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)

Obstructive jaundice, pruritus, and malabsorption developed in twin brothers in infancy. Early liver biopsy specimens showed intracellular and canalicular cholestasis with normal bile ducts. By the age of 3 years, both had cirrhosis and portal hypertension. Each died during the teen years from hepatocellular carcinoma. These brothers represent the tenth reported family with familial cholestatic cirrhosis, and they are the first patients with this syndrome in whom hepatoma developed.
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PMID:Hepatoma in familial cholestatic cirrhosis of childhood: its occurrence in twin brothers. 21 1

The various factors are reviewed which may contribute to the appearance of jaundice in patients with cirrhosis. During the prehepatic phase, hemolysis, spenomegaly and a drop in coagulation factors constitute the main physiopathological mechanisms, whereas intrahepatic cholestasis, alcoholic hepatitis, hepatoma and terminal hepatic insufficiency are the principal mechanisms cited for the hepatic stage. In the posthepatic stage, attention is drawn to the increased frequency of lithiasis in cirrhotic patients and the choledochal lesions seen in chronic pancreatitis.
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PMID:[Icterus and cirrhosis: physiopathology]. 22 39

CT can clearly demonstrate dilation of intra- and extra-hepatic bile ducts due to mechanical obstruction. Note is made that the intrahepatic bile must not necessarily participate in dilation in obstructive jaundice. The cause in 27 cases observed in our institutions was as follows: 16 pancreatic tumors; 1 stone; 2 extrahepatic bile duct obstructions; 4 liver lesions (tumor and cirrhosis) and 4 with cause unknown. Furthermore, CT is helpful in the evaluation of hepatogenic non-obstructive jaundice such as due to primary liver cell carcinoma (hepatoma), metastases to the liver and advanced cirrhosis of the liver. The value of CT in the evaluation of different types of cholestasis is demonstrated by several exemplary cases; and the problems of differential diagnosis are pointed out.
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PMID:[Computerized tomography in the evaluation (author's transl)]. 22 56

Serum glutamic oxaloacetic transaminase (GOT), mitochondrial GOT (GOTm), glutamic-pyruvic transaminase (GPT) and glutamate dehydrogenase activities were determined in 43 healthy controls and in 280 cases of liver diseases. A simplified column chromatographic method coupled with UV assay was employed for separation of GOTm. The activity was measured by following decrease in abosrbance of NADH at 340 nm. The lowest activity of GOTm determined with a coefficient of variation below 10% was 6 mIU/ml. High GOTm activities were found in acute hepatitis (acute stage), subacute hepatitis and primary biliary cirrhosis and were generally associated with high total GOT (GOTt) activities. The activity ratio of GOTm/GOTt varied depending on the stage and severity of liver diseases. The GOTm/GOTt ratio was decreased in acute, fulminant and subacute hepatitides. No significant reduction in the ratio was found in bile duct obstruction, alcoholic liver injury or metastatic liver cancer. Although relatively high GOTm/GOTt ratios were found in some patients with severe hepatic injury, they had no definite association with poor prognosis. These results indicate that the marked elevation in GOTt over GPT in advanced chronic hepatitis, liver cirrhosis and primary hepatoma was mainly due to preferential leakage of cytoplasmic GOT (GOTs).
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PMID:The mechanism of the release of hepatic enzymes in various liver diseases. 1. Alterations in cytoplasmic and mitochondrial enzyme activities in serum. 22 31

Duodenofiberscopy with endoscopic retrograde cholangiopancreatography (ERCP) was performed in 102 patients with obstructive jaundice. Peritoneoscopy and peritoneoscopic cholecystocholangiography were done in patients whose ERCP was inconclusive. The causes of obstructive jaundice were carcinoma of the pancreas in 14 cases, carcinoma of the papilla of Vater in 12 cases, choledocholithiasis in 37 cases, carcinoma of the common bile duct in seven cases, hepatocellular carcinoma (HCC) in seven cases, intrahepatic cholestasis in three cases and miscellaneous causes in eight cases. No final diagnosis was made in 14 patients. The duodenofiberscopic examination with biopsy revealed the cause of obstructive jaundice directly in eight cases, when carcinoma of the pancreas or papilla of Vater extended to the duodenal mucosal surface. In 34 of the 37 patients with choledocholithiasis, ERCP alone was successful in making the diagnosis. Percutaneous transhepatic cholangiography and ERCP were used together to reach a diagnosis in the remaining three patients. We propose a classification for HCC on ERCP which may be useful for the study of icteric type HCC.
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PMID:Endoscopic approaches in the diagnosis of obstructive jaundice--with special reference to endoscopic retrograde cholangiopancreatography. 136 12

Two cases of Alagille syndrome are reported, father and son. This, a 6-year-old boy, presented with neonatal cholestasis but thereafter evolved with progressively decreasing jaundice and persisting pruritus. A liver biopsy confirmed the absence of intrahepatic bile ducts with preservation of hepatic architecture and no fibrosis. The patient had a characteristic phenotype: short stature, triangular face, deep eyes with hypertelorism, partial embryotoxon and data of peripheral pulmonary artery stenosis. His father died 43-year-old by a hepatocarcinoma. His liver biopsy showed also absence of intrahepatic bile ducts. In addition to the association Alagille's syndrome hepatocarcinoma (previously reported in six cases, three into the same family), it should be stressed in this case the long survival and the fact he had many children: the case with Alagille's syndrome, five children in good health, and one who died shortly after birth.
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PMID:[Alagille's syndrome: a family case and its association with hepatocellular carcinoma]. 165 82

Serum CA 19-9 and alpha-fetoprotein (AFP) levels were determined in 211 patients with liver cirrhosis and 27 with primary hepatocellular carcinoma (HCC) associated with liver cirrhosis. This was done to determine the usefulness of CA 19-9 level with respect to AFP level in distinguishing between these two illnesses, and to assess the influence of some clinical and biochemical variables on these tests in patients with liver cirrhosis with or without primary HCC. Pathologic AFP values were found in 23 of 27 (sensitivity, 85%) patients with HCC; CA 19-9 levels increased in only 12 of 27 (sensitivity, 44%) HCC patients, the values being comparable with those of patients with liver cirrhosis. In liver cirrhosis a substantial number of false-positive values was found for both markers, although they were higher for CA 19-9 (50 of 211 versus 39 of 211). In liver cirrhosis correlations were found between AFP level and alanine amino-transferase level; and between CA 19-9 level and (1) total bilirubin value, (2) alkaline phosphatase level, and (3) pseudocholinesterase level. The authors conclude that CA 19-9 level is a poor biochemical marker, inferior to AFP level, in the detection of a carcinomatous transformation of liver cirrhosis. The finding of false-positive AFP values in liver cirrhosis seems mainly attributable to cellular proliferation and necrosis. Cholestasis seems to greatly affect serum CA 19-9 level variations, probably by reducing its liver metabolism.
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PMID:Serum CA 19-9 and alpha-fetoprotein levels in primary hepatocellular carcinoma and liver cirrhosis. 138 Dec 71

The alpha 1-antitrypsin deficient subject (protease inhibitor (PI) phenotype ZZ) has an increased susceptibility to liver disease. The condition is most commonly identified in early infancy as a conjugated hyperbilirubinaemia with hepatitis (11%) or a bleeding state due to vitamin K malabsorption (2%). 50% of cases have cirrhosis and 25% die in the first decade of life. A further 2% present with cirrhosis in later childhood. Adult males are at risk of hepatoma development with or without cirrhosis. Diagnosis is by isoelectric focussing or allele-specific oligonucleotide hybridization. The treatment is that of cholestasis and cirrhosis including transplantation. The pathobiology of the deficiency state, the mechanism of liver damage and the vulnerability of the newborn liver are discussed in this review. A plea is made for a trial of infusions of alpha 1-antitrypsin in early infancy, as is used safely but without proven efficacy in the emphysematous PIZZ subject. Prospects of therapy by gene modification are also reviewed.
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PMID:Alpha 1-antitrypsin deficiency and liver disease: clinical presentation, diagnosis and treatment. 174 15

During the first 18 months of liver transplantation program for adult patients we evaluated 98 potential candidates for this treatment. Forty five patients were refused for transplantation and 53 were accepted. Forty six out of these 53 cases were transplanted. Ten (22%) out of the 46 patients undergoing transplantation had chronic hepatic cholestasis, 31 (67%) chronic hepatic diseases of non biliary origin (3 patients had an associated hepatocarcinoma), and 5 patients (11%) suffered an acute hepatic failure. All transplanted patients with previous chronic hepatic diseases had clinical and biological signs of advanced hepatic failure. There were no operative deaths. During the follow-up period 6 transplanted patients (13%) died. The survival probability among the 46 operated patients was about 84% at 12 months after the transplant. This survival was theoretically higher than that expected to occur without transplantation. The survival probability among the 46 transplanted patients was significantly higher (p = 0.0001) than that recorded in 36 patients with comparable hepatic diseases who were evaluated during the same study period and who were not considered for transplantation due to several reasons. The survival probability at the first year in the later group of 36 patients was 20%.
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PMID:[Liver transplantation: candidate selection and results of a program for adult patients]. 202 74

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


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