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)

Hepatocellular carcinoma (HCC) is the commonest primary tumor of the liver; of late, its incidence has increased in the Western world. The authors report their experience with 42 patients affected with HCC; 36 cases were confirmed by fine-needle biopsy (FNAB), and 2 by surgery. All patients were studied with US and CT; 25 of them underwent color-Doppler US, and 30 angiography. In 9 patients, Lipiodol-CT was performed after hepatic arterial chemo-embolization. Thirty-six expansive and expansive-infiltrative lesions were observed, 4 infiltrative ones, and 1 neoplastic thrombosis of the portal vein with no evidence of parenchymal mass; 28 cases were multinodular in nature. US showed the primary lesion in all cases, while CT missed 2 lesions of 15 mm in diameter. In 19 of 25 cases studied with color-Doppler US, arterial pathologic signals were observed. Angiography confirmed all the primary lesions diagnosed by US in 30 patients and was found to be the most sensitive method to reveal multinodular lesions 8-15 mm phi, whereas Lipiodol-CT had higher resolution in detecting nodules up to 3 mm phi. The retrospective review of our results pointed out the capabilities of diagnostic imaging techniques in characterizing and staging HCCs--which is the reason why the role of biopsy has not been emphasized. The whole of the morphofunctional data obtained with the different techniques allowed lesion tissue characterization.
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PMID:[Integrated imaging of hepatocarcinoma. Personal experience]. 185 15

Effects of growth hormone (GH) overproduction were studied in transgenic mice expressing murine metallothionein I-GH fusion genes. The most obvious consequence was the acceleration of growth, which led to substantial increases in body weight of up to more than twice that seen in controls. Growth of the internal organs was stimulated, with hepatomegaly and nephromegaly as the most prominent features. GH transgene expression was also reflected in increased skeletal growth which affected various bones to different extents. The mean life-span of human GH transgenic mice with serum levels of hGH ranging from 3 x 10(3) to 9 x 10(5) ng/ml was drastically reduced at 160 days in both sexes. Severe renal lesions were the primary cause of the decrease in life expectancy and were characterized by marked nephron atrophy, obsolescence of numerous glomeruli, and a massive cystic dilation of the tubules. Initial changes involved the glomeruli, which showed significant enlargement and sclerotic lesions. The liver exhibited a pronounced hepatocellularmegaly and progressive degenerative as well as hyperplastic changes. One-third of the hGH transgenic animals displayed myocardial fibrosis. Hepatocellular carcinoma was found in bovine GH transgenic mice older than 12 months. Our observations are compared with results of other investigators.
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PMID:Accelerated growth and visceral lesions in transgenic mice expressing foreign genes of the growth hormone family: an overview. 191 Nov 31

Liver transplantation is now accepted as the treatment of choice for tyrosinemia type I (hereditary tyrosinemia). In an effort to determine whether any factors in these patients would aid in predicting optimal timing of the transplant procedure, we evaluated several clinical, biochemical, and radiographic parameters in five successive patients undergoing liver transplant for tyrosinemia type I at the University of Minnesota. All five patients evidenced prolonged periods of clinical and metabolic stability with dietary therapy and four of five remained stable at the time of evaluation for transplantation. Nevertheless, all five suffered significant and unexpected complications of tyrosinemia prior to the time of liver transplant. Four developed renal stones, two were in liver failure, and one developed a neurologic crisis that left him completely paralyzed. Hepatocellular carcinoma was found in one of the five at transplant. We could identify no clinical, biochemical, or radiographic study that was predictive of the likelihood of significant complications of the disorder. Survival from the transplant procedure itself was 100%. The inability to predict or prevent significant complications of tyrosinemia and the favorable outcome from transplantation lead us to recommend liver transplant for all patients with tyrosinemia type I by 12 months of age.
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PMID:Early liver transplantation is indicated for tyrosinemia type I. 191 40

Hepatocellular carcinoma may present in various ways, but only a few instances present with symptoms of distant metastases. This report describes a case of hepatocellular carcinoma presenting with acute haemothorax and haemorrhagic shock secondary to spontaneous rupture of chest wall metastasis. Hepatocellular carcinoma is a frequent malignancy in Asia and should be considered in the list of differential diagnosis of spontaneous haemothorax.
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PMID:Hepatocellular carcinoma presenting as acute spontaneous haemothorax. 196 83

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
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PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

Hepatocellular carcinoma with osteoclast-like giant cells (hepatic giant cell carcinoma [HGCC]) is a rare entity, with only three cases reported. The tumor is histologically similar to giant cell tumor (GCT) of bone, and the origin of the multinucleated giant cells and mononuclear stromal cells has not been determined. The purpose of this report is to present a case of this rare tumor and compare its ultrastructural and immunohistochemical features with those of a conventional GCT of bone. Histologically, the HGCC consists of sheets of osteoclast-like giant cells with a background of mononuclear cells. The giant cells lack the pleomorphism seen in hepatocellular carcinomas with anaplastic giant cells. At the light microscopic level, most of this tumor was nearly identical to a GCT of bone, but several microscopic fields (less than 5% of the tumor) had the histologic appearance of a "usual" hepatocellular carcinoma. The hepatic tumor was negative for HAM 56, epithelial cytokeratins, muramidase, and alpha-1-antitrypsin, with only focal positivity for chymotrypsin in mononuclear and giant cells. The GCT was strongly positive for alpha-1-antitrypsin and chymotrypsin in both the mononuclear and giant cells and showed focal, weak staining for AE1 and AE3 in the mononuclear stromal cells. Ultrastructurally, both mononuclear and giant cells of the HGCC showed features typical of hepatocellular carcinoma. Although the patient presented in this report died, the pattern of growth was different from most hepatocellular carcinomas. The overall histologic features of this tumor are distinctive and appear to justify separating this variant from other types of hepatocellular carcinoma.
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PMID:Hepatic giant cell carcinoma. An ultrastructural and immunohistochemical study. 215 1

Results of liver transplantation in 10 patients with tyrosinemia are reviewed. The indications for transplantation were: hepatoma in three, acute liver failure in two, and progressive chronic liver disease in five. One patient died during surgery. Of the remaining nine who survived the operation, one died at six months as a result of bronchial aspiration and aspiration pneumonia, and a second transplanted for hepatoma died five months later with metastases. Seven patients are alive 6 months to 6 1/2 years following transplantation. Of these seven patients, six have normal liver function and a good performance status. One is awaiting retransplantation for chronic rejection. Hepatocellular carcinoma (HCC) was found either preoperatively or incidentally in five patients, all older than 2 years at the time of their transplant. Four of these are alive and well without evidence of tumor with follow-ups between 3 1/2 and 6 1/2. Four of the five patients less than 2 years of age had hepatocellular dysplasia without evidence of carcinoma on histologic examination of the resected liver. This experience suggests that liver transplantation should be considered seriously for children with hereditary tyrosinemia who are more than 2 years of age because beyond that age the incidence of hepatocellular carcinoma (HCC) increases substantially.
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PMID:Liver transplantation for tyrosinemia. A review of 10 cases from the University of Pittsburgh. 215 69

Hepatocellular carcinoma is a hormone-sensitive tumor. It has been reported that thyroxine and prolactin significantly stimulated hepatoma growth, whereas growth hormone failed to do so. To learn whether the growth hormone receptor is present in human hepatocellular carcinoma, we used radioreceptor assays in samples of human hepatocellular carcinoma. The liver tissues adjacent to hepatocellular carcinoma (mostly cirrhotic) and control liver tissues (taken during various surgical procedures) were also studied. The study results showed that the affinity constant and capacity of high-affinity growth hormone receptor in normal liver tissues were 6.6 +/- 2.0 x 10(10) mol/L-1 (mean +/- SE, n = 7) and 20.7 +/- 11.5 fmol/mg protein, respectively. The affinity constant and capacity of low-affinity growth hormone receptor in normal liver tissues were 8.9 +/- 3.3 x 10(9) mol/L-1 and 64.7 +/- 32.1 fmol/mg protein, respectively. The absence of growth hormone receptor in human hepatocellular carcinoma and cirrhotic liver samples may explain the absence of growth hormone in the stimulation of hepatoma growth and the decrease of somatomedin levels in cirrhosis.
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PMID:Absence of growth-hormone receptor in hepatocellular carcinoma and cirrhotic liver. 222 28

We report 2 cases of type I glycogen storage disease (Von Gierke's disease) discovered in 2 brothers at the age of 7 and 5 years, respectively. Both developed hepatic adenoma at the age of 19 and 17. Hepatocellular carcinoma occurred in the older brother the discovery of adenoma 4 years after. The frequency of these tumors in patients with type I glycogen storage disease raises problems concerning the treatment and modality of regular surveillance of the liver in these patients. The policy for the detection and treatment of these tumors, and particularly the indications for liver transplantation are discussed.
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PMID:[Hepatic adenoma and hepatocellular carcinoma in 3 brothers with type I glycogenosis]. 215 41

Between July 1973 and September 1988, 119 patients with hepatocellular carcinoma underwent hepatic resection at Keio University Hospital, Tokyo. Hepatic resection was performed not only for patients with liver cirrhosis and obstructive jaundice but also for patients with advanced disease. Eighty (67.2%) of the 119 patients had liver cirrhosis and four patients had obstructive jaundice. Two or more segments of the liver were resected in 56 (47.0%) patients, 29 of whom had liver cirrhosis. Eleven patients died within 30 days after surgery, an operative mortality rate of 9.2%. Seven additional patients could not be discharged from the hospital, resulting in a hospital death rate of 5.9%. Seventeen of these 18 patients had cirrhosis. Selection of patients with sufficient reserve function of the remaining liver portion, caused a great reduction of the incidence of postoperative death. The 5-year actuarial survival rate for the 101 patients who were discharged from the hospital was 39%, and 13 patients lived longer than 5 years, the longest survival period being 13 years 10 months. Hepatocellular carcinoma is amenable to hepatic resection if patients with sufficient reserve function of the liver are selected.
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PMID:Hepatic resection for hepatocellular carcinoma. 215 90


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