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 review of 180 patients with either chronic hepatitis or hepatocellular carcinoma (HCC) indicate a significant association. 40 patients with chronic hepatitis were seen between 1975-79. 6/25 of chronic active hepatitis and 7/15 with chronic persistent hepatitis were HBsAg positive (RIA). In the 41 patients with HCC, 15 (37%) were alcoholic, 10 cirrhosis (HBsAg positive), 5 haemochromatosis 5 cryptogenic cirrhosis, 2 probably due to sex steroids and in 4 no aetiological factor was apparent. HBsAg was present in 10/22 (45%) of HCC with cirrhosis, 15/256 (6%) for alcoholic cirrhosis, 5/16 (33%) for haemachromatosis and 5/30 (16%) cryptogenic cirrhosis. 8/80 (10%) who had acute viral hepatitis (B) are antigen positive at 6 months. This report shows that Hepatitis B virus infection is now a significant causes of liver injury in 180 patients studied. The majority of patients who have HBsAg positive cirrhosis do not have a history of acute hepatitis.
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PMID:An Australian experience of hepatitis B infection, cirrhosis and hepatocellular carcinoma. 625 12

Carcinoembryonic antigen (CEA) has been studied with a radioimmunoassay technique with an antiserum obtained from hepatic metastases of colonic cancer (Sorin Biomedica, Saluggia). The normal range of seric CEA varies from 0 to 10 ng/ml; 10 ng/ml is the higher value found in a smoker healthy subject. Seric CEA than 10 ng/ml has been found in 27% of cirrhoses, 39% of acute viral hepatitis (HBsAg+), 13.3% of chronic active hepatitis, 7.7% of chronic persistent hepatitis, 36% of alcoholic hepatitis and 100% of hepatomas. The diminished hepatic clearance of the antigen, or the derepression of its regulator gene, or the formation of CEA-like substances may cause the increase of seric CEA in hepatic diseases. The antiserum obtained from hepatic metastases of colonic carcinoma may explain the positivity in all the patients with hepatoma.
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PMID:[Assay of the carcinoembryonic antigen (CEA) in acute and chronic liver diseases and hepatocellular carcinoma]. 626 78

Patients with liver cirrhosis have the opportunity of receiving blood transfusions rather frequently. Accidental transfusion of blood containing HBs Ag occurred in such a case. Recently, we encountered a case of hepatocellular carcinoma based on posthepatitic cirrhosis in which an emergency blood transfusion because of massive hematemesis from a gastric ulcer was followed by acute B type viral hepatitis. The remainder of the transfused blood was preserved an we tested it serologically when the symptoms of acute viral hepatitis were manifested. We are able to detect hepatitis B surface antigen in the serum. In this patient, the preceding liver cirrhosis did not influence on the clinical course of acute B type viral hepatitis and conversely, the acute B type viral hepatitis did not have any influence on the subsequent clinical course of the liver cirrhosis.
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PMID:Acute type B viral hepatitis due to accidental transfusion of blood containing HBs Ag in a patient with liver cirrhosis. 627 74

The presence of hepatitis Be antigen (HBeAg) and antibody (anti-HBe) was investigated by immunodiffusion in 144 patients with chronic liver disease, and 129 with hepatocellular carcinoma (HCC). Most of the patients were HBsAg-positive. In 62 patients with chronic active viral hepatitis B, 17 (27%) were positive for HBeAg and 25 (40%) for anti-HBe. HBeAg and anti-HBe were not related to the degree of histological activity or serum alanine aminotransferase activities, but were related more frequently to higher HBsAg titer and younger age; whereas anti-HBe generally correlated in an opposite manner. Two patients seroconverted from HBeAg to anti-HBe in 13 and 20 months respectively. HBs antigenemia was not eliminated in either HBeAg or anti-HBe positive patients. The prolonged interval in seroconversion and an age-related declining frequency of HBeAg, accompanied by a reciprocal increase in anti-HBe in chronic infection, suggest anti-HBe as a chronologic indicator in HBs antigenemia in chronic HBsAg carriage. In HCC, regardless of coexisting cirrhosis, a predominant frequency of anti-HBe (62%) was found as in cirrhosis (54%), suggesting longstanding HBsAg carriage in these patients.
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PMID:Hepatitis Be antigen and antibody in chronic liver diseases and hepatocellular carcinoma. 628 25

Alpha 1-antitrypsin (alpha 1 AT) is a glycoprotein of hepatic origin which functions as a systemic protease inhibitor (Pi). Its production is controlled by two autosomal-codominantly transmitted alleles. Among the numerous genetic variants some alleles (predominantly PiZ) may induce alpha 1 AT-deficiency, facultatively associated with childhood liver disease. However, the pathogenesis of this congenital disorder, which may progress to complete cirrhosis remains obscure at present. In addition, no clear cut relationship has been proven between alpha 1 AT-deficiency and deranged liver architecture, observed in advanced aged adults. Possibly this may reflect a more accidental coincidence with the consequences of chronic viral hepatitis (Non A-Non B-type). Nevertheless, this hypothesis is hitherto unestablished as it holds for the supposed association between alpha 1 AT-deficiency and the occurrence of malignant hepatoma.
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PMID:[Alpha 1-antitrypsin deficiency and the liver (author's transl)]. 628 50

Dramatic advances in the understanding of the pathogenesis, pathophysiology, prevention, and treatment of the major viral diseases of the liver have been made. Hepatitis B and A viruses have been identified, with specific diagnostic serologic assays commercially available for these infections. The diagnosis of non-A, non-B hepatitis is currently made by exclusion. Morphological alterations in viral hepatitis are similar, regardless of the etiologic agent. Chronic viral hepatitis may be associated with hepatitis B and non-A, non-B, but not with hepatitis A. Persistent infection with hepatitis B virus is associated with an increased incidence of primary hepatocellular carcinoma. Viruses similar to the hepatitis B virus cause the same spectrum of liver disease in certain animals. With the development of a vaccine against hepatitis B virus infection, it may be possible to prevent a large proportion of worldwide chronic liver disease, as well as primary hepatocellular carcinoma.
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PMID:The biology of viral hepatitis. 628 89

In spite of many animal experiments and clinical observations, the etiologic aspects of primary hepatocellular carcinoma remain obscure. In 20 cases of primary hepatocellular carcinoma occurring in cases of liver cirrhosis, the author clarified the etiologic aspects. In 10 out of 20 cases of primary hepatocellular carcinoma, an early history of blood transfusion could be detected. In eight cases, an early history of acute viral hepatitis including three cases of posttransfusion hepatitis could be clarified. In the five remaining cases, etiologic factors were unknown but an early history of anicteric hepatitis could not be ignored. In four out of 20 cases, HBs Ag in the serum could be detected. In spite of these findings, the close relationship between hepatitis virus infection and the pathogenesis of primary hepatitis virus infection and the pathogenesis of primary hepatocellular carcinoma must be taken into consideration. The period of time from blood transfusion and/or the onset of acute viral hepatitis to initial diagnosis of primary hepatocellular carcinoma appears to be reasonable for the occurrence of the disease. The question remains open as to what role hepatitis virus plays in the pathogenesis of primary hepatocellular carcinoma.
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PMID:Clinical study on etiologic aspects of primary hepatocellular carcinoma. 629 25

The activity of L-GGT (EC 2.4.1.66), an enzyme catalyzing the intracellular biosynthesis of collagen, was determined in human primary hepatic cancer, acute viral hepatitis and cirrhotic liver tissues and compared to the mean level of enzyme activity in normal human liver tissues. The mean levels of L-GGT activity in primary hepatocellular carcinoma (PHC), acute viral hepatitis and cirrhotic tissues were 7.78, 2.69 and 2.16 times the mean level of enzyme activity in normal human liver tissues. The mean level of L-GGT activity in PHC was 3.61 times the mean level of L-GGT activity in cirrhosis and 2.90 times the mean value of liver enzyme activity in acute viral hepatitis. The findings in this study provide a basis for the highly elevated serum values of this intracellular enzyme in patients with primary hepatic cancer and the data indicate that L-GGT activity may be increased in primary liver cancer to compensate for an increased rate of collagen synthesis.
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PMID:Elevation of liver-galactosylhydroxylysyl glucosyltransferase activity in human primary hepatocellular carcinoma. 631 46

Total prolyl hydroxylase protein was measured in hepatic tissues of 8 patients with primary hepatocellular (PHC), 5 with acute viral hepatitis, and 5 with cirrhosis (3 alcoholic and 2 with secondary biliary cirrhosis). The mean values were compared with the mean value of 10 normal hepatic tissues. The mean values were all highly significantly elevated (P less than 0.001) in PHC, acute viral hepatitis and the cirrhotic patients, respectively. The mean L-IRPH value in PHC was about 9.50 times the control mean, while in acute viral hepatitis, and cirrhosis the mean L-IRPH values were about 3.00 and 2.30 times the control mean respectively. The mean level of L-IRPH in PHC was 4.06 times the mean level of L-IRPH in cirrhosis and 3.14 times the mean value in acute viral hepatitis. The findings of this study provide a basis for the elevated serum values of this intracellular enzyme of collagen synthesis in patients with primary hepatocellular carcinoma and the data indicate that this enzyme may be elevated to compensate for an increased rate of collagen synthesis in the malignant liver tissue.
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PMID:Liver immunoreactive prolyl hydroxylase protein in human primary hepatocellular carcinoma. 632 76

Among the three types of viral hepatitis agents-A, B and non-A, non-B-the hepatitis B virus (HBV) has been best characterized by immunologic and recombinant DNA technologies. The indefinite persistence of hepatitis B virus infection in 85% to 90% of perinatally infected infants and in about 10% of those infected later in life accounts for a worldwide epidemiologic reservoir of more than 200 million carriers who are at a high risk for the development of delta-infection, chronic liver disease and hepatocellular carcinoma. Active immunization with a safe and effective vaccine, derived from the plasma of carriers of hepatitis B surface antigen (HBsAg), is envisaged to avoid viral hepatitis type B and its chronic sequelae. In addition to serologic and immunohistochemical markers of hepatitis B virus infection, hybridization assays using cloned HBV DNA have provided new insight into the biology of this virus, its persistence and its oncogenic potential in humans and in animal models. Genetic similarities have been recognized between HBV and the antigenically distinct non-A, non-B agents implicated in some cases of transfusion-associated chronic hepatitis. Structurally this unique group of HBV and HBV-like agents are DNA viruses with functional attributes of integration and replication analogous to the retroviruses.
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PMID:Hepatitis B virus infection. Current concepts of chronicity and immunity. 632 74


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