Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Focal hepatic atrophy has numerous causes and in many cases is associated with compensatory hypertrophy. We have observed this phenomenon on CT in patients with hepatic neoplasms. Of 12 patients studied, eight had hepatic metastases, two had hepatocellular carcinoma, and two had bile-duct carcinoma. Focal changes in liver morphology (i.e., atrophy with compensatory hypertrophy) were found in five patients at presentation and developed after treatment with systemic or intraarterial chemotherapy in the others. Atrophic changes affected the right lobe in eight patients, the left lobe in three, and part of both lobes in one. Compensatory hypertrophy of part or all of the unaffected liver was found. Ten patients had obstruction of the portal vein branch to the atrophic segment, four of these 10 also had hepatic vein obstruction, and two of these 10 also had bile duct obstruction. Portal vein obstruction appears to be the most important element in the production of focal hepatic atrophy in patients with hepatic neoplasms. After treatment with chemotherapy, tumor regression and atrophy may be associated with compensatory hypertrophy and enlargement of the uninvolved part of the liver. This must not be mistaken for progression of disease.
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PMID:Atrophy with compensatory hypertrophy of the liver in hepatic neoplasms: radiographic findings. 325 66

Retention cysts may arise from periductal glands of the hepatic ducts. These cysts are usually asymptomatic. Presented here is the first case with jaundice secondary to obstruction of the hepatic ducts by periductal cysts. Two other cases involved asymptomatic cysts in the presence of cirrhosis, portal vein thrombosis, and hepatocellular carcinoma. This confirms the previously noted association of cysts and portal vein thrombosis. The possibility of obstruction caused by benign cysts should be considered when investigating patients with intrahepatic bile duct obstruction.
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PMID:Hepatic cysts of periductal gland origin presenting as obstructive jaundice. 362 29

Hepatocellular carcinoma can be complicated by obstructive jaundice with tumor growing into the extrahepatic bile duct. This complication is an autopsy finding in most reported cases and, rarely, is recognized ante mortem. We report two patients with hepatocellular carcinoma who presented initially with obstructive jaundice. Clotted blood and tumor, which caused bile duct obstruction, was removed operatively and the biliary tract was drained in both patients. We conclude that blood clot and fleshy debris removed from the common bile duct at operation for obstructive jaundice suggests the possibility of hepatocellular carcinoma; the differential diagnosis of jaundice and fever in patients known to have hepatocellular carcinoma should include intrabiliary tumor causing obstruction and cholangitis; and the association of obstructive jaundice and hepatocellular carcinoma may occur more often than previously recognized.
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PMID:Obstructive jaundice caused by hepatocellular carcinoma. 609 Aug 14

Tumor debris, free-floating in the major biliary ductal system, is a cause of intermittent biliary obstruction that has previously not been recognized. Six patients had hepatic neoplasms with episodic jaundice and/or cholangitis due to floating tumor debris. Diagnosis included metastatic adenocarcinoma of the colon (n = 3), cholangiocarcinoma (n = 1), hepatocellular carcinoma (n = 1), and cavernous hemangioma (n = 1). All patients underwent biliary exploration, with hepatic resection and transhepatic intubation in two and T-tube placement in four. One patient died in the early postoperative period, and the major complication rate in the five survivors was 0%. Four of the five survivors had no further episodes suggestive of major bile duct obstruction. Our experience emphasizes the importance of distinguishing extrahepatic obstruction secondary to tumor debris from the more common causes of jaundice in patients with tumors and suggests that safe and effective palliation can be achieved in these patients.
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PMID:Floating tumor debris. A cause of intermittent biliary obstruction. 609 35

Serum gamma-glutamyl transpeptidase zymograms were examined by 4--26% polyacrylamide gradient gel slab electrophoresis using sera from 90 patients with various hepatobiliary diseases. The isozyme bands were separated into 13 bands in order from post albumin fraction. Characteristic patterns of the zymograms were obtained in cases of hepatocellular carcinoma and cholestasis. Bands I, II and II' may be specifically related to hepatocellular carcinoma. Band I was observed frequently in hepatocellular carcinoma, however it was also occasionally observed in alcoholic liver injury and metastatic liver cancer. Both band II and II' were only observed in hepatocellular carcinoma cases. The origin of band II and/or II' was not clarified but band I might appear through some proteolytic process in hepatoma tissue and also liver affected by alcohol. In cholestatic cases the activity of bands III and IX were prominent. The frequency of band VI decreased according to the severity of jaundice and a negative correlation appeared to exist between bands III and VI. This phenomenon may be partially related to lipid metabolism disorder which is frequently observed in cholestasis. Results of analysis of the frequency of appearance of these bands did not permit differentiation between intra- and extrahepatic cholestasis.
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PMID:Clinical significance of appearance of serum gamma-glutamyl transpeptidase isozyme. 611 91

Analysis of tissue from a recent case of fibrolamellar liver cell carcinoma by several staining and spectrophotometric methods demonstrated elevated copper and copper-binding protein (CBP) in malignant hepatocytes. Production of CBP has not previously been described for this or any other type of hepatocellular carcinoma. Identification of CBP in liver cell carcinoma adds further evidence that this protein is a normal synthetic product of liver cells which may reappear in chronic cholestasis or hepatic malignancy. The mechanism of disturbed copper homeostasis in this case is uncertain.
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PMID:Copper and copper-binding protein in fibrolamellar liver cell carcinoma. 618 96

This report describes four siblings affected with familial intrahepatic cholestasis detected in early infancy. In the two male siblings, biliary cirrhosis and fatal hepatocellular carcinoma later developed, whereas the female siblings have had persistent hepatomegaly and recurrent episodes of cholestasis. Sequential biopsies show that this rare disorder of unknown etiology must be added to the many causes of giant cell transformation of the liver in infancy. Its oncogenic risk, particularly in males, has not been generally appreciated.
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PMID:Hepatoma in siblings with progressive familial cholestatic cirrhosis of childhood. 626 30

Serum apoprotein A-I and A-II levels were determined by electroimmunoassay in patients with liver diseases and cholestasis. Significant decreases in apoprotein A-I and A-II levels were observed in such patients. The decreases were especially pronounced in the early phase of acute hepatitis and cholestasis. The decreases in A-II levels were more prominent than the decreases in A-I in severe hepatic dysfunction or cholestasis. Accordingly, the A-I/A-II ratio showed no change in the convalescent phase of acute hepatitis or chronic hepatitis but increased significantly in the early phase of acute hepatitis, cirrhosis of the liver, hepatoma, and cholestasis. The results suggested the existence of a high density lipoprotein with an abnormal apoprotein composition or a more profound decrease of HDL3 than of HDL2 in severe hepatocellular dysfunction of cholestasis.
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PMID:Serum apoprotein A-I and A-II levels in liver diseases and cholestasis. 627 23

For a long time, it has been assumed that the liver plays an important role in the formation and excretion of bile acids and that the metabolism of bile acids, therefore, can be disturbed to some extent in liver diseases. Pathophysiological aspects of the disturbed metabolism of bile acids remained obscure at the time when procedures of qualitative and quantitative analyses, identification and estimation of bile acids began to be utilized in practice 20 years ago. Since then, the metabolism of bile acids has been clarified in individuals under normal as well as pathological circumstances. Because of a functionally and morphological close relation between hepatic epithelial cells and the metabolism of bile acids, the pathophysiological aspects of the disturbed metabolism of bile acids in parenchymatous inflammatory diseases of the liver, fatty liver, cholestasis and primary hepatocellular carcinoma are attracting considerable attention. First applied to the measurement of human bile acids in blood plasma in 1965, gas-liquid chromatography has been utilized as a standard method in medical practice. Recently, radioimmunoassay and enzyme linked radioimmunoassay have been utilized. This progress in the estimation of bile acids has awoken our interest in the pathophysiological significance of bile acids in liver diseases. The author reviewed the information on bile acid metabolism in liver diseases which has been reported up to the present.
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PMID:Clinical aspects of bile acid metabolism in liver diseases. 628 49

Many hepatic lesions, ranging from subcellular alterations to malignant tumors, have been attributed to the use of anabolic steroids (AS) and contraceptive steroids (CS). These lesions that have been attributed to AS and CS are discussed with focus on the following: biochemical changes; subcellular alterations; intrahepatic cholestasis; vascular complications (sinusoidal dilatation, peliosis hepatitis, Budd-Chiari syndrome); hyperplasia and neoplasia (diffuse hyperplasia, nodular transformation, focal nodular hyperplasia, hepatocellular adenoma, hepatocellular carcinoma, and miscellaneous malignant tumors); and miscellaneous effects (effects of preexisting liver disease, cholelithiasis, and pancreatitis). OCs have a number of physiologic effects on the liver. These include decreased bile flow, diminished secretion of organic anions, and decreased synthesis and secretion of bile acids. Retention of bromosulfophthalein has been noted with AS during late pregnancy and in the puerperium. It is well established that the CS can lead to elevations of serum ceruloplasmin and copper levels. Subcellular alterations have been reported in both humans and rats on AS or women on CS and involve multiple organelles of the several systems of the liver. Both AS and CS have been implicated in intrahepatic cholestasis. Jaundice usually develops after 2-5 months of therapy with AS or after 3 months of OC use. The lesions attributed to CS and AS can involve any of the systems of the liver. At times more than 1 system is affected simultaneously. Most of the steroid related lesions resemble similar ones caused by other etiologies. Some, such as peliosis hepatitis, are rarely related to other etiologies, but others can be termed steroid specific. A number of diseases associated with the CS or AS also occur in pregnancy. Acute fatty metamorphosis of pregnancy and the periportal hemorrhagic necrosis characteristic of eclampsia have not been reported in patients on CS. Spontaneous rupture of the liver during pregnancy has not been attributed to the CS.
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PMID:Hepatic lesions caused by anabolic and contraceptive steroids. 628 45


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