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)

Antibody to hepatitis B core antigen (anti-HBc) was measured by radioimmunoassay using CORAB (Abbott Laboratories) in 10 cases of chronic persistent hepatitis (CPH), 46 cases of chronic aggressive hepatitis (CAH), 33 cases of liver cirrhosis (LC) and 53 cases of hepatocellular carcinoma (HCC) in relation to hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs). Ninety-eight point four percent of patients with HBsAg and 93.8% of patients with anti-HBs were positive for anti-HBc and the titers of anti-HBc in patients with HBsAg were significantly higher than those with anti-HBs. Thirty-five point five percent of patients negative for either HBsAg or anti-HBs were positive for anti-HBc. The titers of anti-HBc in patients with CPH, CAH and LC were relatively low, whereas 7 (46.8%) of the HCC patients negative for either HBsAg or anti-HBc had high titers of anti-HBc. The significance of the presence of anti-HBc alone is discussed.
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PMID:Determination of antibody to hepatitis B core antigen by radioimmunoassay in chronic liver disease. 625 99

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

Hepatocellular carcinoma associated with hepatitis B virus (HBV) infection occurring in a boy who was 6 years 2 months old is reported. The patient is thought to have been infected with HBV by exchange blood transfusion (horizontal infection) in the neonatal period. Jaundice appeared eight months after birth. He was subsequently treated and follow-up with a diagnosis of hepatitis B surface (HBs) antigen (Ag)-positive chronic persistent hepatitis. His mother and other family members were HBsAg-negative. Postmortem examination revealed a multinodular growth of hepatocellular carcinoma of trabecular and solid pattern, mainly of the right lobe, complicated with mild fibrosis of the liver. Numerous HBsAg-positive hepatocytes demonstrated by orcein staining and the indirect immunoperoxidase method were present in the noncancerous area. This hepatocellular carcinoma is considered to have occurred within six years two months after HBV infection and not to have been associated with liver cirrhosis. The present case may be valuable for assessing the oncogenic properties of HBV and the incubation period of HBV infection before it develops into hepatocellular carcinoma.
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PMID:A 6-year-old boy having hepatocellular carcinoma associated with hepatitis B surface antigenemia. 625 92

Immune complexes were investigated in the clinical course of 35 patients with the liver disease diagnosed by clinical and laboratory criteria, including the liver biopsy. Immune complexes were assayed by use of radio-labelled polyclonal rheumatoid and C1q as reactants with immune complexes. Although the highest amounts of immune complexes were determined in a few number of sera from patients with primary biliary cirrhosis, significantly higher amounts of immune complexes were observed in sera from patients with fulminant hepatitis, liver cirrhosis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma. However, no significant increase in immune complexes was seen in the clinical course of patients with chronic aggressive hepatitis (2A), chronic persistent hepatitis and acute hepatitis. Clinical follow-up studies of patients with higher amounts of immune complexes showed significant changes in the amounts of immune complexes in parallel with clinical, biochemical and immunological variables. The ultracentrifugal analysis demonstrated that immune complexes involved in the liver disease seemed to be larger than 19s in the size, since their concentration fluctuated according to the clinical course, although smaller complexes sedimenting at 7s and those between 8s and 19s were recognized without any significant changes in the clinical course.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 7. Immune complexes in the clinical course and their ultracentrifugal analysis. 626 81

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

Peripheral blood killer cell (K-cell) population of patients with chronic hepatitis was investigated by means of a plaque-assay method using sheep red blood cells. The mean K-cell population of 14 control subjects was 5.1 +/- 2.0% (mean +/- SD), and that of 28 patients with chronic hepatitis was 4.4 +/- 3.1%. These 28 patients were divided into three groups: CPH, CAH 2A and CAH 2B. The mean K-cell population of each group was decreased in order of the severity of the disease. Especially, that of patients with CAH 2B was a statistically significant decrease (p less than 0.01) from control subjects. In the course most patients with CAH, K-cell population did not change for three months after admission. K-cell population was observed to decrease in the patients with active stage of liver cirrhosis, but not in patients with the terminal stage of liver cirrhosis, even in hepatoma patients. It is suggested that the K-cell population may play an important role of pathogenesis of chronic hepatitis.
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PMID:Killer cell (K-cell) population in chronic liver disease. 626 41

Two hundred and eighty-seven autopsy cases of hepatocellular carcinoma (HCC) in Chinese were reviewed. The analyses included histological study of the tumour and of the non-cancerous liver tissue, the cause of death and metastases. Bleeding of oesophageal varices was more frequent but rupture of tumour less common in cases associated with cirrhosis than in those without cirrhosis. There was a significantly higher incidence of bilobar involvement by tumour in the clear cell type of HCC and in cases unassociated with cirrhosis compared to other histological types of HCC and HCC with cirrhosis, possibly because of longer survival of the former groups. A strong association was found between cirrhosis and hepatic fibrosis with HCC and hepatitis B surface antigen (HBsAg), suggesting an oncogenic effect of chronic persistent hepatitis B virus (HBV) infection on hepatocytes.
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PMID:An autopsy study of hepatocellular carcinoma in Hong Kong. 627 77

We performed a follow-up study on 70 patients with acute non-A, non-B (NANB) posttransfusion hepatitis and a retrospective study on 283 chronic hepatitis, 70 cirrhosis and 53 hepatocellular carcinoma patients of type NANB. In acute NANB post-transfusion hepatitis, as judged by the transaminase levels, th duration of the disease exceeded 6 months in 46/70 = 65.7% and 1 year in 32/70 = 45.7%. The histological diagnosis of the 32 cases persisting for more than 1 year was chronic active hepatitis in 5, chronic persistent hepatitis in 2 and unresolved hepatitis in 6. The frequency of previous transfusion in chronic hepatitis, cirrhosis and hepatocellular carcinoma of type NANB was 42.8, 37.1 and 15.1%, respectively, whereas the incidence of early posttransfusion hepatitis was 8.5, 8.6 and 7.5%, respectively. in chronic liver diseases with a history of jaundice and/or hepatitis, previous transfusions are more frequently associated with type NANB than with type B disease. The present study demonstrates that NANB posttransfusion hepatitis tends to develop to chronic liver disease when analyzed prospectively as well as retrospectively.
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PMID:The significance of blood transfusion in non-A, non-B chronic liver disease in Japan. 628 37

A simple, direct molecular hybridization test was employed to detect hepatitis B virus (HBV) DNA sequences in human serum. In 61 HBsAg carriers, many with HBV-related diseases (chronic persistent hepatitis, chronic active hepatitis, or posthepatitic cirrhosis), 28/28 (100%) who were HBeAg+ and 16/32 (50%) who were anti-HBe+ had HBV DNA sequences in their serum. Among 22 South African black patients with hepatocellular carcinoma, 7 (32%) had detectable HBV DNA in their serum but at reduced levels when compared to HBsAg carriers without hepatocellular carcinoma, suggesting that viral replication is suppressed or inactive in many hepatocellular carcinoma patients. Hybridization analysis also distinguished carriers with high, moderate, or low amounts of HBV DNA in serum. Ten to 20% of HBsAg+/HBeAg+ carriers showed high serum levels of HBV DNA but, surprisingly, a similar percentage of HBsAg+/anti-HBe+ carriers also showed relatively high serum levels of HBV DNA. Five patients who had undergone immunosuppression therapy and most of whom were on chronic hemodialysis had very high serum levels of HBV DNA, in the range observed during acute HBV infection. By epidemiologic analysis, two of these individuals were implicated in transmission of hepatitis to other hemodialysis patients, paramedical personnel, or intimate family contacts. Serum HBV DNA hybridization analysis identifies carriers with high serum levels of HBV irrespective of HBeAg/anti-HBe status and may define individuals with potentially high risk of transmitting infection to their immediate contacts.
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PMID:Detection of hepatitis B virus DNA directly in human serum by a simplified molecular hybridization test: comparison to HBeAg/anti-HBe status in HBsAg carriers. 630 65

HBeAg and anti-HBe were sought by RIA in the serum of 320 HBsAg-positive and 27 HBsAg-negative Greek patients with acute and chronic liver diseases. The incidence of HBeAg and anti-HBe in the group of 60 patients with acute hepatitis B was 23% and 77%, respectively. Among the 35 patients with chronic active hepatitis 6 (17%) were HBeAg-positive and 24 (69%) anti-HBe positive; among the 25 patients with chronic persistent hepatitis 3 (12%) were HBeAg-positive and 22 (88%) anti-HBe positive. Similar results were found in the groups of patients with cirrhosis and hepatoma. These findings show that all cases of acute hepatitis B were HBeAg-positive at the onset of the disease and a seroconversion to anti-HBe appeared very early in most of the cases. The extremely high incidence in particular of anti-HBe in the Greek patients with chronic liver diseases is in disagreement with the results of other studies from other populations. These differences may express differences in the immune response of the host in the different populations, or in the nature of the infecting strain commonly present in each country. Most of the HBsAg-negative patients with cirrhosis were found to be HBeAg or anti-HBe-positive.
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PMID:HBeAg/anti-HBe antigenic system in liver diseases in Greece. 632 77


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