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)

A detailed morphological study concerning the liver of 71 patients suffering from idiopathic haemochromatosis was carried out. These patients were subjected to long-term venesection therapy, which lasted from 1 to 12 years. The mean duration of therapy was 7 years for each patient. The material consisted of needle biopsies of the liver. Three to seven biopsies were performed in each patient; the initial biopsy, the biopsy following venesection therapy, and the follow-up biopsies. In 30 cases the follow-up was performed in autopsy material. It was found that the final histological appearance of the liver remained unchanged in 44 (62%) cases, became worse in 23 (32%) cases, and improved in 4 (5%) cases. However, the change for the worse is generally retarded and consequently the mean survival of the patients is increased. Two out of 4 cases that showed improvement (i.e. changing from cirrhosis to fibrosis) are strongly supported by the fact that the follow-up study was performed in autopsy material after 2-5 needle liver biopsies. A high incidence of hepatocellular carcinoma (18%), as well as of a malignant neoplasia in another organ (8.4%), was noted in spite of the long-term venesection therapy. It follows therefore that the longer survival of patients with idiopathic haemochromatosis increases the possibility of hepatocellular carcinoma or of a malignancy in another organ.
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PMID:Cirrhotic process, liver cell carcinoma and extrahepatic malignant tumors in idiopathic haemochromatosis. Study of 71 patients treated with venesection therapy. 283 15

Previous reports have emphasized the association of primary hepatocellular carcinoma in patients with idiopathic hemochromatosis with cirrhosis. In contrast, patients with idiopathic hemochromatosis without cirrhosis have no increased risk of hepatocellular carcinoma. Phlebotomy therapy, by preventing the accumulation of parenchymal iron and subsequent cirrhosis, is believed to prevent hepatocellular carcinoma in the precirrhotic stage of the disease. We report the case of a 67-yr-old man with a 32-yr history of idiopathic hemochromatosis complicated by cirrhosis, who had reversal of cirrhosis with phlebotomy therapy, yet developed hepatocellular carcinoma. There was no serologic or tissue evidence of hepatitis B infection.
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PMID:Primary hepatocellular carcinoma in idiopathic hemochromatosis after reversal of cirrhosis. 284 22

A primary hepatocellular carcinoma associated with underlying hemochromatosis appeared as a metastatic mandibular lesion. A swelling of the retromolar area and mandibular paresthesia were the presenting complaints. Hepatocellular carcinoma rarely metastasizes to the orofacial area. To our knowledge, only 18 cases have been reported. The clinical, radiographic, and histologic features of an additional case of hepatocellular carcinoma metastatic to the left posterior alveolar ridge is reported, and the literature is reviewed.
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PMID:Hepatocellular carcinoma presenting as an oral cavity lesion. 284 39

Two patients with primary haemochromatosis are reported in whom hepatocellular carcinoma supervened despite removal of excess iron after venesection therapy. These are the first patients described in whom hepatocellular carcinoma has complicated primary haemochromatosis in the absence of concomitant cirrhosis.
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PMID:Hepatocellular carcinoma in primary haemochromatosis in the absence of cirrhosis. 285 Feb 72

The liver is, under normal conditions, mitotically inactive and relatively resistant to chemical carcinogenesis. When rat or mouse hepatocytes are stimulated to divide, however, the liver becomes exquisitely sensitive to carcinogenesis. The heightened sensitivity of dividing liver cells to carcinogens is one of the most dramatic phenomena in the field of experimental chemical carcinogenesis and is reproducible with a wide variety of chemical agents and experimental conditions. This same phenomenon seems to apply to humans, as circumstances that produce a sustained hepatocellular proliferation in man are associated with an increased risk of hepatocellular carcinoma (HCC). These include inborn errors of metabolism (e.g., haemochromatosis, Wilson's disease, hereditary tyrosinaemia) as well as alcoholism. A recent editorial in this Journal suggested that any condition resulting in cirrhosis is also associated with an increased risk of HCC, and this may in turn be due to regenerative hyperplasia always present in cirrhotic liver (Johnson PJ, Williams R. J Hepatol 1987; 4: 140-147). In the case of HCC associated with hepatitis B virus (HBV) infection, the possibility must be entertained that chronic HBV infection serves to produce a sustained hepatonecrosis with concurrent (regenerative) hyperplasia. This proliferative state would in theory serve to increase the liver's susceptibility to environmental dietary carcinogens and may tend to increase the risk of HCC by this indirect mechanism. Until a molecular mechanisms is demonstrated whereby HBV produces a defined cellular lesion that endows hepatocytes with a malignant phenotype, it should not be assumed that HBV is a direct cause of HCC.
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PMID:Cell proliferation and the aetiology of hepatocellular carcinoma. 285 89

Idiopathic hemochromatosis is a hereditary disease characterized by a progressive iron overload secondary to high intestinal iron absorption. After a latent period of many years, manifestations of liver cirrhosis, diabetes mellitus, cardiac failure, hypogonadism, skin hyperpigmentation and arthropathy can occur. Liver cirrhosis is the most common feature and it is complicated by hepatocellular carcinoma in 30% of cases. Tests of high sensibility are available for early diagnosis. Repeated phlebotomy can prevent clinical features in asymptomatic patients and can improve prognosis in symptomatic subjects. Current concepts in idiopathic hemochromatosis are reported in this review.
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PMID:[Idiopathic hemochromatosis]. 298 52

In evaluating nuclear magnetic tomography for the diagnosis of liver disease, one must differentiate between circumscribed and diffuse lesions. Nuclear magnetic tomography provides additional information for lesions which are echogenic on ultrasound and can differentiate between metastases, haemangiomas and hamartomas. In diffuse parenchymal disease measurement of relaxation time can differentiate between fatty liver, cirrhosis (alcoholic, primary biliary), haemochromatosis (cirrhotic transformation) and hepatoma. NMR spectroscopy is a method for the future.
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PMID:[Differential diagnosis of liver diseases in the nuclear spin tomogram]. 298 31

Patients with cirrhosis present a continuing diagnostic and therapeutic challenge. The status of their disease frequently changes, necessitating intensive serial evaluation. CT is an invaluable tool in the management of these patients because it can noninvasively provide vital information concerning liver size, contour, and occasionally hepatic parenchyma. More importantly, CT can demonstrate superficial and deep varices, assess the patency of the extrahepatic portal system, and detect other complications including ascites, hepatic steatosis, hemochromatosis, and hepatocellular carcinoma.
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PMID:Computed tomography in the evaluation of cirrhosis and portal hypertension. 298 57

The risk of hepatocellular carcinoma (HCC) and other internal malignancies was examined in patients with genetic hemochromatosis (GH) by following 208 patients from the time of diagnosis to June 1983 and by comparing the numbers of cancers they developed with expected values constructed from cancer registry incidence data by means of actuarial methods. In addition, cancers occurring in a comparison group of 148 subjects with other chronic nonalcoholic liver diseases (CLD) were determined. Among the GH group, 16 new cases of HCC occurred subsequent to the diagnosis of GH, together with 8 other malignancies. The 16 cases of HCC reflect a 200-fold excess risk, which from all indications represents the first quantitation of the risk of this tumor in GH. There appears to be no increased risk of other malignancies in this disease. Among the CLD group only 1 HCC and 1 other malignancy occurred.
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PMID:Cohort study of internal malignancy in genetic hemochromatosis and other chronic nonalcoholic liver diseases. 298 5

Nuclear Magnetic Resonance (NMR) tomography has already attained a position in clinical use beside the established techniques ultrasound (US) und computerized tomography (CT) for the examination of the liver and its related diseases. In assessing its methodical significance one has to differentiate between focal liver lesions and damages of the liver parenchyma. Focal lesions may be identified with NMR just as safely as with US and CT. However, NMR produces additional information, especially in the echo-dense lesions in US, where both NMR and angio-CT can differentiate between echo-dense metastases, haemangiomas and fatty tumours. In damages of the liver parenchyma NMR seems to become the method of choice. Quantitative tissue differentiation is possible by determining the relaxation times. In fatty degeneration of the liver focal fatty infiltration and circumscribed cirrhotic changes can be discerned. It is possible to identify cirrhoses directly and not merely by indirect criteria as is the case with US and CT. NMR can also differentiate between aethylic (prolonged T1) and primary-biliary cirrhosis (shortened T1). Haemochromatosis may be identified with CT, the accompanying secondary cirrhotic change, however, can only be detected by NMR. In liver cell carcinoma, e.g. secondary to cirrhosis, cancer nodes and cirrhotic regeneration nodes may be differentiated. Whole body NMR spectroscopy is still under research. Once it is perfected for clinical use it will change the entire laboratory medicine.
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PMID:[Nuclear magnetic resonance tomography in the study of the liver and its diseases]. 299 7


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