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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An association of alcoholic cirrhosis of the liver, hepatoma, extensive aortic thrombosis, and chronic bleeding peptic ulcer of the duodenal bulbus in a patient who survived only three days after hospitalisation is reported. An explanation of each disease is given and the fact that a basically hypocoagulative situation (cirrhosis) can give rise to thrombosis of the aorta is stressed. Production and release into the circulation of thromboplastins by the hepatoma (paraneoplastic syndrome), leading aortic atherosclerosis and slow circulation due to haemorrhagic cardiocirculatory collapse was the most likely explanation.
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PMID:[Association of liver cirrhosis, hepatoma, extensive aortic thrombosis and chronic duodenal peptic ulcer in the same patient]. 626 18

The records of 20 Alaskan Native patients with primary hepatocellular carcinoma (PHC) diagnosed in the 11-year period 1969-1979 were reviewed. The annual incidence of PHC was found to be high among Alaskan Native males and especially high among Alaskan Eskimo males (7.6 and 11.2 per 100,000 respectively) in comparison to Greenland and Canadian Eskimos and US white males. Familial and geographic clustering of PHC patients was noted in areas known to be hyperendemic for hepatitis B virus (HBV) infection. A bimodal age distribution among PHC patients occurred with peaks at 15-25 years and 40-65 years. A high prevalence of hepatitis B surface antigen (HBsAg) in serum of patients in the younger age group suggests that HBV infection might be a factor associated with the development of PHC in young Eskimos. PHC in Alaskan Natives is apparently not closely associated with alcoholic cirrhosis.
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PMID:Primary hepatocellular carcinoma in Alaskan natives, 1969-1979. 627 29

Despite Scotland's well-recognised alcohol problem, there is scant information of the aetiology of cirrhosis in this country. This study of 222 patients, reviewed 197 cases presenting as cirrhosis and 25 cases presenting as primary liver cell carcinoma (PLCC) in the East Tayside area of Scotland between 1975 and 1979. The survey was based on an analysis of all histologically proven cases of cirrhosis and PLCC encountered during a five-year period. There was a constant rate of presentation of cirrhosis of about 40 new patients per year, with a stable pattern of aetiology. About 55 per cent were due to alcohol, and there was no significant change in this proportion over the study. No evidence was found for an increasing female susceptibility or earlier female morbidity in alcoholic cirrhosis. Cryptogenic cirrhosis, cardiac cirrhosis and secondary biliary cirrhosis were more often diagnosed at post mortem. Ninety one per cent of patients with primary biliary cirrhosis were females, but the expected male preponderance in haemochromatosis was not present. In addition to the 25 patients presenting with PLCC, three of the cirrhotic patients developed the tumour by the end of 1979. Seventy one per cent of PLCC cases arose in already cirrhotic livers, none were HBsAg positive. Bronchopneumonia, hepatic failure, gastrointestinal bleeding and cardiac failure were the most frequent causes of death.
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PMID:Cirrhosis and primary liver cell carcinoma in Tayside: a five year study. 627 84

We compared the presence of serologic markers of hepatitis B virus (HBV) infection with the presence of the viral DNA in the livers of patients with alcoholic liver disease with or without hepatocellular carcinoma. Among 51 patients with various kinds of alcoholic liver disease but without hepatocellular cancer, 19 had one or more serologic markers of HBV, but only three had viral surface antigen in their serum. These three patients, as well as three others who had HBV antibodies but no viral antigen in their serum and two others who had no serologic markers of any kind, had HBV DNA in their liver cells. In at least five of the eight patients with viral DNA in the liver, the DNA was integrated into the genome. Among 20 patients with alcoholic cirrhosis and hepatocellular carcinoma, nine of the 16 tested had serologic markers of HBV infection, but all 20 had HBV DNA integrated into the genome of the neoplastic liver cells. These data suggest that HBV plays a part in the pathogenesis of primary liver-cell cancer in alcoholics.
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PMID:Evidence that hepatitis B virus has a role in liver-cell carcinoma in alcoholic liver disease. 628 40

The development of hepatocellular carcinoma (HCC) is probably related to infection with hepatitis B virus (HBV). Hepatocytes in livers of patients with HCC have been reported to show putative preneoplastic changes such as hyperplasia, dysplasia, or adenomatous regeneration. To determine quantitatively whether these morphologic changes are associated with HBV-infected cells, the authors performed morphometry of hepatitis B surface antigen (HBsAg)-positive hepatocytes in the nontumorous portion of 10 livers with HCC and in 10 livers without HCC. The diameter of nuclei and cytoplasm of HBsAg-positive hepatocytes was measured after demonstration of HBsAg by the peroxidase-antiperoxidase method. As controls, HBsAg-negative hepatocytes in the same liver sections were measured as well as hepatocytes of 20 age-matched HBsAg-negative patients with normal liver or alcoholic cirrhosis. HBsAg-positive hepatocytes exhibited significantly larger nuclei and a higher nucleocytoplasmic ratio than control hepatocytes. In addition, HBsAg-positive cells were often arranged in foci that consisted of two cell populations: hypertrophic (enlarged nuclei and nucleocytoplasmic ratio) and hyperplastic (two-cell-thick plates of small cells with a high nucleocytoplasmic ratio). While precancerous cells have been difficult to identify, these morphologic changes are frequently associated with the development of malignant neoplasia.
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PMID:Morphometric study of hepatocytes containing hepatitis B surface antigen. 632 Jun 48

Plasma immunoreactive calcitonin (iCT) is elevated in primary liver cancer and its measurement has been proposed as a tumour marker. Since iCT is also frequently raised in alcoholic liver cirrhosis, it would be of practical relevance to distinguish this condition from primary hepatoma by measuring the plasma level of iCT. We measured plasma iCT levels in 23 subjects with primary liver cancer, in 27 with hepatic cirrhosis and in 42 healthy subjects who served as normal controls. A gel-chromatography analysis was carried out on the plasma of two cases of hepatoma, two of cancer and cirrhosis, and two of alcoholic liver cirrhosis. The subjects with primary liver cancer had values of plasma iCT (pg/ml; mean +/- SE) of 342 +/- 41; those with liver cirrhosis 159 +/- 22, and normal controls 73 +/- 3. The increase in primary liver cancer was significant in comparison both healthy subjects (P less than 0.001) and with cirrhotic patients (P less than 0.001). Twenty-two out of 23 patients with primary liver cancer and 13 out of 27 with liver cirrhosis had elevated iCT values (upper normal limit 113 pg/ml). There was no significant difference between plasma iCT values of patients with cancer and those with cirrhosis. However, we measured iCT values higher than 400 pg/ml only in patients with primary liver cancer. The gel-filtration analysis showed 3 or 4 peaks of iCT with a molecular weight higher than synthetic human calcitonin. The results suggest that plasma iCT levels can be considered a reliable marker of liver cancer, whereas its discriminating power between liver cancer and cirrhosis was not entirely satisfactory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcitonin in hepatoma and cirrhosis. 632 18

A total of 512 people from a defined population in west Birmingham served by a district general hospital were found to have cirrhosis in the period 1959-76. The annual incidence rose from 5.6 per 100 000 to a peak of 15.3 per 100 000 in 1974. This was due to an increase in the incidence of alcoholic cirrhosis, which in the last six years accounted for two-thirds of cases. The proportion of patients with decompensated cirrhosis when first seen (65%) did not alter during the 18 years. This was reflected in a death rate of 78% among the 468 patients traced up to the end of 1978. Liver failure, hepatoma, and gastrointestinal haemorrhage accounted for almost three-quarters of the deaths. The proportion of patients who survived for five years was 36% for alcoholic cirrhosis, 14% for cryptogenic cirrhosis, and 60% for chronic active hepatitis, and these figures too remained constant throughout the 18 years. Modern methods of treatment for decompensated cirrhosis did not improve prognosis and only abstention in patients with alcoholic cirrhosis had a beneficial effect on survival. Since alcoholic cirrhosis is now the most common form of the disease it is important to recognise those at risk and to encourage abstinence; also, more efforts are needed to identify the causes of cryptogenic cirrhosis. Whatever the cause, cirrhosis needs to be diagnosed before decompensation occurs, if treatment is to have any effect.
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PMID:A 20-year prospective study of cirrhosis. 677 78

The case of a 70-year-old man with clinically-compensated alcoholic liver cirrhosis is illustrated. His serum alpha-fetoprotein level was on the increase but Ultrasonography and Magnetic Resonance detected no focal lesion of the liver. Five months after Ultrasonography, Computed Tomography and Magnetic Resonance were performed because the patient's alpha-fetoprotein level indicated hepatocellular carcinoma, but none of these tests succeeded in locating the neoplasm. Digital subtraction angiography was performed and only then was a small hepatocellular carcinoma revealed under the diaphragm. The patient underwent transcatheter arterial chemo-embolization with the result that the alpha-fetoprotein level dropped immediately and is still normal after 15 months. The case described is a model of what the ideal function of a marker of neoplasia should be, namely early detection, and subsequent precise confirmation of the continuing efficacy of the treatment adopted.
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PMID:A case of hepatocellular carcinoma that resisted identification. 752 3

Sixty-three patients with alcoholic cirrhosis were retrospectively studied for the prevalence of antibodies to core (P22) and nonstructural (C100) region of hepatitis C virus (HCV). The prevalence rate of anti-P22 antibodies in patients with alcoholic cirrhosis was higher than that of anti-C100 antibodies (63.5% vs. 54.9%). The positivity rate of anti-C100 and/or anti-P22 antibodies was 73.0% (46/63) in alcoholic cirrhosis. We performed a multivariate analysis on the effects of age, sex, cumulative alcohol intake, anti-HCV antibodies, indocyanine green excretion test, and serum albumin on the development of hepatocellular carcinoma HCC in patients with cirrhosis, using Cox's proportional-hazards model, which revealed that anti-HCV positivity was the only independent prognostic variable for HCC in patients with alcoholic cirrhosis. The probability of HCC was significantly higher in the anti-HCV-positive patients than in the negative patients with alcoholic cirrhosis (p < 0.05). The 3-, 5- and 10-yr cumulative occurrence rate of HCC was, respectively, 13.3%, 41.3%, and 80.7% for anti-HCV-positive patients with alcoholic cirrhosis, compared with 0%, 8.3%, and 18.5% for anti-HCV-negative patients. In nonalcoholic patients with type C cirrhosis, the 3-, 5-, and 10-yr cumulative occurrence rate of HCC was 7.3%, 23.1%, and 56.5%, respectively. The follow-up studies indicate that hepatocarcinogenesis is hastened significantly in patients with alcoholic cirrhosis if they are positive for anti-HCV antibody, and that heavy alcohol consumption also is a risk factor for the development of HCC in patients with type C cirrhosis.
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PMID:Prevalence of hepatocellular carcinoma in patients with alcoholic cirrhosis and prior exposure to hepatitis C. 767 68

Progression of alcoholic liver disease is closely related to drinking habits. However, prognosis of alcoholic liver disease is not determined just by drinking habits, but also by other factors. In this study, the roles of alcohol-altered liver membrane antibody and hepatitis C virus infection were analyzed in alcoholic patients who were followed up for various lengths of time. Serial changes of liver histological appearance were analyzed in 39 patients with alcoholic liver disease who were followed for long periods (49.7 +/- 34.3 mo) and who underwent liver biopsy at least two times. Prognoses of 35 patients with alcoholic cirrhosis who were followed for more than 1 yr were also evaluated. Development of cirrhosis in alcoholic liver disease was significantly higher in the alcohol-altered liver membrane antibody-positive patients than in the patients negative for this antibody. On the other hand, hepatitis C virus markers were not related to development of cirrhosis. However, hepatocellular carcinoma developed more frequently in the hepatitis C virus marker-positive patients. In patients with cirrhosis, the cumulative rates of hepatocellular carcinoma development were significantly higher in the hepatitis C virus marker-positive patients than in the marker-negative patients. Cumulative survival rates in the hepatitis C virus marker-positive patients were significantly lower than rates in the hepatitis C virus marker-negative patients, even in noncancer patients. However, such differences were not observed in the alcohol-altered liver membrane antibody-positive and alcohol-altered liver membrane antibody-negative cirrhotic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The alcohol-altered liver membrane antibody and hepatitis C virus infection in the progression of alcoholic liver disease. 767 78


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