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)

Histidine-rich glycoprotein is a 3.8s alpha 2-glycoprotein of human plasma originally isolated in 1972 [1,2]. The biologic function of histidine-rich glycoprotein, however, is unknown. A recent report suggests that histidine-rich glycoprotein binds to the high-affinity lysine-binding sites of plasminogen and that histidine-rich glycoprotein may retard fibrinolysis by interfering with the binding of plasminogen to fibrin [3]. We have measured the plasma titers of histidine-rich glycoprotein in normal subjects and patients with advanced hepatic cirrhosis by single radial immunodiffusion with a monospecific antiserum. The levels in 22 patients were 7.0 +/- 2.5 mg/dl (mean +/- SD), whereas those in 20 control subjects were 11.8 +/- 2.7 (p less than 0.001). Upon two-dimensional crossed immunoelectrophoresis, the pattern of histidine-rich glycoprotein in liver cirrhosis was similar to that of normal histidine-rich glycoprotein. Since histidine-rich glycoprotein seems to function as an antifibrinolytic agent, the decreased titers in cirrhosis may be one factor contributing to the enhanced fibrinolysis commonly seen in this disorder.
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PMID:Reduced histidine-rich glycoprotein levels in plasma of patients with advanced liver cirrhosis. Possible implications for enhanced fibrinolysis. 711 73

Carcinoembryonic antigen (CEA), an oncofetal glycoprotein, has been originally suggested as a tumor marker for colorectal cancer and afterwards has been regarded as a specific marker for different cancers. The determination of CEA in 73 patients with "benign" hepatic diseases points out the limitation of test's diagnostic value on account of the not infrequent observation of false positives in the examined cases. In particular the greatest incidence and intensity of elevated levels of CEA has been found in hepatic cirrhosis. However must be mentioned that the highest values of CEA has been documented nearly constantly in the comparison's group of some forms of malignancies, between which nevertheless there have been sporadically false negatives.
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PMID:[Carcinoembryonic antigen (CEA) and non-oncological liver diseases (case report)]. 724 73

To evaluate the diagnostic significance of tenascin, the extracellular matrix glycoprotein in chronic liver disease, serum tenascin levels were measured by a newly developed ELISA in 21 patients with chronic persistent hepatitis, in 55 with chronic active hepatitis, in 59 with liver cirrhosis, in 31 with hepatocellular carcinoma, in 26 with acute hepatitis and in 66 healthy subjects. The serum tenascin level was significantly elevated in the patients with chronic active hepatitis, liver cirrhosis, hepatocellular carcinoma, and acute hepatitis when compared with the healthy subjects (p < 0.001). The serum tenascin level also increased with increasing severity of chronic liver diseases. A significant correlation was observed between the serum tenascin levels and serum levels of various extracellular matrix proteins such as type III procollagen N-aminoterminal peptide (PIIIP), laminin and the 7S domain of type IV collagen (p < 0.001). A strong positive correlation was observed between the serum tenascin levels and histologic findings, particularly in the degree of hepatic fibrosis. This is the first report documenting serum tenascin level increases in patients with various chronic liver diseases. The measurement of the serum tenascin levels may provide additional information relevant to the study of connective tissue.
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PMID:Serum tenascin levels in chronic liver disease. 752 6

Adenomatous hyperplasia in the human liver with cirrhosis is similar to the hyperplastic nodule in rat hepato-carcinogenesis in that the mdr gene or its product P-glycoprotein is overexpressed. We immunohistochemically stained archival formalin-fixed, paraffin-embedded sections of 15 adenomatous hyperplasias with or without hepatocellular carcinoma in livers with cirrhosis, using the avidin-biotin-complex method and the JSB-1 monoclonal antibody which specifically binds the cytoplasmic epitope of P-glycoprotein. Of 15 cases with adenomatous hyperplasia, four were found solely in livers with cirrhosis. In six cases, adenomatous hyperplasia and hepatocellular carcinoma were found in the same liver separately. Hepatocellular carcinoma was discovered within adenomatous hyperplasia in five cases. All 15 livers with cirrhosis and those with adenomatous hyperplasia were positively stained for P-glycoprotein. When the grade of staining was compared between adenomatous hyperplasia and the surrounding liver, P-glycoprotein was overexpressed in 12 of 15 cases with adenomatous hyperplasia. P-glycoprotein was also stained more strongly in well-differentiated hepatocellular carcinoma than in the liver, but the staining grade of hepatocellular carcinoma was weaker than that of adenomatous hyperplasia. Moreover, the glycoprotein expression was less when the tumor was less differentiated.
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PMID:Overexpression of P-glycoprotein in adenomatous hyperplasia of human liver with cirrhosis. 754 Jun 36

The appearance of desialo-transferrin (De-TF) in serum has been reported to be a biochemical marker of chronic alcoholism. However, conclusive evidence of whether De-TF is a marker for chronic alcohol drinking or for alcoholic liver disease (ALD) has not yet been obtained. Glycoproteins can be divided into two groups, a transferrin (TF) group and an alpha 1-acid glycoprotein (A1-AG) group, based on the characteristics of microheterogeneity (M-HTG) of each protein. In the present study, the appearance of M-HTG in serum TF and A1-AG in alcohol drinkers was compared. In 96 patients with ALD, M-HTG of TF was found in 66 patients (68.8%), and M-HTG of A1-AG was found in 61 patients (63.5%). In 20 patients with alcoholic pancreatitis, the detection rate of M-HTG of A1-AG was significantly higher than that of TF. In six patients with pancreatitis but not liver disease, M-HTG of TF was not detected. In 14 alcoholics without liver or pancreas disease, M-HTG of TF was not detected, whereas M-HTG of A1-AG was detected in 6 cases--a significant difference. The amount of alcohol consumed was not different in patients with and without liver disease. In non-ALD, M-HTG of both proteins was detected only in patients with decompensated liver cirrhosis. The detection rate of M-HTG in TF was significantly higher than in A1-AG. These results suggest that M-HTG of serum TF is a marker of ALD and that of serum A1-AG is a marker of chronic alcohol drinking.
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PMID:Microheterogeneity of serum glycoproteins in alcoholics: is desialo-transferrin the marker of chronic alcohol drinking or alcoholic liver injury? 804 44

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
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PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8

alpha 1-Acid glycoprotein, an acute phase reactant synthesised by the liver, has been reported to be increased in neoplastic conditions and reduced in chronic liver disease. We measured serum alpha 1-acid glycoprotein by a nephelometric method in 186 subjects (112 males, 74 females): 55 had mild chronic liver disease (chronic hepatitis and steatofibrosis), 45 cirrhosis, 38 hepatocellular carcinoma, 15 extra-hepatic malignant disease; 33 healthy subjects were used as controls. Analysis of variance demonstrated a significant variability among groups (F = 17.08, P = 0.0000). Higher concentrations of alpha 1-acid glycoprotein were detected in malignant extra-hepatic disease than in all other groups (P < 0.01); concentrations of alpha 1-acid glycoprotein were higher in hepatocellular carcinoma than in cirrhosis (P < 0.01). Multiple regression analysis by groups (dependent variable = alpha 1-acid glycoprotein; group 1 = mild chronic liver disease + cirrhosis; group 2 = hepatocellular carcinoma) showed a significant correlation for both group 1 (r = 0.6264, F = 8.005, P = 0.0000) and group 2 (r = 0.8947, F = 13.643, P = 0.0000). The significant standardised regression coefficients were: cholinesterase, C-reactive protein, gamma-glutamyltransferase and iron (negative) for regression upon group 1; C-reactive protein, alpha 1-antiproteinase, gamma-glutamyltransferase, iron (negative) for regression upon group 2. A difference between the 2 regression equation coefficients was detected (F = 5.209, P = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase of serum alpha 1-acid glycoprotein despite the decline of liver synthetic function in cirrhotics with hepatocellular carcinoma. 810 7

alpha 1-antitrypsin (alpha 1-AT) is a glycoprotein called an acute phase reactant, which increases in blood in a variety of inflammations. alpha 1-AT deficiency with an inherited remarkable reduction of alpha 1-AT in blood has two major disorders, pulmonary emphysema and liver diseases, particularly an infantile cirrhosis. It is of great interest that each disorder has peculiar mechanisms based on an imbalance between proteases and protease inhibitors. alpha 1-AT constitutes genetic polymorphism of which alpha 1-AT deficiency presents rare PiZ or PiZ-like variants. alpha 1-AT deficiency is an inherited metabolic disorder associated with not only a severe reduction of alpha 1-AT in blood, but also amino acid substitutions of alpha 1-AT due to gene variations.
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PMID:[Liver cirrhosis associated with alpha 1-antitrypsin deficiency]. 811 96

The asparagine-linked sugar chains in serum transferrin purified from patients with hepatocellular carcinoma (n = 13), healthy individuals (n = 5) and patients with liver cirrhosis (n = 6) were compared. Sugar chains released with N-glycanase from desialylated and pepsin-digested transferrin were derivatized by reductive pyridylamination. Analysis of the sugar chains by high performance liquid chromatography in combination with exoglycosidase digestion revealed an increase of a biantennary complex-type sugar chain with a fucosylated trimannosyl core; Gal beta 1-4GlcNAc beta 1-2Man alpha 1-6(Gal beta 1-4GlcNAc beta 1-2Man alpha 1-3) Man beta 1-4GlcNAc beta 1-4(Fuc alpha 1-6)GlcNAc in 7 of 13 cancer patients and an increase of a sugar chain with a fucosylated trimannosyl core and bisecting N-acetylglucosamine; Gal beta 1-4GlcNAc beta 1-2Man alpha 1-6(GlcNAc beta 1-4) (Gal beta 1-4GlcNAc beta 1-2Man alpha 1-3)Man beta 1-4GlcNAc beta 1-4(Fuc alpha 1-6)GlcNAc in one of the 13 cancer patients. Further, the fucosylated alteration of the sugar chain was detected also in alpha 1-antitrypsin, hemopexin, alpha 1-acid glycoprotein and alpha 2-HS glycoprotein from one of the patients with increased fucosylated transferrin.
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PMID:Alteration of asparagine-linked glycosylation in serum transferrin of patients with hepatocellular carcinoma. 817 73

Differential value of ACE activity and acid alpha 1-glycoprotein was evaluated in the selected liver and biliary tract diseases. The study involved 75 patients divided into 4 subgroups, according to the character of their disease: patients with the acute viral hepatitis, chronic viral hepatitis, liver cirrhosis, and cholelithiasis. It was found that ACE activity was significantly increased in all pathologies involving liver parenchyma, and normal in patients with extrahepatic cholestasis. It was also shown that simultaneous assays of ACE and acid < alpha 1-glycoprotein may serve as a sensitive test differentiating jaundice in parenchymal hepatic diseases from that in the course of extrahepatic pathology.
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PMID:[Activity of angiotensin converting enzyme I and levels of acid alpha glycoprotein in selected liver and biliary tract diseases]. 823 40


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