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

The etiologic relationship of parasitic liver disease to primary liver cancer has long been debated. For this reason, a review of 4611 necropsies was carried out to determine the frequency with which hepatocellular carcinoma occurred in association with schistosomiasis. Of 227 cases of hepatocellular carcinoma, 24 (10.6%) were associated with schistosomiasis japonica. This was significantly higher than the incidence of this carcinoma without schistosomiasis (2.78%). The majority of the 24 cases exhibited the features of a mixed macronodular and micronodular cirrhosis (Gall's posthepatitic cirrhosis); this was super-imposed upon and caused a masking of schistosomiasis fibrosis. By radioimmunoassay hepatitis B antigen was positive in 27% of these cases. A review of the literature indicated that chronic schistosomiasis, on its own, is unlikely to be the cause of primary liver cell carcinoma. Histologic features resembling post-hepatitic cirrhosis combined with a high frequency of hepatitis B antigen suggest that viral hepatitis rather than S. japonicum is the more likely etiologic factor involved, or has a synergistic effect on carcinogenesis.
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PMID:Primary liver cancer coincident with Schistosomiasis japonica. A study of 24 necropsies. 16 89

During a 23 year period at Memorial Hospital, the diagnosis of liver cell carcinoma was made in 42 patients who were 11 to 40 years old. Ninety per cent were Caucasian, mostly born in the United states. No occupational hazard was detected. Serum hepatitis antigen was demonstrated in only one patient. Alpha fetoprotein was found in the serum of 55 per cent of nine patients tested. Eight-three per cent were Rh positive, 43 per cent were ABO groups, A or O, respectively. Twenty-three per cent of 13 patients with sufficient material for study had an associated cirrhosis. Of these, active hepatitis with cirrhosis was present in one patient; postnecrotic cirrhosis was present in another. Approximately 7 per cent had a history of previous liver disease. One patient had infectious mononucleosis, and nearly 13 per cent gave a family history of cancer. Weight loss or pain in the right upper abdominal quadrant was present in 65 per cent, and hepatomegaly was found in 88 per cent. Only one patient presented with hemoperitoneum simulating an acute condition within abdomen. The liver profile examinations characteristically revealed an elevation in serum alkaline phosphatase, 5 nucleotidase, and Bromsulphalein retention with normal bilirubin level. The most common finding, upon roentgenographic examination, was an elevated right hemidiaphragm. Selective celiac and superior mesenteric angiography and 99mTc sulfur colloid liver scans were both done in 13 patients. There was a 75 per cent accuracy rate in localization of the tumor. At laparotomy, the tumor was found to be confined to one lobe in seven patients and involved both lobes in ten. Twenty-seven patients were thought to have multicentric tumors and 15 unicentric lesions. Only ten were found to be candidates for hepatic lobectomy. Five and ten years survival rates were 20 per cent; the operative mortality rate was 40 per cent. Twenty per cent died within a year, ten per cent, one patient, is alive with disease at 28 months and another is free of disease at 31-months. Paraneoplastic syndromes were erythrocytosis in two patients, terminal stage of hypoglycemia in one patient, and hypocholesterolemia with associated excess beta globulin in one patient.
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PMID:Liver cell carcinoma during the prime of life. 17 34

Hepatoma has been related to chemical, dietary, metabolic, infectious, and genetic factors. therapeutic hepatic irradiation has never been associated with hepatoma. A case of hepatocellular carcinoma is presented that occurred two decades after radiotherapy for presumed hepatic hemangioma. Radiation-related liver disease is discussed in general, with emphasis placed on radiation hepatocarcinogenesis.
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PMID:Hepatoma occurring two decades after hepatic irradiation. 17 8

The cytoplasmic bodies in hepatocytes thought to indicate possession of the Z allele for alpha 1-antitrypsin deficiency were found in necropsy in 10 of 64 adults with cirrhosis, four of nine with hepatic fibrosis, and four of 15 with hepatocellular carcinoma. They were also found in six of 76 adults with severe panacinar emphysema, and in four of a control series of 110 adults with neither emphysema nor liver disease. The association of the bodies with each of the three liver diseases was statistically significant, but the association of the bodies with emphysema was not. It is considered probable that heterozygous (PiMZ) alpha 1-antitrypsin deficiency is associated with an increased incidence of cirrhosis, hepatic fibrosis, and hepatocellular carcinoma.
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PMID:Alpha-1-antitrypsin bodies in the liver. 19 72

The antibody to hepatitis B core antigen (anti-HBc) is belived to be a marker for natural infection with hepatitis B virus (HBV). In order to study the etiological role of HBV in relation to primary hepatocellular carcinoma (PHC), the anti-HBc in sera of 31 PHC patients was surveyed by the immune adherence hemagglutination method which was about 10 times more sensitive than the complement fixation method. Twenty two out of 31 PHC cases were positive for anti-HBc (71.0%). The is a higher rate of incidence than that of HBs-Ag (51.6%). However, high anti-HBc titer above 2(10) which might reflect current infection with HBV was observed in 15 of these 22 cases. The remaining 7 cases had a titer lower than 2(8); 5 of these patients had neither HBs-Ag nor anti-HBs in their sera. As control, 37 anti-HBs positive blood donors with no definite liver disease were surveyed for anti-HBc titer. Thirty-four of them were positive, but in the majority of cases, the serum titer was less than 2(9), which might only reflect previous infection with HBV. These findings indicate that not only the prevalence of anti-HBc, but also the determination of its real titer is quite important for studying the relationship of HBV to PHC.
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PMID:Anti-HBc titer in relation to the etiological role of hepatitis B virus in primary hepatocellular carcinoma. 19 28

This paper gives, in detail, the causes of either liver disease or hepatomegaly in 100 patients, mostly adults, admitted to the medical wards of Angau Memorial Hospital, Lae, during 1968 and 1969. The major findings included liver cell carcinoma, cirrhosis (often with chronic active hepatitis), tropical splenomegaly, pericholangitis and hepatitis. There were 27 with miscellaneous findings including ten with normal, or almost normal, livers despite the definite enlargement. Patients with liver cell carcinoma presented late in the course of their illness and had a poor prognosis. Others, with pericholangitis, had clinical features of portal hypertension indistinguishable from that complicated cirrhosis. There was an unexpected number with chronic active hepatitis and a liver biopsy is essential for such a diagnosis. Hepatic sinusoidal lymphocytosis is almost invariably found in patients with TS but may occasionally be found in those with a non-palpable spleen. Patients with right heart failure of chronic respiratory disease, and jaundice of acute pneumonia were excluded from the study.
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PMID:Liver disease in Papua New Guinea. 19 19

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

A retrospective examination in South-west Scotland of formalin-fixed paraffin-embedded liver tissue by an immunoperoxidase technique revealed hepatitis B surface antigen (HBsAg) in eight out of 81 cases (10%) of primary hepatocellular carcinoma (PHC) and in four out of 82 cases (5%) of cirrhosis. No positive staining was found in 112 controls without overt liver disease matched for age and sex. Unlike most previous studies showing an association between HBsAg and PHC, the present investigation was carried out in an area where HBs antigenaemia is infrequent and PHC is an uncommon tumour. While possibly hepatitis infection is an important cause of PHC, the association between HBsAg and PHC could be due merely to activation by the tumour of latent virus B in a previously infected person.
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PMID:Incidence in South-west Scotland of hepatitis B surface antigen in the liver of patients with hepatocellular carcinoma. 20 8

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

Sera of 173 patients with various forms of liver disease along with serum precipitates produced by polyethylene glycol were screened for the presence of a microsomal antigen referred to as ubiquitous tissue antigen (UTA) and its antibody by double diffusion precipitation in agarose gel. UTA was detected in 7 or 26 patients with chronic active hepatitis, 1 of 5 with alcoholic hepatitis, 2 of 14 with alcoholic cirrhosis and 18 of 98 with hepatoma. Antibodies to UTA were found only in 2 patients with chronic active hepatitis, 1 with alcoholic cirrhosis and 1 with hepatoma. No UTA or its antibody were noted in sera of 5 patients with alcoholic fatty liver, 10 patients with hepatitis B, and 15 asymptomatic carriers of HBsAg. Positivity for the UTA or its antibody was restricted to severe, chronic cases irrespective of diagnosis, indicating that persistent tissue destruction might be necessary for antigen release or antibody formation.
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PMID:Detection of a microsomal antigen and its antibody in human liver diseases. 22 26


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