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)

The general use of synthetic estrogens like DC pointed out that near many skilled collateral effects, some others that are showing with a decrease of bile excretion (cholestasis), reversible with their administration interruption; with hepatic cells adenoma that are potentially premalignant and can transform into hepatocellular carcinoma; with vascular complications such as (most frequently in carcinomatousis) "hepatic peliosis" and "thrombosis" of suprahepatic veins (Budd-Chiari's syndrome). There is no overall increase in the incidence of gallbladder disease (cholelithiasis and cholecystitis).
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PMID:[Oral contraceptive and hepatic effects]. 210 Nov 66

Tissue plasminogen activator (t-PA) in plasma obtained from patients with acute hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, drug-induced intrahepatic cholestasis, obstructive jaundice, fulminant hepatitis or disseminated intravascular coagulation (DIC), was analysed chromatographically. Liver disease cases showed a new peak (peak C) on HPLC fractionation. The protein of peak C had a lower molecular weight than ovalbumin. Lysine- and zinc- chelating affinity chromatography revealed that the peak C consist with the light chain (L-chain) of t-PA. The L-chain was also found in patients with DIC, but disappeared after improvement of DIC. Therefore, it was suggested that appearance of the L-chain would be related to acceleration of secondary fibrinolysis in plasma. The L-chain was especially high in plasma obtained from patients with decompensated liver cirrhosis. These results indicated that high increase of the L-chain in cases of severe liver disease may be due to either impaired clearance of t-PA in the liver or secondary hyperfibrinolysis accompanied by DIC. We concluded that determination of the L-chain of t-PA may contribute to clarify the mechanism of hyperfibrinolysis in liver diseases.
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PMID:[Qualitative analysis of tissue plasminogen activator in plasma obtained from various liver diseases by gel filtration and affinity chromatography]. 210 95

Patients with liver disease frequently have hemostatic abnormalities which include accelerated fibrinolysis. In order to assess the fibrinolytic state in liver disease, plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP), and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 36 patients with liver disease (six patients with acute hepatitis, seven with chronic hepatitis, ten with liver cirrhosis, 11 with hepatocellular carcinoma, and two with intrahepatic cholestasis). As compared with healthy subjects, mean plasma levels of FbDP (1,083 +/- SD 1,254 vs. 236 +/- 100 ng/ml, P = 0.005) and TDP (1,773 +/- 1,814 vs. 669 +/- 212 ng/ml, P = 0.001) were significantly elevated in patients with liver disease, whereas FgDP was normal (389 +/- 202 vs. 396 +/- 132 ng/ml, P = 0.87). Plasma FbDP correlated very well with TDP (r = 0.986, P less than 0.00001) in liver disease. In addition, FbDP and TDP but not FgDP correlated with plasma concentrations of thrombin-antithrombin III complex. When plotted by the disease categories, the magnitude of elevations of FbDP and TDP was the most prominent in acute hepatitis followed by hepatocellular carcinoma. These findings indicate that activation of fibrinolysis occurs following thrombin generation, but increased primary fibrinogenolysis is rare in liver disease.
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PMID:Fibrinolysis and fibrinogenolysis in liver disease. 219 67

The methods to detect antimitochondrial antibodies (AMAs), which are characteristically positive in primary biliary cirrhosis (PBC), have some problems in technical difficulty, sensitivity and specificity. Based on the finding that one of the major antigens corresponding to AMAs was the E2 component of pyruvate dehydrogenase complex (PDH), a very simple enzyme-linked immunosorbent assay (ELISA) to detect anti-PDH antibody (anti-PDH) has been developed in this study. Among 68 patients with PBC, IgG class anti-PDH and IgM class anti-PDH were detected in 64 patients (94.1%) and in 55 patients (80.8%), respectively, while only three cases (4.4%) were both negative. Mean optical densities (O.D.) of sera from patients with PBC were 0.536 +/- 0.386 (mean +/- SD) in IgG class and 0.308 +/- 0.342 in IgM class. No positive cases were detected in the following patients by this ELISA: 20 patients with acute viral hepatitis, 24 with chronic persistent hepatitis, 32 with chronic active hepatitis, 19 with liver cirrhosis, 19 with hepatocellular carcinoma, 19 with acute intrahepatic cholestasis, 10 with autoimmune hepatitis, and six with systemic lupus erythematosus. Among nine AMAs negative cases with PBC by conventional indirect immunofluorescence (IF) assay, seven cases were found to be positive by this ELISA. The inter-assay coefficient of the variation of this method ranged from 4.9% to 5.8% and the intra-assay coefficient of variation from 3.8% to 5.1%. Therefore, this ELISA is useful for diagnosis of PBC.
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PMID:Detection of anti-pyruvate dehydrogenase complex antibody in primary biliary cirrhosis by an enzyme-linked immunosorbent assay. 221 Feb 21

We have measured the plasma PIVKA-II levels in 188 cases of various liver disease with HCC and malignant diseases in other organs by an EIA, using a monoclonal antibody (E-1023 kit, Eisai), and also have measured the plasma vitamin K levels in cases of HCC and cholestasis by an HPLC. Plasma PIVKA-II was detected in many cases of HCC (67%, 35 of 52 cases) and cholestasis (60%, 6 of 10 cases). In contrast, the positivities of PIVKA-II in the other diseases including benign liver diseases were very low. Combination assays of PIVKA-II and vitamin K revealed that PIVKA-II correlates with vitamin K in cholestasis but not in HCC, suggesting that PIVKA-II in HCC does not depend on a systemic deficiency of vitamin K. From these results, it was concluded that PIVKA-II is a reliable marker which can reflect the clinical course of HCC.
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PMID:[Evaluation of plasma PIVKA-II as a new marker for hepatocellular carcinoma]. 246 9

This study was undertaken in order to compare the ability of 4 tumour markers to discriminate between liver cirrhosis patients with or without hepatocellular carcinoma (HCC). Serum alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), CA 19-9 and tissue polypeptide antigen (TPA) were determined in 63 patients with liver cirrhosis and in 25 patients with HCC in liver cirrhosis. All 4 serum markers were found to be increased in a number of liver cirrhosis patients, regardless of the presence of HCC. AFP was found to be more elevated in HCC patients as compared to the other group; no difference was observed for CA 19-9, CEA and TPA. A significant correlation was detected in HCC patients between AFP and TPA. Significant correlation were detected in all except HCC patients between liver function tests and TPA. We can conclude that AFP determination remains as yet the only suitable marker able to detect HCC in liver cirrhosis. The newly introduced serum marker CA 19-9 is, as previously reported, unhelpful for CEA. TPA can in some instances (i.e. in the absence of an important hepatic cell necrosis or cholestasis) provide a clue to neoplastic growth.
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PMID:Do CA 19-9 and TPA play a minor role as compared to AFP in diagnosing primary hepatocellular carcinoma? 247 97

Alagille's syndrome is a common form of familial intrahepatic cholestasis. In addition to the hepatobiliary system, many other organ systems are affected. Most of the affected patients survive through adulthood. Hepatic involvement is the cause of death in about one-third of patients. Hepatocellular carcinoma complicating the course of this disease is very rare and has been reported previously in only three cases. We report a family in which three of four siblings with this syndrome developed hepatocellular carcinoma and died as a result of it. None of these children had a liver disease, other than Alagille's syndrome, that could account for the development of such a tumor. This experience suggests that Alagille's syndrome, or at least chronic cholestasis, may be a predisposing factor for the development of hepatocellular carcinoma. Annual determination of alpha-fetoprotein and abdominal computed tomography (CT) scan may detect the development of a hepatocellular carcinoma in such cases while they are still resectable.
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PMID:Hepatocellular carcinoma in Alagille's syndrome: a family study. 254 4

A 57-year-old man with hepatocellular carcinoma (HCC) invading the hepatic duct was treated with transcatheter arterial embolization (TAE). The dilated hepatic duct was decompressed his jaundice disappeared and he survived for 10 months after the first TAE, succumbing due to bleeding from gastric erosion. Although total bilirubin was 26.7 mg/dl and massive ascites was noted on occasion of the first TAE, hepatic dysfunction did not worsen and both icterus and ascites decreased, disappearing one month after the therapy. Autopsy revealed HCC with trabecular arrangement originating in the left lobe and growing into the left hepatic duct accompanied by liver cirrhosis and follicular carcinoma of the thyroid gland. Severe icterus caused by bile duct obstruction does not correlate with the grade of hepatic failure in HCC with liver cirrhosis, so TAE was effective and should be tried as a first choice therapy in such a poor risk case.
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PMID:A case report of transcatheter arterial embolization of cholestatic type of hepatoma. 254 3

Thirty-one patients with primary biliary cirrhosis were observed in Picardy during the decade 1975-1984. Mean annual incidence was 2.6 per 10(6), and point prevalence, 13 per 10(6) inhabitants in 1984. Asymptomatic cases (without clinical manifestations of cholestasis) constituted 32% of all patients. In five of the 21 symptomatic patients, ascites and/or digestive hemorrhage due to ruptured esophageal varices revealed the disease. Nine patients (2 with initially asymptomatic PBC) died during the follow-up period. Cholelithiasis was present in 10 patients (32%) and one case of hepatocellular carcinoma was found at autopsy.
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PMID:[Asymptomatic forms of primary biliary cirrhosis seen in 10 years in Picardie]. 294 18

A patient is described with micronodular cirrhosis, partial (heterozygous, MZ) deficiency of alpha-1-antitrypsin (AAT) and hepatocellular carcinoma. The patient did not drink alcohol and all serological markers of infection with hepatitis B virus were absent. Death was due to intra-peritoneal bleeding from a multifocal liver tumour. Histology revealed multiple intracytoplasmic AAT globules in hepatocytes at the periphery of the cirrhotic nodules. Copper granules, present in the same non-neoplastic liver cells may have resulted from minor cholestasis. Within the neoplastic hepatocytes AAT globules were sparse and copper deposits co-existed with the globular variant of Mallory bodies. The case is presented in support of the postulated association of partial deficiency of AAT, chronic liver disease and hepatic neoplasia.
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PMID:Cirrhosis and hepatocellular carcinoma in a patient with heterozygous (MZ) alpha-1-antitrypsin deficiency. 300 53


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