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 prevalence of HDAg in the liver of Chinese patients with chronic hepatitis and hepatocellular carcinoma was determined using direct immunofluorescence and immunoperoxidase. Overall, 6 patients (6.31%) out of 95 HBsAg carriers with inflammatory liver disease and neoplasia were found to be HDAg positive. HDAg was detected in the livers of 6 (7.59%) out of 79 chronic hepatitis patients. The relative frequency of HDAg in cirrhosis-B, CAH-B and CPH-B was 14.3%, 7.1%, and 5.89%, respectively. These results suggest that a sizeable number of HBsAg carriers are also carriers of HDV. In view of the large number of HBV carriers in China, the relatively minor but distinct presence of HDV represents an important health problem.
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PMID:Immunohistochemical research of HDV infection in Chinese patients with chronic liver disease. 217 Feb 57

Using spectrophotometric method, we studied the activities of serum alpha-L-fucosidase, N-acetyl-beta-D-glucosaminidase and alpha-D-mannosidase in 94 patients, of whom 32 had acute hepatitis, 4 subacute fulminant hepatitis, 27 chronic active hepatitis, 22 posthepatitic cirrhosis and 9 hepatocellular carcinoma. In comparison with normal controls, the activities of the three glycosidases in the patients were significantly increased. The degree of the elevation of alpha-L-fucosidase activity correlated to the clinical phases and the course of acute infection of hepatitis B virus (HBV). The levels of glycosidase activities could reflect to a certain degree the pathological variations of the liver. Monitoring the levels of glycosidase activities, especially alpha-L-fucosidase, would be helpful in the diagnosis and medical care of viral hepatitis and hepatocellular carcinoma.
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PMID:Activities of serum enzymes in patients with viral hepatitis B, posthepatitic cirrhosis and hepatocellular carcinoma. 217 63

Non-A, non-B hepatitis (NANB), whether following the transfusion of blood products or occurring sporadically without percutaneous exposure, is complicated in approximately 50% of cases by the development of chronic hepatitis. Emerging as a consistent observation is the insidious progression of such cases of chronic NANB hepatitis to cirrhosis. Among patients with chronic NANB hepatitis followed for up to 10 years, cirrhosis is demonstrable in 20%. In May, 1988, the identification of the agent of NANB hepatitis was described by Houghton and colleagues of the Chiron Corporation. Hepatitis C, a 10,000 nucleotide single-stranded RNA virus with properties similar to those of flavivirus, was identified by developing a cDNA library from the genetic material in a chimpanzee inoculum of high infectivity and locating a clone which elaborated a virus-specific protein. Serologic evidence for HCV infection can be detected in 60-90% of cases of transfusion-associated hepatitis and 50% of cases of sporadic NANB hepatitis. Antibody to HCV (anti-HCV) can be detected in 30% of chronic hepatitis B, in 10-46% of alcoholic cirrhosis, in 40-70% of cases of hepatocellular carcinoma HBsAg negative and in 0-83% of patients with auto-immune chronic active hepatitis. Assays for HCV antigen will require technology more sensitive such than current immunoassays, such as the polymerase chain reaction. The introduction into blood banks of a screening test for anti-HCV is expected to reduce the risk of transfusion-associated NANB hepatitis and is highly recommended.
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PMID:[Non-A, non-B hepatitis: hepatitis C]. 217 14

We investigated expression of HBV markers in chronic liver disease positive for antibody to HCV (anti-HCV). Sera from 107 patients with chronic non-A, non-B liver disease, 65 HBs antigen carriers with chronic liver disease and 14 asymptomatic HBV carriers were tested for the presence of anti-HCV. Anti-HCV was detected in 83 (78%) patients with chronic non-A, non-B liver disease, irrespective of the past history of blood transfusion, and anti-HCV prevalence was similar in each category of chronic liver disease. Fifty-three (64%) out of these 83 sera positive for anti-HCV has also antibodies to HBV. Anti-HBc antibody was detected frequently in liver cirrhotics with hepatocellular carcinoma than in chronic persistent hepatitis, chronic active hepatitis and cirrhotics without hepatocellular carcinoma. In addition, titers of anti-HBc antibody were significantly higher in cirrhotics with hepatocellular carcinoma than in the other groups. On the other hand, anti-HCV was detected in 7 out of 65 patients with HBV-related liver disease. Four out of these 7 were patients with HBV-related hepatocellular carcinoma. Anti-HCV was detected in none of asymptomatic HBV carriers. These findings suggest that infection with both HBV and HCV is likely to cause more serious liver disease than infection with a single agent.
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PMID:[Expression of hepatitis B virus (HBV) markers in chronic liver disease positive for antibody to hepatitis C virus (HCV)]. 217 12

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

Critical considerations are expressed on scientific approach to liver cirrhosis, a nosological entity based on both analytical inquiry and long term observation of a large number of cirrhotic patients. The main points taken into consideration are: the etiopathogenesis of cirrhosis; a systematic of diagnostic elements; some preventional aspects of the disease and of its major sequelae. In the histogenetical analysis, the following steps are identified and analysed: a) hepatocellular death (necrosis), b) inflammatory process, c) fibrosis, d) hepatocellular regeneration and disorganized vascular architecture as a consequence of nodular regeneration. The hepatotoxic action of the three most studied and widespread etiologic agents of cirrhosis, alcohol, HBV, iron, is also considered. Finally, as a last pathogenetic step and peculiar to liver cirrhosis, the complex vascular rearrangement that leads to a relative increase of the liver blood flow is analysed. Clinical experience suggests a distinction between active and inactive liver cirrhosis. In the former we find a chronic active hepatitis associated with nodular regeneration and subsequent compensatory blood flow rearrangement. No signs of chronic active hepatitis can be found in the latter which is characterized by irreversible alteration of the liver architecture, reduction of the liver function and hemodynamic rearrangement (portal and arterial). Both nosologic entities can be either clinically characterized or not by symptoms of the major sequelae and complications of cirrhosis. On the basis of the clinical experience, among the complications of cirrhosis spontaneous bacterial peritonitis, gastrointestinal bleeding, hepatorenal syndrome and hepatocarcinoma appear to have a great prognostic value. Association between hepatocarcinoma and liver cirrhosis, which seems to be independent of single etiologic factors of cirrhosis itself, also has a great reliance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Epistemology of liver cirrhosis]. 227 60

Two variants of dysplastic hepatocytes are revealed: small and large which are characterized by cell atypia and probably result from the disturbance of regenerative processes. The disturbance of the liver lobule architectonics is also a feature of dysplasia. The degree of hepatocyte dysplasia assessed by morphometric indices (nuclei surface, ratio of ellipticity) and its frequency increase with progression of the pathological process: chronic persistent hepatitis----chronic active hepatitis----liver cirrhosis----hepatocellular carcinoma. More frequent observation of the hepatocyte dysplasia in viral liver conditions (HBsAg in dysplastic hepatocytes) indicates the role of hepatitis B virus in the development of hepatocyte dysplasia. Increase of DNA content and nuclei polymorphism are observed in small and large dysplastic hepatocytes when the degree of dysplasia is increasing, this making these cells closer to cells of hepatocellular carcinoma and favouring the concept of hepatocellular carcinoma development in the foci of dysplastic hepatocytes, particularly in liver cirrhosis.
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PMID:[The morphological characteristics of hepatocyte dysplasia]. 228 82

Lymphocytes were propagated with interleukin 2 from liver tissue removed at transplantation from patients with primary biliary cirrhosis or autoimmune chronic active hepatitis. Phenotypic analysis of the cultured lymphocytes as well as the infiltrating cells in situ indicated that the culture technique did not select for a particular phenotype. Eight cultures were tested for cell-mediated lympholysis activity against a bile duct tumor line as well as a hepatocellular carcinoma line, but no specific killing was seen. In addition, no natural killer activity was detected. However, the lymphocyte cultures were able to kill the targets in a lectin-dependent cytotoxicity assay, indicating their cytolytic effector activity. Preliminary studies have demonstrated that lymphocytes extracted from hepatic tissue and hilar lymph nodes from a patient with primary biliary cirrhosis proliferated in response to autologous biliary epithelial cells. These methods might be useful in studying the pathogenesis of primary biliary cirrhosis and other liver diseases with autoimmune features.
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PMID:Propagation and characterization of lymphocytes infiltrating livers of patients with primary biliary cirrhosis and autoimmune hepatitis. 235 71

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.
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PMID:Detection of antibodies against the polymerase gene product in hepatitis B virus infection. 239 Oct 62


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