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)

Thirty-eight patients with porphyria cutanea tarda (PCT) have been seen in the last 18 years. Five of these patients (13%) developed hepatocellular carcinoma (HCC) during follow-up. We analyzed the differences in clinical, laboratory and liver histology findings at presentation, between patients who developed HCC during follow-up (HCC-group, n = 5) and those who did not (PCT-group, n = 33). Of the clinical features the duration of skin-symptoms was longer in the HCC-group (mean: 10.4 +/- 1.1 years) than in the PCT-group (mean: 1.4 +/- 1 years) (p less than 0.001). No differences in routine laboratory findings were found. Although 11/38 (29%) patients had serologic evidence of a past hepatitis B virus infection and 7/38 (18%) patients had antibodies against hepatitis C virus, no differences in these parameters were found between the PCT-group and the HCC-group. In all 34 liver biopsies a variable degree of siderosis was found (PCT-group vs. HCC-group: NS). Only piecemeal necrosis (p less than 0.01) and advanced fibrosis or cirrhosis (p less than 0.001) were more common in liver biopsies in the HCC-group. In conclusion, factors related to an increased risk of HCC in PCT are: a) a long symptomatic period before start of treatment and b) the presence of chronic active hepatitis and/or advanced fibrosis or cirrhosis in liver biopsies.
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PMID:Hepatocellular carcinoma in porphyria cutanea tarda: frequency and factors related to its occurrence. 132 Jan 75

Magnetic resonance demonstrated siderotic regenerating nodules in a patient with hepatocellular carcinoma with accompanying liver cirrhosis. The siderosis disappeared when iron deficiency anemia developed in association with biliary hemorrhage. Magnetic resonance was sensitive enough to follow changes in the siderosis. The mechanism of iron deposition in regenerating nodules that accompanied liver cirrhosis did not seem to be related to the severity of the liver damage.
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PMID:Siderotic nodules in hepatic cirrhosis disappearing after biliary hemorrhage: MR imaging. 165 91

It has been pointed out that hepatocellular carcinoma (HCC) develops more frequently in cirrhotic liver with siderosis than in liver without iron deposition, that excess copper in hepatocytes inhibits hepatocarcinogenesis, and that an increase in copper and a decrease in zinc are seen in the sera of patients with various malignant tumors. Iron, copper and zinc concentrations in the serum and liver were estimated in normal subjects and cirrhotic patients with and without HCC. Serum copper level was significantly higher in cirrhotic patients with or without HCC than in normal subjects. No significant differences were observed in the levels of these trace elements in the serum and liver of cirrhotic patients with and without HCC. The current study seems to indicate that iron, copper and zinc do not play an important role in the development of HCC in cirrhotic patients in Japan.
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PMID:Iron, copper and zinc levels in serum and cirrhotic liver of patients with and without hepatocellular carcinoma. 255 Aug 61

We report the findings in 53 biopsies from 45 patients with porphyria cutanea tarda (PCT). Red autofluorescence and birefringent acicular cytoplasmic inclusions were constant findings in all untreated cases. Autofluorescence occurs in other hepatic porphyrias, but acicular inclusions appear to be specific for PCT; we have seen them in subclinical porphyria and before development of cutaneous symptoms. They are probably uroporphyrins and they trend to disappear during rinsing by water during most staining procedures. We recommend unstained paraffin sections for their demonstration. Liver damage in PCT has features distinct from other liver diseases, including alcoholic liver disease. These include constant but mild periportal siderosis, focal lipofuscin deposition, focal lobular hepatocyte necrosis associated with groups of pigment-laden macrophages, focal steatosis, marked hepatocyte hyperplasia and the presence of periductal lymphocyte aggregates. The latter have not been previously described in PCT and were present in 43% of our cases. There is a direct relationship between increasing age and progressive distortion of liver architecture, with fibrosis present at a mean age of 48 years, cirrhosis at 57 and hepatocellular carcinoma at 66. The characteristic liver histology and the natural history of PCT are against this being the result of any non-specific liver damage and favour instead a specific liver disease whose pathogenesis may be mainly the result of the metabolic defect of PCT.
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PMID:The pathology of the liver in porphyria cutanea tarda. 625 81

A male infant with neonatal iron storage disease, also known as neonatal hemochromatosis (NH), underwent orthotopic liver transplantation (OLT) at the age of 55 days. The native liver contained an incidental hepatocellular carcinoma. Scant iron accumulation was found in a biopsy specimen of the implanted liver on the seventh postoperative day (POD); successive biopsies showed increasing siderosis. On POD 62, the patient died of a cardiac arrhythmia. Autopsy showed siderosis at many sites, including the implanted liver. We discuss the possibility that hemochromatosis recurred in the liver allograft and review possible factors contributing to the siderosis.
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PMID:Rapid development of hepatocellular siderosis after liver transplantation for neonatal hemochromatosis. 895 82

Iron overload has been shown to impair the immune response of the liver, and induce hepatic fibrosis and cirrhosis. Opinions differ concerning the relative risk of developing hepatocellular carcinoma (HCC) in siderotic patients as compared with patients with hepatic fibrosis and cirrhosis and the possible mechanism of liver carcinogenesis in genetic hemochromatosis is still unknown. The purpose of this study is to assess hepatic iron overload, fibrosis and cirrhosis in liver tissue adjacent to hepatocellular carcinoma and in liver tissue of controls in population at risk for hepatocellular carcinoma. Liver tissue was available for examination in 147 biopsies with HCC collected in South Africa. As controls we used liver samples from 211 age and sex matched Africans who died in accidents. Tissue samples were processed routinely, stained with H and E, Sweet's reticulin, Masson's trichrome for fibrous tissue, Prussian blue for iron stain and immunohistochemically for HBsAg. Iron content was assessed with the method described by Brissot. Iron overload was detected in 42.1% of cancerous livers and in 43.7% of livers from controls. The presence of siderosis and iron content gradually increased with the age of studied similarly in cases and in controls. Cirrhosis was present in 32% of cancerous livers and was associated with iron overload in 13%. No cirrhosis and 6% of mild periportal fibrosis not related with siderosis was observed in controls. HBsAg was stainable in 80% of cancerous livers of patients below 25 years of age and in 40% of patients over 35 years. HBsAg in controls was positive in 9%. No relationship of HBsAg and amount of stainable iron in cancerous and livers of controls was found. In conclusion, African siderosis can not play important role in the etiopathogenesis of HCC.
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PMID:Hepatic siderosis, fibrosis and cirrhosis: the association with hepatocellular carcinoma in high-risk population. 942

Although HLA-linked hemochromatosis greatly increases the risk for hepatocellular carcinoma in people of European ancestry, iron overload in Africa is not thought to be etiologically related to this malignancy. To determine if African iron overload may be associated with hepatocellular carcinoma, we reviewed 320 consecutive diagnostic liver biopsies processed at the University of Zimbabwe from 1992 to 1994 and we selected for analysis 215 biopsies from adults that were suitable for the histological assessment of hepatocellular iron. Subjects were stratified according to hepatocellular iron grades of 0-2+ (normal levels to mild siderosis; n = 183) and grades of 3+ and 4+ (distinctly elevated levels consistent with iron overload; n = 32). Thirty-six subjects had hepatocellular carcinoma. Logistic regression modeling revealed a significant association between iron overload and hepatocellular carcinoma after adjustment for age, sex and and the presence of portal fibrosis or cirrhosis (p = 0.041). The odds of hepatocellular carcinoma in subjects with iron overload was 3.1 (95% confidence interval of 1.05-9.4) times that of subjects without iron overload. While we could not test for exposure to viral hepatitis or to aflatoxins in this study, our findings suggest that iron overload may be a risk factor for hepatocellular carcinoma in Africa.
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PMID:African iron overload and hepatocellular carcinoma (HA-7-0-080). 945 25

The synergistic effects of iron overload and ethanol on the liver of mice were studied over a period of 46 weeks. The determination of several parameters (iron, calcium, magnesium, alpha-hydroxyproline, lipid peroxidation, hepatomegalic and splenomegalic indexes) showed that ferrous and ferric lactates provoke an increase of calcium in the liver, higher than that of ethanol in the control animals. The relationship between liver calcium homeostasis modification and the increase of collagen and lipid peroxidation is discussed. Histological examinations showed differences in the tissular characteristics especially when iron and ethanol were given together. These findings suggest the liver calcium homeostasis changes found as a synergistic effect in the early stages of chronic iron overload may be of importance as a trigger of events leading to the pathway of fibrosis-->cirrhosis-->hepatocarcinoma reported in pathologies such as nutritional siderosis and hemochromatosis.
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PMID:Iron-ethanol synergism and pathological liver transformation. 1021 26

Genetic haemochromatosis constitutes a high risk factor for the development of hepatocellular carcinoma. It is widely accepted that venesection prevents the evolution of cirrhosis in haemochromatosis and indirectly protects against the development of hepatocellular carcinoma. Clinical, pathological and radiological data are presented on three patients who did not conform to the 'siderosis-cirrhosis-carcinoma' sequence and in whom prompt and adequate iron depletion did not prevent the development of cancer. This is the first report of hepatocellular carcinoma intervening in non-cirrhotic liver in two siblings with genetic haemochromatosis. The current literature on the subject is reviewed. The direct oncogenic role of iron remains to be elucidated. Hepatocellular carcinoma should be considered as a differential diagnosis in patients with non-cirrhotic genetic haemochromatosis who present with clinical deterioration during the course of an otherwise uneventful venesection programme.
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PMID:Hepatocellular carcinoma arising in the absence of cirrhosis in genetic haemochromatosis: three case reports and review of literature. 1051 28

Hepatocellular carcinoma (HCC), following liver cirrhosis as a complication of chronic hepatitis B or C viruses (HBV or HCV)and iron overload, has been reported in thalassemia patients. This study assessed HCC incidences, the role of iron and possible antitumor activity of chelators in 57 thalassemia major (TM) and nine thalassemia intermedia (TI) patients using deferoxamine (DFO) therapy. Antibodies against HCV were detected in 23/57 (40.4%) TM patients, chronic HCV and cirrhosis were diagnosed in 13/23 (56.5%), 7/12 did not respond to antiviral therapy and 2/7 progressed to HCC (incidence 2/57, 3.5%). Three (33.3%) TI patients with liver siderosis and fibrosis and late introduction of iron chelation developed HCC without a history of hepatitis. The incidence was higher in TI (p = 0.032). The main risk factor for HCC was HCV infection in TM patients but it was iron activity in TI patients. Iron chelation with DFO appeared to play a protective role.
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PMID:Incidence of hepatocellular carcinoma in a thalassemia unit. 2052 12


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