated AFP-L3 and AFP-P4+P5, were analyzed with Lens culinaris agglutinin A and AFP-P4+P5 with erythroagglutinating phytohemagglutinin, respectively, in an attempt to determine the utility and significance of these macromolecules as early indicators of hepatocellular carcinoma during the periodic follow-up of cirrhotic patients. The subjects were 51 of 190 consecutive cirrhotic patients in whom hepatocellular carcinoma developed during a 6-year follow-up period and 21 cirrhotic patients without hepatocellular carcinoma. Serum AFP levels were of limited value to diagnose and predict hepatocellular carcinoma. The relative levels of AFP-L3 and AFP-P4+P5 in patients with hepatocellular carcinoma at the time of tumor detection were significantly higher than those in patients with cirrhosis. The sensitivity was 61%, and the specificity was 90%. Fourteen patients (48%) of 29 patients with small hepatocellular carcinomas less than 2 cm in diameter showed elevated percentage of lectin-reactive AFP. Retrospective examination of 21 patients who were positive for lectin-reactive AFP at diagnosis of hepatocellular carcinoma showed that 41% of them had already expressed lectin-reactive AFP 12 months before the direct detection of hepatocellular carcinoma by diagnostic imaging. These results lead us to conclude that the level of lectin-reactive AFP is a suitable predictive marker for the early recognition of hepatocellular carcinoma in the follow-up of patients with cirrhosis, and that measurements of the level of lectin-reactive AFP should be added to the screening methods that are now in use.
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PMID:A clinical study of lectin-reactive alpha-fetoprotein as an early indicator of hepatocellular carcinoma in the follow-up of cirrhotic patients. 754 56

Diagnostic kits for determination of alpha-fetoprotein (AFP) carbohydrate chain microheterogeneity were developed using lectin affinity electrophoresis with Lens culinaris agglutinin-A (LCA-A) and erythro-agglutinating phytohemagglutinin-E4 (PHA-E4). Separated AFP bands by electrophoresis were detected with high sensitivity by antibody-affinity blotting and immunoenzymatic amplification. Densitometry was used to apportion lectin reactive AFPs. The within-run S.D. for proportions of AFP bands was below 3%. Band intensity was linearly related to AFP concentration between 2 and 200 ng/ml. Profiles of lectin reactive AFPs were compared in serum samples from 55 patients having liver diseases. The average values of lectin reactive AFPs for chronic hepatitis and liver cirrhosis patients were both below 13%, but those of hepatocellular carcinoma patients were above 25%. Correlation of data with disease states suggests that the methods can greatly facilitate the discrimination between benign and malignant liver diseases.
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PMID:Establishment of assay kits for the determination of microheterogeneities of alpha-fetoprotein using lectin-affinity electrophoresis. 768 Sep 70

This paper is a study to identify the clinical significance of high-molecular-mass alkaline phosphatase (ALP:E:C..3.1.3.1.), ALP-lipoprotein-X complex (LP-X) and intestinal variant ALP. We used cellulose acetate and agarose gels and techniques including wheat germ lectin, cetavlon-diethyl ether, thermostatability, neuraminidase and L-phenylalanine to improve the electrophoretic separation of the alkaline phosphatase isoenzymes. Patients' serum samples were electrophoresed from a diverse group of individuals ill with cholestasis, neoplastic disease metastatic to the liver, hepatocellular carcinoma, cirrhosis, diabetes mellitus, and chronic renal disease. Agarose gels provided better separation of ALP isoenzymes than cellulose acetate gels. The results also indicated that high-molecular mass ALP is present in patient's serum in conditions associated with cholestasis especially caused by hepatic malignancy. High-molecular mass ALP was frequently found to co-exist with the liver isoenzyme and LP-XALP complex. The intestinal variant was identified in patients with malignancy, cirrhosis, chronic renal disease and diabetes mellitus. Intestinal ALP coexisted concomitantly with a variant intestinal ALP. Intestinal variant ALP is most likely composed of intestinal ALP attached to a cellular membrane-binding domain, or may be an artifact produced by neuraminidase incubation.
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PMID:Clinical significance of serum high-molecular-mass alkaline phosphatase, alkaline phosphatase-lipoprotein-X complex, and intestinal variant alkaline phosphatase. 804 46

The peribiliary vascular plexus (PVP) plays an important role in the pathophysiology of the biliary tree. We histologically examined vascular endothelial cells of the intrahepatic PVP in various hepatobiliary diseases by immunohistochemistry and lectin histochemistry with antibodies to factor VIII-related antigens (F-VIII-R-Ag) and Ulex europaeus agglutinin I (UEA-I). The PVP around the intrahepatic large bile ducts (LBDs) and septal bile ducts (SBDs) in normal livers consists of three layers: inner layer vessels immediately adjacent to the epithelium, intermediate layer vessels within the ductal wall, and outer layer vessels outside the ductal wall. In some bile ducts that show active inflammation in hepatolithiasis, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and extrahepatic biliary obstruction (EBO), vessels in the intermediate layer and, to a lesser degree, in the inner layer, are increased in number. In sclerotic bile ducts of PSC, EBO, and hepatolithiasis, the number of inner and intermediate layer vessels are markedly and variably reduced, respectively. In liver cirrhosis or chronic advanced liver diseases, the vessels in all three layers, particularly those in the outer layer, are increased in number and dilated, probably reflecting intrahepatic microcirculatory disturbance. The PVP showed several types of numerical and luminal changes, each of which may be related to disease processes in the intrahepatic biliary tree as well as to intrahepatic microcirculatory disturbance.
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PMID:Intrahepatic peribiliary vascular plexus in various hepatobiliary diseases: a histological survey. 808 71

Serum cholinesterase (ChE) (E.C. 3.1.1.8) is a glycoprotein which has 36 potential sites of asparagine-N-linked sugar chains. The structures of oligosaccharides released from ChE on hydrazinolysis were studied by serial lectin affinity column chromatography, exoglycosidase digestion, and methylation analysis. Seventy-three % of the sugar chains occurred as biantennary oligosaccharides and the remainder as C-2 and C-2,4/C-2,6 branched tri- and tetraantennary oligosaccharides. Several percentages of the Lewis X antigenic determinant and fucosylated mannose core were linked to them, and their sialic acid residues were linked to nonreducing terminal galactose residues at the C-3 and C-6 positions. Aleuria aurantia lectin-reactive ChE with the Lewis X antigenic determinant increased in hepatocellular carcinomas and liver cirrhosis compared with chronic hepatitis; on the other hand, Aleuria aurantia lectin-reactive ChE did not change significantly after transcatheter arterial embolization and was not related to the serum levels of alpha-fetoprotein and carcinoembryonic antigen in patients with hepatocellular carcinomas. Accordingly, the analysis of Aleuria aurantia lectin-reactive ChE is clinically useful for differentiating liver cirrhosis from chronic hepatitis and to identify high risk groups for hepatocellular carcinomas, i.e., cirrhotic patients in Child's A grade.
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PMID:Increase of fucosylated serum cholinesterase in relation to high risk groups for hepatocellular carcinomas. 826 62

Acute (hepatitis) and chronic (cirrhosis) liver injuries were experimentally induced in BALB/c-mice by administration of D-galactosamine and carbon tetrachloride, respectively. In both experimental liver diseases the incidence of hepatic tumor colonization of sarcoma L-1 was significantly reduced as compared to non-treated control animals. Thus, it seems that either dysfunction or loss of organ-characteristic lectins (galactosyl-specific hepatic lectins) prevented liver colonization. Histochemical staining of liver sections from D-galactosamine or carbon tetrachloride-treated mice with appropriate galactose-containing (neo)glycoproteins supported this hypothesis, since the lectin-dependent binding was greatly reduced as compared to sections from non-treated animals.
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PMID:Hepatocellular injury inhibits lectin-mediated tumor colonization into BALB/c-mice livers. 833 80

We have established an enzyme-linked immunosorbent assay (ELISA) for total serum cholinesterase (ChE) using 2 new monoclonal antibodies (mAbs) to ChE (E.C.3.1.1.8). The ELISA results correlated very well with the results of a serum ChE activity assay, which has been widely used for differentiating patients with liver diseases, such as hepatocellular carcinoma, liver cirrhosis and chronic hepatitis, from normal individuals. We next established an ELISA for Aleuria aurantia lectin (AAL)-reactive serum ChE using one of the anti-ChE mAbs and AAL, which specifically recognizes L-fucose alpha 1-->2, L-fucose alpha 1-->3, and L-fucose alpha 1-->6 structures. The ratio of AAL-reactive ChE to total ChE in sera determined by the two ELISA procedures was increased in patients with hepatocellular carcinoma and liver cirrhosis compared with patients with chronic hepatitis and normal individuals. We then applied the ELISA for AAL-reactive ChE directly to 10-fold-diluted serum samples, and by using a cut-off value of the mean + 2S.D. for normal individuals, we could effectively differentiate liver cirrhosis from chronic hepatitis. This single ELISA for AAL-reactive ChE could be a useful aid in clinical diagnosis.
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PMID:Enzyme-linked immunosorbent assay (ELISA) for Aleuria aurantia lectin-reactive serum cholinesterase to differentiate liver cirrhosis and chronic hepatitis. 874 9

Circulating hyaluronan is mostly derived from lymph, fibroblast and Ito cells in the liver, and more than 90% of hyaluronan is degraded in hepatic sinusoidal endothelial cells. Thus, elevated serum hyaluronan is regarded as an indication of hepatic fibrosis with activated Ito cells and dysfunctional sinusoidal endothelial cells. We studied the distribution of hyaluronan in human liver sinusoids to determine the influences on elevated hyaluronan levels in sera. Histochemical examination was made using hyaluronan-binding protein (HABP) and serial sections of liver tissue for staining of alpha-smooth muscle actin (ASMA) (an indicator of activated Ito cells) and of ulex europaeus agglutinin I lectin (UEA-1) (closely related to hepatic sinusoidal capillarization). Positive staining, indicating the presence of hyaluronan, was noted in fibrous regions around the portal tracts, areas of focal necrosis in the liver parenchyma, and walls of the sinusoids in chronic hepatitis. In this group, hyaluronan-positive areas corresponded to positive ASMA staining and faint staining of UEA-1. On the contrary, in liver cirrhosis, UEA-1-positive areas were essentially identical to hyaluronan-positive areas and to ASMA-negative areas in sinusoidal walls. Hyaluronan and ASMA could be detected in the same areas of sinusoidal walls in chronic hepatitis, but not in liver cirrhosis. Hyaluronan appears to be mainly related to the staining of activated Ito cells in chronic hepatitis. Therefore, we concluded that in chronic hepatitis, the production of hyaluronan was accelerated in Ito cells; however, degradation of hyaluronan by sinusoidal endothelial cells continued. On the contrary, in liver cirrhosis, hyaluronan production decreased in Ito cells, and a marked transformation of sinusoidal endothelial cells with hepatic sinusoidal capillarization indicated loss of the ability to degrade hyaluronan. These different mechanisms in chronic hepatitis and liver cirrhosis may operate in the sinusoidal walls and may cause the elevation of hyaluronan in sera.
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PMID:Localization of hyaluronan in human liver sinusoids: a histochemical study using hyaluronan-binding protein. 902 14


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