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)

HBV infection acquired during infancy and early childhood has a high likelihood of progressing to chronic infection, which can lead to chronic hepatitis, cirrhosis, and primary hepatocellular carcinoma. In areas of the world where HBV infection occurs predominantly in infants and young children, routine infant immunization with hepatitis B vaccine is the most appropriate vaccination strategy. In the United States, the majority of HBV infections occur in adults with behaviors or occupations that put them at risk for HBV infection. Nevertheless, infection acquired during infancy and early childhood contributes significantly to the burden of chronic liver disease in the United States. Until recently, the vaccination strategy in the United States has included HBsAg screening of pregnant women and vaccination of infants born to infected women and vaccination of people in groups at high risk for HBV infection. Because of the difficulties in accessing and vaccinating persons from high-risk groups and the recent findings that HBV infection occurs more commonly among children in some groups in the United States than previously appreciated, the Immunization Practices Advisory Committee of the US Public Health Service and the American Academy of Pediatrics in 1991 endorsed a strategy of universal immunization of infants for hepatitis B. This strategy has the advantages of accessing infants in the United States through preexisting vaccine delivery systems and vaccinating individuals prior to their engaging in high-risk behavior. Continued screening of pregnant women for HBsAg is necessary to prevent perinatal HBV transmission and to identify for vaccination those household and sexual contacts of HBV carriers, a group that is also at high risk of HBV infection.
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PMID:Impact of hepatitis B virus infection on women and children. 153 49

To clarify the potential role for HCV in the development of chronic liver disease in Yatsuka town with a high morbidity of liver disease, epidemiological studies were taken in 459 subjects of Yatsuka town compared with 219 subjects of Mihonoseki town with a low one. In Yatsuka town, the mortality rate of liver cirrhosis was three times higher than the overall rate in Simane prefecture, and the rate of liver cancer rapidly increased in recent years. Age and sex-matched epidemiological studies showed a significantly higher incidence of hepatic dysfunction compared with Mihonoseki town (11.5% vs 3.7%, P less than 0.01). The prevalence of HCV antibody was significantly higher in Yatsuka town than Mihonoseki town (16.6% vs 3.7%, P less than 0.001), although there were no differences in frequencies of HBs antigen and habitual alcohol drinker between the two districts. These data strongly suggest that the high prevalence of HCV may be associated with the high morbidity of chronic liver disease, especially hepatocellular carcinoma in Yatsuka town.
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PMID:[Prevalence of HCV antibodies in Yatsuka town of Simane prefecture, Japan]. 159 74

To determine the factors underlying the apparent reduction in binding ability of thyroxine-binding globulin in hepatocellular carcinoma, hormone-binding characteristics were further examined in patients with this disease and in control subjects. No differences in affinity constants with respect to triodothyronine or serum thyroxine-binding globulin from hepatocellular carcinoma, cirrhotic and normal subjects were found. The affinity for thyroxine was significantly reduced in hepatocellular carcinoma (0.41 +/- 0.13 x 10(10) mol-1) and cirrhotic (0.65 +/- 0.1 x 10(10) mol-1) patients compared with normal subjects (0.94 +/- 0.7 x 10(10) mol-1). Investigations carried out on liver tissue obtained from patients with hepatocellular carcinoma and chronic liver disease showed that thyroxine-binding globulin within tumor tissue was elevated and bound less exogenous tracer hormone compared with that obtained from nontumor tissue. Tumor-derived thyroxine-binding globulin with altered binding properties is, at least partly, responsible for the abnormal behavior of the serum protein in patients with hepatocellular carcinoma.
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PMID:Impaired binding properties of thyroxine-binding globulin in hepatocellular carcinoma and chronic liver disease. 164 37

A questionnaire-based survey involving 11,801 hemophiliacs from 54 hemophilia centers in the USA and Europe documented the occurrence of hepatocellular carcinoma (HCC) in 10 patients. The crude rate of HCC was 3.2/100,000 patients/year, at least 30 times higher than the background incidence of this tumor in the countries of origin of the patients. All patients were Caucasians with hemophilia A, 39 to 74 years of age, and had liver cirrhosis. All had one or more risk factor for cirrhosis and HCC: 5 were positive for serum hepatitis B surface antigen, 4 had the antibody to hepatitis C virus, and 4 had histories of alcohol abuse. Serum alpha-fetoprotein, measured in 6 patients, was significantly elevated in 4 (range: 807-1399 ng/ml), and only moderately elevated in 2 (25 and 171 ng/ml). The onset of HCC was asymptomatic in 5 patients, whereas it was accompanied by jaundice, abdominal pain, or ascites in the remaining patients. Thus, HCC seems to be a more important secondary disease for hemophiliacs than formerly recognized. Since HCC is often asymptomatic, screening hemophiliacs with chronic liver disease with periodic ultrasound scans might increase the changes of detecting HCC at a stage amenable to surgical treatment.
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PMID:Hepatocellular carcinoma in hemophilia. 165 Jan 34

To assess the contribution of the recently identified hepatitis C virus to chronic liver diseases of unknown cause and chronic hepatitis attributed by exclusion to non-A, non-B hepatitis, we tested for antibody to hepatitis C in hepatitis B surface antigen-negative patients with a spectrum of chronic liver diseases. Antibody to hepatitis C virus, a marker of hepatitis C infection, was detected with a first-generation radioimmunoassay at the following frequencies in the following patient groups: 69% of transfusion-associated non-A, non-B hepatitis; 53% of non-transfusion-associated non-A, non-B hepatitis; 26% of hepatitis B surface antigen-negative hepatocellular carcinoma; 8% of cryptogenic cirrhosis; 5% to 7% of autoimmune chronic liver diseases; 19% of patients with miscellaneous types of chronic liver disease; and 0.67% of healthy controls. Among non-transfusion-associated cases, 81% with a history of intravenous drug use but only 18% with occupational exposure as health workers had antibody to hepatitis C virus. Among cases of hepatocellular carcinoma, 63% of Japanese patients but only 11% of American patients had evidence of hepatitis C infection. Comparison in a subgroup of 79 serum samples of a second-generation radioimmunoassay with the first-generation assay demonstrated a 12% increase in antibody frequency from 30% to 42%. We conclude that hepatitis C plays a substantial role in transfusion-associated and non-transfusion-associated non-A, non-B hepatitis as well as in hepatocellular carcinoma, especially in Japan, a limited role in cryptogenic cirrhosis, and essentially no role in autoimmune chronic liver diseases. Application of more sensitive immunoassays will increase the frequency of antibody seropositivity in all subgroups, but relative distinctions among risk groups are likely to remain.
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PMID:Role of hepatitis C virus in non-B chronic liver disease. 165 89

To clarify the discrepancy in hepatitis B surface antigen (HBsAg) subtypes present in the serum and liver, as well as among hepatocytes, liver specimens which were resected from 37 HBsAg-positive patients with hepatocellular carcinoma (HCC) were examined. We evaluated HBsAg and the subtypic determinants of HBsAg and hepatitis B core antigen (HBcAg) using the peroxidase-antiperoxidase (PAP) staining method. Hepatitis B antigens were more frequently detected in small tumors (HBsAg in 67%. HBcAg in 40%) than in large ones (HBsAg in 36%, HBcAg in 14%). The prevalence of each subtypic determinant in the HBsAg positive non-tumorous vs. tumorous areas was 100% vs. 67% in a, 100% vs. 57% in d, 100% vs. not tested in y, 100% vs. 53% in r and 25% vs. 0% in w (a, d, y, r and w represent subtypic determinants). There was virtually no difference in a set of subtypic determinants between the serum and liver. However, there were some variations in a set of subtypic determinants among the hepatocytes. On the other hand, liver tissue of compound subtype adyr in serum contained both cells with a,d,r and with a,y,r as well as a few cells with a,d,y,r. These findings suggest that HBV genomes in hepatocytes of type B chronic liver disease may differ genetically among cells even in the same liver tissue.
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PMID:Expression of hepatitis B surface antigen subtypes in liver of patients with hepatocellular carcinoma; comparison of subtypes in serum and liver. 165 86

A recently introduced enzyme immunoassay procedure for antibodies against the hepatitis-C virus (HCV) was used to test samples from 185 cases with hepatocellular carcinoma (HCC) and 432 hospital controls. The anti-HCV results were examined in conjunction with previously reported data from this study concerning hepatitis-B virus (HBV) serology, hepatitis-D virus (HDV) antibodies, presence of cirrhosis and tobacco smoking. There was evidence for interaction between HBV and HCV in the causation of HCC: as previously reported, the rate ratio (RR) linking the presence of anti-HCV to HCC among subjects positive for hepatitis-B surface antigen (HBsAg) was substantially higher than the corresponding RR among those negative for this marker; furthermore, among HCC patients positive for HBsAg, a high proportion (33/61) of those who were positive for hepatitis-Be antigen (HBeAg) or its antibody were positive for anti-HCV, whereas among HBsAg-positive controls who were also positive for HBeAg or its antibody, none was positive for anti-HCV (0/18; p less than 10(-4)). The anti-HCV-related RR for HCC was also higher among HCC patients with cirrhosis than among those without evidence of co-existing cirrhosis (RR 11.4 vs. 4.4; p = 0.06). In addition, there was some evidence of interaction between tobacco smoking and HCV in the origin of HCC; after controlling for age, sex and HBsAg status, the RR for subjects positive for anti-HCV was 6.8 among smokers but only 3.2 among non-smokers (p = 0.26). By contrast, there was no suggestion of an interaction between anti-HCV and anti-HDV, in agreement with the presumed minimal role, if any, of HDV in HCC etiology. These results support the notion that HCV is involved in the etiology of HCC by advancing, through a chronic liver disease process, carcinogenesis initiated by other factors.
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PMID:Epidemiologic assessment of interactions of hepatitis-C virus with seromarkers of hepatitis-B and -D viruses, cirrhosis and tobacco smoking in hepatocellular carcinoma. 165 59

Hepatitis C virus (HCV) is a recently characterised non-A, non-B hepatitis (NANBH) agent, which appears to be important in both parenteral and sporadic NANBH. HCV infection has been associated with the development of chronic liver disease, cirrhosis and hepatoma. Groups of patients in the western Cape with chronic liver disease and hepatoma were screened for antibodies to HCV and the results were confirmed by standard neutralisation tests. Three of 19 patients with cirrhosis secondary to alcohol abuse or classic auto-immune chronic active hepatitis were considered to have antibodies to HCV at initial screening. All of these were false-positive results. Five of 20 patients with presumptive chronic NANBH were considered possibly to have antibodies to HCV. Only 1 patient with post-transfusional NANBH was confirmed to have specific HCV antibodies. Two of 30 patients with hepatoma had specific anti-HCV antibodies in contrast to 11 others with serum HBsAg positivity. One hundred blood transfusion donors and 25 antenatal patients were tested concurrently and shown to be negative for anti-HCV. Specific antibodies to HCV were present in very few patients with cirrhosis, presumptive NANBH and hepatoma tested in this local survey. False-positive reactions appeared to occur at a higher rate than true-positive results.
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PMID:Hepatitis C virus antibodies in patients with liver disease. The western Cape experience. 165 34

From January 1, 1968 to December 31, 1984, 31,955 autopsies were performed at the Department of Pathology of the University of Trieste. Of these 16,521 were male and 15,434 female which covered about 70% of the population who died in the area over the recent years. Hepatocellular carcinoma (HCC) associated with liver cirrhosis was encountered in 441 cases (380 males and 61 females, M:F ratio 5.8:1) with an overall occurrence of 1.4% in the autoptic population. On the contrary and in the absence of chronic liver disease HCC was only observed in 0.3% of the cases (45 males and 16 females, M:F ratio 2.7:1). Liver cirrhosis accounted for 10% of autopsies (2099 males and 1104 females, M:F ratio 1.8:1). A 15% of cirrhosis was associated with HCC, indicating that major attention should be paid to cirrhotic patients, in particular males after the 5th decade of life. The year distribution of HCC and cirrhosis was fairly constant during the period of time considered. These data suggest that: i) HCC is common in Italy; ii) in the vast majority, HCC occurs in the presence of cirrhosis; and iii) HCC appears to be a rather late disease as it does not reduce the life expectancy of cirrhotic and control populations. Since reliable, nationwide epidemiological data are not available in Italy, it is not known whether these data represent a local realty or whether they may be extrapolated to the entire country. Cooperative and prospective studies appear appropriate in investigating possible geographical differences in HCC distribution and permit a better understanding and prevention of the disease.
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PMID:Incidence of hepatocellular carcinoma in Italy: what could we learn from autoptic studies? 166 Mar 31

Hepatitis viruses, particularly HBV and HCV, are major causes of hepatocellular carcinoma worldwide, due to the induction of chronic liver disease and of cirrhotic transformation of the liver. Cirrhosis certainly represents the most important link between chronic viral hepatitis and HCC. Under these circumstances, risk of HCC development in chronic HBV and HCV infection is strictly dependent on the propensity to cirrhotic transformation. Intervention of other, more direct, molecular events induced by the virus itself are suspected, particularly for HBV which is able to integrate into the host genome, but not yet incontrovertibly proved.
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PMID:Hepatitis viruses as aetiological agents of hepatocellular carcinoma. 166 Mar 32


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