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)

A novel, simple, clinically useful quantitative liver function test, called the galactose single point (GSP) method, was developed by measurement of galactose blood concentration 1 h after galactose was administered (0.5 g/kg). It was quickly infused intravenously in 55 normal healthy volunteers, 73 patients with chronic hepatitis (CH), 36 with cirrhosis and 41 with hepatocellular carcinoma (HCC). Patients with CH diagnosis were assessed by liver biopsy. Cirrhosis was diagnosed by histological examination or a chronic hepatitis history with esophageal varices or ascites, whereas HCC was diagnosed either histologically, or cytologically proved, or as implied in the 'one imagine study' being positive with AFP > 300 ng/dl. Highly significant galactose blood levels were observed between normal healthy volunteers and patients 50, 60 and 70 min after galactose was administered. Galactose elimination capacity (GEC), modified GEC (MGEC) and consecutive GSP tests were performed in 6 healthy volunteers for 2 days. 0.64-16.87% variation was observed for each subject. The significant differences (p < 0.001) in average GSP values were 247 +/- 18.1, 422 +/- 27.3, 629 +/- 42.8 and 579 +/- 43.6 micrograms/ml for normal healthy volunteers, CH, cirrhosis and HCC patients, respectively. Highly significant correlations (p < 0.001) were obtained among GSP, GEC and MGEC for all patients. Positive correlations were observed between GSP, GEC, MGEC and AST (serum aspartate aminotransferase), ALT (serum alanine aminotransferase), serum bilirubin, albumin, prothrombin time and r-globulin. According to results obtained from 202 normal healthy volunteers and patients, the GSP method may be a simple, clinically useful quantitative measurement of liver function for the determination of a patient's residual liver function, the prognosis of liver function for patients with cirrhosis, postoperational follow-up and, finally, the timing of a liver transplant.
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PMID:Assessment of liver function using a novel galactose single point method. 133 11

It is frequently assumed that the risk of hepatocellular carcinoma related to hepatitis B virus is higher when chronic hepatitis B virus infection is acquired early in life. This hypothesis has never been directly evaluated. However, firstborn and secondborn children are exposed to common infections after their school enrollment, whereas laterborn children are exposed much earlier, through their older siblings. The authors analyzed sibship size and birth order data from a large case-control study of patients admitted to Athens, Greece, hospitals between April 1976 and October 1984. The analyses included 185 patients with hepatocellular carcinoma, 35 patients with metastatic liver cancer, and 432 other hospital controls. There was a tendency for cases of hepatocellular carcinoma to concentrate at higher birth orders. When the analysis was restricted to cases and controls who were positive for hepatitis B surface antigen, this tendency was even more notable. These results are compatible with the hypothesis that establishment of chronic hepatitis B virus infection at an early age increases the risk of hepatocellular carcinoma substantially more than does chronic infection with this virus established at a later age.
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PMID:Age at first establishment of chronic hepatitis B virus infection and hepatocellular carcinoma risk. A birth order study. 133 66

Result of hepatic resection in 150 patients with hepatocellular carcinoma (HCC) harboring up to three lesions smaller than 3cm in diameter (PEI candidates) and 144 patients with multiple lesions (TAE candidates) was studied. In PEI candidates, associated liver diseases were liver cirrhosis in 108 patients (72%) and chronic hepatitis in 41 (27.3%). Survival rates at 1-, 3- and 5-years were 98.0%, 83.5% and 61.4%, respectively. Prognosis of the patients with a well-differentiated solitary lesion was particularly good. In TAE candidates, 1-, 3- and 5-years survival rates were 98.5%, 57.8% and 33.7%, respectively. Half of the patients were considered to have multicentric disease, and their prognosis was better than that with intrahepatic metastases. Surgical resection is recommended as a primary treatment of HCC when the patients are feasible for surgery even if nonsurgical treatments are possible. Further study is required to establish the proper indication for nonsurgical procedures as a primary treatment of HCC in patients who are candidates of surgery.
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PMID:[Result of surgical resection of hepatocellular carcinoma in possible candidates for nonsurgical treatments]. 133 12

In the treatment of active chronic hepatitis and hepatocellular carcinoma some effective drugs can produce myelosuppression. Hypersplenism may considerably limit the dosage of such drugs. Splenectomy is an effective treatment for hypersplenism, although it is not without complications. Partial splenic embolization is a good and safe procedure; 15 patients were treated in order to achieve higher platelet and leukocyte counts. Embolization has been performed with gelfoam with local and systemic antibiotics (Spigos' protocol) and 50-75% of the splenic parenchyma was infarcted. All patients could be treated for the underlying hepatopathy with adequate dosages of interferon or chemotherapeutic drugs.
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PMID:Splenic embolization prior to myelosuppressive treatment in hepatocarcinoma and active chronic hepatitis. 133 37

Aflatoxin is implicated as a risk factor for hepatocellular carcinoma in areas of the world with a high incidence of this tumor. The present study was designed to validate the use of aflatoxin-albumin adducts in peripheral blood as a measure of individual exposure to this carcinogen. Dietary intake of aflatoxin was measured at the individual level in 20 residents of Keneba, West Kiang, The Gambia, over a 7-day period and correlated with the level of aflatoxin bound to peripheral blood albumin at the beginning and end of the study. Complementary enzyme-linked immunosorbent assay and high-performance liquid chromatography-fluorescence techniques were used to assay the aflatoxin adducts. All subjects were exposed to aflatoxin originating from several food types, with an average daily intake of 1.4 micrograms/day. A significant correlation (r = 0.55; P = < 0.05) was observed between the dietary intake and the level of albumin-bound aflatoxin at the end of the study. In addition, a good agreement was obtained with the two analytical techniques. A comparison of matched chronic hepatitis B surface antigen carriers with noncarriers did not reveal any difference in adduct formation for a given dietary intake of aflatoxin. These studies demonstrate the validity of aflatoxin-albumin adducts as a marker of human exposure to this carcinogen.
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PMID:Dietary intake of aflatoxins and the level of albumin-bound aflatoxin in peripheral blood in The Gambia, West Africa. 133 83

The DNA-HBV was investigated in 109 serum samples from 75 patients with different forms of infection with the HB virus, using an RIA hybridization technique (Genostic-Abott). DNA-HBV was present in 12 of 18 cases of acute hepatitis, 1 of 3 patients with fulminant disease, 11 of 14 patients with chronic hepatitis and/or cirrhosis, 2 of 10 patients with hepatoma and 6 of 30 asymptomatic chronic carriers. Presence of DNA-HBV beyond 60 days in 7 patients with acute hepatitis established the chronic state. The highest levels were found in patients with chronic hepatitis or cirrhosis (mean 41 +/- 11 pg/ml) and the lowest in chronic carriers and patients with hepatoma. High levels of DNA-HBV denote persistent viral replication and would support antiviral treatment. Thus, investigation of DNA-HBV has diagnostic, prognostic and therapeutic implications in patients with Hepatitis B.
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PMID:[Significance of investigating viral DNA in serum from patients with hepatitis B]. 134 Sep 75

Intercellular adhesion molecule 1 (ICAM-1), a counter-receptor for lymphocyte function-associated antigen 1 on T cells, is critically important to a wide variety of adhesion-dependent leukocyte functions, including antigen presentation and target cell lysis. ICAM-1 expression by hepatocytes is increased in areas of inflammation and necrosis during chronic hepatitis B. Whether induction of ICAM-1 is due to the effect of inflammatory cytokines or involves a direct effect of the hepatitis B virus (HBV) remains unknown. In the present study, transfection of the HBV genome into human hepatoma cell lines resulted in enhanced expression of ICAM-1 protein and RNA in the absence of inflammation. Results of subgenomic transfections indicated that the HBV X protein (pX) induced ICAM-1 expression. Nuclear run-on assays showed that pX induced the ICAM-1 gene by increasing its rate of transcription. Although both pX and interferon gamma induced transcription of ICAM-1, addition of interferon gamma to cells expressing pX did not show an additive or synergistic effect. These results indicate that pX can directly regulate expression of ICAM-1 and may participate in the immunopathogenesis of HBV infection.
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PMID:Up-regulation of intercellular adhesion molecule 1 transcription by hepatitis B virus X protein. 136 Jun 68

Recent advances in epidemiology, virology, of clinical of hepatitis are presented in the paper. The authors pointed out that hepatitis A never becomes chronic. On the other hand, with hepatitis B or B and D, evolution to chronicity is possible. Two distinct forms of non-A non-B hepatitis are now distinguished: parenterally transmitted non-A non-B hepatitis, mainly due to hepatitis C virus; enterically transmitted non-A non-B hepatitis mainly due to hepatitis E virus. C virus hepatitis is characterized by a frequent course to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Chronic forms are associated with the presence of anti-HC antibodies in the serum. These antibodies are rarely present in the acute stage of the disease. Hepatitis E is almost exclusively encountered in developing countries. Like with A virus hepatitis, chronicity never occurs. However, fulminant hepatitis is possible in pregnant women in the third trimester of pregnancy. There is no routine serological test. Development of vaccines against A, E and C viruses can be expected very soon. There is no specific treatment of acute viral hepatitis.
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PMID:[Acute viral hepatitis--present status and perspectives]. 136 29

The concentration of plasma vitronectin was determined and compared with various parameters of liver function including the blood coagulation system in patients with liver diseases. The severity of cirrhosis was graded according to Child's criteria and compared with the plasma vitronectin level. Furthermore, the distribution of vitronectin in the liver of patients with liver diseases was studied by light and electron microscopy using the indirect immunoperoxidase method. The plasma vitronectin level was low in all liver disease groups as compared with the healthy controls. The difference from the controls was significant in patients with hepatocellular carcinoma and decompensated cirrhosis. Moreover, the plasma vitronectin level was positively correlated with the levels of serum cholinesterase, albumin, plasma alpha 2 plasmin inhibitor-plasmin complex and the prothrombin time and results of the hepatoplastin test. Plasma vitronectin decreased with increasing severity of cirrhosis according to Child's criteria. These results suggest that the plasma vitronectin level is a useful parameter of hepatic synthetic function in patients with liver diseases; it may also reflect the severity of cirrhosis. Light microscopy revealed vitronectin in the area of focal necrosis and the portal tracts in the liver of patients with acute viral hepatitis, in the area of piecemeal necrosis in the liver of patients with chronic hepatitis and along the area of fiber deposition in the liver of patients with cirrhosis. Immunoelectron microscopy showed vitronectin in the rough endoplasmic reticulum of hepatocytes. Moreover, vitronectin was seen around inflammatory cells, endothelial cells, Ito cells and hepatocytes in the perisinusoidal area near focal necrosis and piecemeal necrosis and on collagen fibers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitronectin in liver disorders: biochemical and immunohistochemical studies. 137 81

Tenascin is an oligomeric glycoprotein of the extracellular matrix synthesized during embryonic development. It is prominently expressed in a variety of tumors. The role of tenascin in liver tissue is, however, unknown. We used immunocytochemistry to define the localization of tenascin and compare this with the localization of non-collagenous proteins, such as laminin and fibronectin, in normal human liver and pathological liver from patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. In normal liver, tenascin expression was localized along the sinusoidal and vascular wall. In fibrotic liver, tenascin was also observed in the region between the hepatic parenchyma and the fibrosing portal tracts, especially in areas of piecemeal necrosis in chronic hepatitis. Immuno-EM study of liver tissue in chronic hepatitis strongly suggested the synthesis and secretion of tenascin by fat-storing cells into the space of Disse. In hepatocellular carcinoma, tenascin was expressed in both the capsule and lobular septa, but not in the sinusoidal walls of the tumors. These results led us to postulate a close relationship between the occurrence of this protein and disease processes such as fibrosis and cancer invasion.
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PMID:Tenascin expression in human chronic liver disease and in hepatocellular carcinoma. 137 63


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