Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human alpha 1-microglobulin (alpha 1-m) levels were studied in the sera and urine of patients with various liver diseases. In patients with acute hepatitis and chronic hepatitis it was almost within the normal range. A significant decrease of serum alpha 1-m, however, was demonstrated in patients with compensated liver cirrhosis (p less than 0.05) as well as in those with decompensated liver cirrhosis (p less than 0.001). The most striking decrease was noted in patients with fulminant hepatitis (p less than 0.001). Its concentration in hepatoma was generally within the normal range, but there was 1 hepatoma case with the high concentration of alpha 1-m. Serum alpha 1-m levels correlated significantly with serum albumin, plasma fibrinogen and cholinesterase activity. As compared with the level in normal individuals, the patients with decompensated liver cirrhosis had significantly low urinary alpha 1-m (p less than 0.005), reflecting the findings for sera. These results indicated that the liver plays an important role in alpha 1-m synthesis, and its quantitation may be used for evaluating severe liver damage.
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PMID:Human alpha 1-microglobulin in various hepatic disorders. 619 36

The pattern of serum cholinesterase (ChE) isozyme appeared to be characteristically abnormal in liver cirrhosis and hepatoma. In liver cirrhosis an abnormal fast moving peak was observed in 92.5% of fifty three patients studied. Further, diminishing activities of ChE 3 and 4, accompanied by an emergence of weak bands with unusual rates of flow, were noted in 58.5%. The latter abnormality was always associated with the former one. The pattern in hepatoma was essentially the same with liver cirrhosis, though diversity of bands was also present in some cases. It was ascertained that these abnormalities was due to sialic acid content bound to the enzyme, but was not due to production of abnormal enzyme protein moiety. It was suggested by clinical analysis that the degree of the abnormality of the isozyme may be useful for the diagnosis and prognostic evaluation of liver cirrhosis.
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PMID:Abnormalities of serum cholinesterase isozyme in liver cirrhosis and hepatoma (Part II). 625 50

Two cases of hepatocellular carcinoma (HCC) were described, in whom hypercholinesterasemia was found. Histochemical examinations revealed that there was a significantly increase in enzyme activity of cholinesterase in liver tissue slice obtained from the part of carcinoma in case 1. It was found that cholinesterase activity in homogenized liver tissue in part of carcinoma was much higher than that of non-carcinoma, and even in other HCC cases, hepatic cirrhosis and control liver tissues. These results suggested that HCC cells were capable of producing cholinesterase and, therefore, that hypercholinesterasemia was an additional paraneoplastic syndrome in HCC.
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PMID:Hypercholinesterasemia in patients with hepatocellular carcinoma: a new paraneoplastic syndrome. 630 85

Serum arylesterase isozyme patterns were studied in 184 normal healthy individuals, 290 cancer patients and 466 patients with various diseases. No abnormal patterns were seen in the normal healthy subjects. Several abnormal patterns found in the group of cancer patients and patients with various diseases are described. In the majority of patients with cancer of the liver there is an abnormal additional cathodal band. The most cathodal band in normals or the two most cathodal bands in the patients with hepatoma with double cathodal bands stained for cholinesterase as well as for arylesterase. We also studied serum arylesterase activity on the basis of the kinetic release of beta-naphthol in these groups. The mean activity in normal healthy individuals agrees with that reported earlier. In patients with cancer and with miscellaneous other diseases, the mean activity is lower but the range of values in the two groups is very wide.
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PMID:Arylesterase isoenzymes and activity in normal healthy adults and in patients with cancer and with other diseases. 741 94

We measured urokinase-type plasminogen activator (u-PA) plasma levels in patients with various chronic liver diseases, including hepatocellular carcinoma (HCC), also measuring these levels in healthy volunteers. Plasma u-PA levels in the group of patients with decompensated liver cirrhosis (mean modified Pugh score of 14 points) were markedly elevated and significantly higher than those in the patients with decompensated liver cirrhosis with HCC (modified Pugh score of 10 points), those with compensated liver cirrhosis with HCC, and those with compensated liver cirrhosis. Patients in all these three latter groups had moderately and significantly elevated u-PA levels compared to levels in the chronic hepatitis group and the healthy volunteers, but the levels were not significantly different from each other. There was no relationship between u-PA plasma level and the type of HCC tumor invasion or number or size of tumors. Significant correlations were found between u-PA plasma levels and the results of seven different liver function tests in three groups without associated HCC; u-PA antigen and prothrombin time (%), hepaplastin test (%), serum cholinesterase, serum albumin, serum total cholesterol, and indocyanine green clearance correlated negatively, while u-PA antigen and serum total bilirubin correlated positively. These results suggest that plasma u-PA is associated with deterioration of liver function but not with HCC invasion.
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PMID:Elevated urokinase-type plasminogen activator plasma levels are associated with deterioration of liver function but not with hepatocellular carcinoma. 787 70

The authors measured immunoenzymatically circulating intercellular adhesion molecule-1 (cICAM-1) concentration in 135 patients with liver disease of either viral or toxic etiology: 13 had acute hepatitis; 58 had mild chronic liver disease; and 64 had cirrhosis (superimposed in 30 by hepatocellular carcinoma). Forty patients with extrahepatic diseases (19 with malignancies) and 28 healthy blood donors were tested as controls. One-way analysis of variance demonstrated a significant variability of cICAM-1 concentration among groups (F = 76.67, P < .0001), the highest value being recorded in acute hepatitis (Bonferroni's test for pairwise comparisons, P < .01). Total bilirubin showed a strong correlation with cICAM-1 (R = 0.766, P < .001). By stepwise multiple regression analysis the independent predictors of cICAM-1 concentration were chosen in the following order: total bilirubin; aspartate aminotransferase; cholinesterase; alpha-1-antitrypsin; and immunoglobulins. Thus, in addition to inflammation, cholestasis and decline of functioning hepatic mass may influence cICAM-1 concentration.
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PMID:Circulating intercellular adhesion molecule-1 (cICAM-1) concentration in liver disease. Relationship with cholestasis and functioning hepatic mass. 794 24

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

We measured serum erythropoietin (EPO) immunoenzymatically in 245 subjects (151 male, 94 female) to investigate the pathophysiology of its liberation in patients with liver disease. Twelve patients had acute hepatitis, 60 mild chronic liver disease (CLD), 50 cirrhosis (CIR), 43 hepatocellular carcinoma (HCC), 16 malignant extrahepatic disease, 32 benign extrahepatic disease (BEN); 32 subjects served as healthy controls. Higher EPO levels were found in all groups of patients as compared with controls (Bonferroni's test, P < 0.01); CIR and HCC had higher values than CLD and BEN (P < 0.01). By multiple regression analysis, EPO correlated with haematocrit, cholinesterase and C-reactive protein (F = 18.63, P < 0.0001). Thus, circulating EPO increases in patients with liver disease, particularly in its more advanced forms. Besides anaemia, both impairment of liver function (possibly via decreased EPO metabolism) and inflammation seem to play contributory roles in elevating serum EPO.
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PMID:Evidence for a multifactorial control of serum erythropoietin concentration in liver disease. 755 88

The activities of lecithin-cholesterol acyltransferase (LCAT) and lipid transfer protein (LTP) were assayed using sensitive radioassay methods in controls (n = 113) and in patients with various liver diseases (n = 72). Plasma LCAT activity decreased with progression of hepatocellular damage. Plasma LTP activity in controls was 216 +/- 68 nmol/mL/h, and there were no significant differences between controls and patients with chronic hepatitis ([CH], 193 +/- 70), compensated liver cirrhosis (LC) with or without hepatocellular carcinoma ([HCC], 197 +/- 48 and 193 +/- 62, respectively), or decompensated liver cirrhosis ([dLC], 182 +/- 65). In acute viral hepatitis, LTP activity decreased significantly; however, the degree of reduction was not as dramatic as that for LCAT. There was no correlation between LCAT and LTP activity both in controls and patients with various liver diseases. LCAT activity was positively correlated with serum albumin (r = .52, P < 0.1) and cholinesterase (r = .37, P < .01) levels, and inversely correlated with serum bilirubin level (r = -.38, P < 0.1); there was no correlation between plasma LTP activity and these parameters of liver function. That plasma LTP activity did not change with hepatocellular damage may indicate that the liver in humans may not be the primary site of LTP production.
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PMID:Lecithin-cholesterol acyltransferase and lipid transfer protein activities in liver disease. 844 43

Molecules governing cellular interactions have been suggested to be involved in the spurious elevation of alpha 1-fetoprotein (AFP) in non-neoplastic liver disease. To explore this controversial issue, we measured AFP, circulating intercellular adhesion molecule 1 (cICAM-1), and common liver function tests in 111 patients (71 male, 40 female). Eighty-four patients had non-neoplastic chronic liver disease and 27 had hepatocellular carcinoma. The concentration of cICAM-1 was determined immunoenzymatically. In patients with non-neoplastic chronic liver disease, univariate analysis demonstrated a significant correlation between AFP and cholinesterase (R = -0.397, P < 0.001), aspartate aminotransferase (R = 0.421, P < 0.001), bilirubin (R = 0.231, P < 0.05) and cICAM-1 (R = 0.430, P < 0.001). Multivariate analysis among these variables and AFP indicated cICAM-1 to be the strongest independent predictor of AFP. We conclude that cICAM-1 compares favourably with liver function tests in predicting non-specific AFP variations in non-neoplastic chronic liver disease, suggesting a link between targeting of the inflammatory damage to the hepatocyte and development of neoplasia.
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PMID:Circulating intercellular adhesion molecule 1 predicts non-specific elevation of alpha 1-fetoprotein. 864 48


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