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

The presence of fat in hepatic masses narrows the range of differential diagnoses down to hepatic angiomyolipoma, lipoma, adenoma, hepatoma, metastatic fatty tumors of the liver, focal fatty infiltration of the liver, and extrahepatic fatty masses such as intraperitoneal implants from malignant teratomas, and packed omentum. We report six hepatic tumors containing fat (lipoma, hepatocellular carcinoma, and calcified mass with fat-fluid level) with CT and magnetic resonance (MR) imaging. The distribution of fat was diffuse in the lipomas and some hepatocellular carcinomas and localized in other hepatocellular carcinomas and fat-fluid masses. The density ranged from - 100 to 0 HU. High intensity areas on both T1- and T2-weighted MR images corresponded to the hypodense areas on CT.
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PMID:CT and MR imaging of fatty tumors of the liver. 302 96

A 46-year-old woman underwent right hepatic lobectomy for the removal of a solitary liver tumour from a non-cirrhotic liver. The macroscopic and light microscopic features were those of a liver cell adenoma but the cells appeared oncocytic. Electron microscopy confirmed the numerous mitochondria characteristic of oncocytes. The difficulty of distinguishing oncocytic liver cell adenoma from fibrolamellar hepatocellular carcinoma is discussed.
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PMID:Oncocytic liver cell adenoma. 303 29

Twenty-four patients with liver cell adenomas were referred to Paul Brousse Hospital between 1976 and 1987. This represents the largest reported surgical experience of this pathology from a single centre. Six patients had multiple adenomas, which were associated with glycogen storage disease in four. Two patients had polyadenomatosis, one of whom underwent successful liver transplantation after malignant transformation to hepatocellular carcinoma. Eighteen patients (median age of 33 years, range of 17-45 years) had either a solitary adenoma or two adenomas. Eighty-three per cent were women 87% of whom had received oral contraceptives or other hormone therapy before diagnosis (median duration of 11 years, range of 3-15 years). Fifty per cent of these patients presented with acute hemorrhage into an adenoma. Seventeen patients underwent surgical resection of their adenomas, with the remaining patient currently being treated by arterial embolizations to reduce the tumor size before surgery. There was no operative mortality or serious morbidity, and all patients remain well upon follow-up. Surgical excision of liver adenomas, where this can be done without causing mortality, is recommended. Resection relieves symptoms and removes both the risks of hemorrhaging into the tumour and of malignant transformation to hepatocellular carcinoma.
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PMID:Liver cell adenomas. A 12-year surgical experience from a specialist hepato-biliary unit. 319 Feb 82

Mortality, major causes of moribundity, and spontaneous tumors in CD-1 mice were studied in 891 males and 890 females, which were used as controls in 11 different 2-year chronic and oncogenicity studies during the past 5 years. Average mortality of males and females at 83 weeks of age was 32.6% and 28.6%, respectively, and at 109 weeks of age was 66.4% and 63.3%, respectively. Mortality was significantly lowered in males and females born after 1980 in accordance with an abruptly decreased occurrence of systemic amyloidosis in these animals. The major cause of death or moribundity included systemic arteritis, systemic amyloidosis, auricular thrombosis, glomerulosclerosis, lymphoma, and pulmonary adenocarcinoma in both sexes. Dysuria and hepatocellular carcinoma in males and mammary adenocarcinoma in females were also critical lesions. The major tumors occurring at more than 3% incidence were systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver and adenoma/adenocarcinoma of the Harderian gland for males, and systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver, leiomyoma/leiomyosarcoma of the uterus, adenoma/adenocarcinoma of the pituitary (anterior), adenoma/adenocarcinoma of the mammary gland and adenoma/adenocarcinoma of the Harderian gland for females. Intralaboratory heterogeneities in the incidence were recorded as follows: systemic lymphoma in 1 of 11 control groups (1/11) and adenoma/adenocarcinoma in 1/11 for males, and systemic lymphoma in 3/11, adenoma/adenocarcinoma of the lung in 2/11, adenoma/adenocarcinoma of the liver in 1/11, and adenoma/adenocarcinoma in 1/11 for females.
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PMID:Mortality, major cause of moribundity, and spontaneous tumors in CD-1 mice. 319 56

Classification of rat hepatocellular proliferative lesions can vary between pathologists as the many qualitative histologic criteria have not been satisfactorily evaluated and ranked for prognostic value. Computer-assisted morphometry offers an objective method to evaluate certain cellular features. The Solt-Farber resistant hepatocyte model was used in this study to produce populations of rats with a full range of hepatocellular proliferative lesions. Cellular features within the lesions were then measured morphometrically and the data were analyzed by animal age and by subjective lesion diagnosis. The nuclear/cytoplasmic ratio followed by the cell area and nuclear area were found to be the most important parameters for separating microscopic foci and islands of cellular alteration, an early hyperplastic lesion, from other hepatocellular proliferative lesions. The coefficient of variation, as a relative measure of heterogeneity, increased in a linear manner for cell, nuclear and nucleolar areas as the animals aged and was significantly higher for cell and nuclear area in hepatocellular carcinoma compared to other hepatocellular proliferative lesions. Hepatocyte nodules (representing primarily late hyperplastic lesions) and persistent hepatocyte nodules (lesions with similarities to hepatocellular adenoma) could not be satisfactorily separated within the limits of this study. As these borderline lesions show a continuum of cytologic change, other features, such as architectural change, are necessary to satisfactorily classify them on a subjective basis. An alternative approach is to use discriminant functions derived from morphometric studies.
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PMID:Morphometric evaluation of hepatocellular proliferative lesions in the rat liver. 322 23

This is a broad review (140 literature citations) of the possible effects of oral contraceptives on the liver. The oral contraceptives considered consist of combined preparations of estrogens and progestogens although the so-called "minipills" contain only a progestogen. The effects are divided into 1) decrease in excretory liver function; 2) influence on bile acid formation, including cholesterol metabolism; 3) increased synthesis of various transport proteins (ceruloplasmin, transferrin, thyroxine-binding protein, and cortisol-binding protein); 4) the effects of increased tissue circulation caused by sexual hormones and anabolic steroids as a cause for more frequent cavernous angiomas and peliosis hepatis; 5) interference with the metabolism of other drugs by the competitive action of the hepatic metabolites of steroid hormones. This includes the increased formation of delta amino levulinic-acid synthetase, the key enzyme for porphyrin synthesis. The gestagen component of oral contraceptives is responsible for enzyme induction in the smooth endoplasmic reticulum. Morphological liver changes caused by oral contraceptives include parenchyma changes, hepatosis, reactive hepatitis, hepatitis resembling viral hepatitis, vascular changes, sinusoid ectasia, Budd-Chiari syndrome, hyperplasias and neoplasias, focal nodular hyperplasia, adenoma and liver cell carcinoma.
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PMID:[Effects of oral contraceptives on liver function and structure]. 332 30

The effects of four isomeric forms of aminophenols, ortho-, meta-, para-aminophenol and acetaminophen (o-, m-, p-AP and AAP, respectively) on liver and kidney carcinogenesis initiated by N-ethyl-N-hydroxyethylnitrosamine (EHEN) were tested. Rats were given 0.1% EHEN (in their drinking water for 2 weeks) and then diet containing these compounds at concentrations of 0.8% for 49 weeks. Administration of o-AP and AAP significantly decreased the number and area of preneoplastic foci staining immunohistochemically for glutathione S-transferase placental type (GST-P) per unit area of liver section as compared with the values for rats given EHEN alone. o-AP and AAP also significantly decreased the incidence of hepatocellular carcinoma. In contrast, p-AP and AAP significantly increased quantitative values for kidney preneoplastic lesions and renal cell adenoma. It is suggested that the cytotoxic effects of these chemicals preferentially suppressed the proliferation of preneoplastic liver cells, but stimulated the mitotic activity of preneoplastic tubular lesions in the kidney.
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PMID:Reciprocal modifying effects of isomeric forms of aminophenol on induction of neoplastic lesions in rat liver and kidney initiated by N-ethyl-N-hydroxyethylnitrosamine. 362 66

Diagnostic criteria for hepatoproliferative lesions of Fischer 344 rats are presented to permit more complete categorization of the spectrum of lesions observed in two-year chemical carcinogenicity studies. A nomenclature recently adopted by the National Toxicology Program differs from previous classification schemes in that hepatocellular hyperplasia and hepatocellular adenoma are to be used for lesions which were previously combined under the diagnosis of neoplastic nodule. The term hyperplasia is reserved for proliferative lesions that are perceived to be secondary, nonneoplastic responses to degenerative changes in the liver. Foci of cellular alteration, hepatocellular adenoma, and hepatocellular carcinoma are believed to represent a spectrum of changes that comprise the natural history of neoplasia. This change in nomenclature was made subsequent to a peer review of representative hepatoproliferative lesions from two-year carcinogenicity studies. The revised nomenclature is consistent with traditional pathologic diagnoses for proliferative lesions in other epithelial tissues and should facilitate the interpretation of conventional toxicity and carcinogenicity studies in rats. Morphologic features of other selected rat liver lesions are also presented.
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PMID:National Toxicology Program nomenclature for hepatoproliferative lesions of rats. 376 23

The pathology lesions from three studies, two with butylated hydroxyanisole (BHA) and one with butylated hydroxytoluene (BHT), are reviewed. When BHA was fed at 0.5 and 2.0% of the diet to F344 rats for two years, there was an increase in epithelial hyperplasia of the forestomach at both treatment levels. Papilloma and squamous-cell carcinoma of the forestomach were increased at the 2.0% level. When BHA was fed to beagle dogs at 1.0 and 1.3% of the diet for 180 days, no lesions/tumours of the distal oesophagus or stomach could be identified either at gross necropsy or by light or electron microscopy. The BHT was fed to Wistar rats at 0, 25, 100 and 250 mg/kg body weight. At the highest dose there was an increase in the number of rats with hepatocellular adenoma and with hepatocellular carcinoma.
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PMID:Pathology of BHA- and BHT-induced lesions. 380 18

The presence of duck hepatitis B virus (DHBV) DNA in liver and serum and its state (integrated vs. free) were studied in 23 ducks from Chi-tung county in China by spot hybridization and Southern blot hybridization, respectively. In 16 of 23 (70%), DHBV DNA was detected in serum and/or in liver tissue. These infected ducks showed a variety of pathological changes including advanced chronic disease in the liver. In contrast, none of the virus-negative ducks had advanced hepatic changes. One DHBV DNA-seropositive duck had a large hepatocellular carcinoma. Southern blot analysis demonstrated integrated DHBV DNA in neoplastic tissue and abundant episomal DHBV DNA in non-neoplastic tissue of the liver. In one noninfected duck with a small adenoma, no viral DNA was detected in tumor or non-neoplastic tissue. The detection of integrated DHBV DNA in hepatocellular carcinoma suggests that DHBV behaves like human and woodchuck hepatitis viruses in relation to chronic liver disease and hepatocarcinogenesis.
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PMID:Duck hepatitis B virus DNA in liver and serum of Chinese ducks: integration of viral DNA in a hepatocellular carcinoma. 386 Aug 52


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