Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10 of a series of 108 patients with alcoholic liver disease presented with cholestasis associated with non-cirrhotic alcoholic liver disease and without evidence of extrahepatic biliary obstruction. In 7 patients liver histology and the associated conditions presenting as cholestasis were heterogeneous. However, in 3 patients who had been drinking excessively before cholestatic jaundice developed, cholestasis was a major feature of liver histology. The term acute alcoholic cholestasis is suggested for this apparently distinct syndrome of cholestatic jaundice in the absence of hepatitis.
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PMID:Cholestasis in acute alcoholic liver disease. 7 24

The infant with elevated direct-reacting bilirubin levels requires an early specific diagnosis to identify those who would require early surgical intervention and those in whom the bilirubin levels will eventually return to normal. This study compares the accuracy of three tests: the serum lipoprotein-X (LP-X), the I131 rose bengal (IRB) excretion and the serum alpha-fetoprotein (AFP) in making a specific diagnosis in 15 patients. When used individually the accuracy of the tests varies from 56-100%. The LP-X and IRB excretion are more specific and when in agreement are 100% acurate in the diagnosis of the neonatal hepatitis syndrome (NHS) or extrahepatic biliary obstruction (EHBO). This study suggests that both the LP-X and IRB excretion should be used in the investigation of the infant with conjugated hyperbilirubinemia.
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PMID:Lipoprotein-X and other tests in the diagnosis of obstructive jaundice in the infant. 8 96

Quantitative determination of the abnormal plasma lipoprotein of cholestasis LP-X has been performed in 81 LP-X positive patients with different liver disorders. Great variations in the plasma concentration of LP-X were demonstrated both in the 45 patients with intrahepatic cholestasis (acute hepatitis, toxic hepatitis, primary biliary cirrhosis and cholangitis) and in the 36 patients with extrahepatic cholestasis (extrahepatic biliary obstruction by tumours and choledocholithiasis). The plasma concentratkons of LP-X in the patients with extrahepatic cholestasis (median 158 mg/100 ml) were significantly (psmaller than 0.001) higher than in the patients with intraphepatic cholestasis (median 25 mg/100 ml) was exceeded by 42% of the patients with extrahepatic biliary obstruction, and 33% of the patients with extrahepatic biliary obstruction, had LP-X LEVELS ABOVE 400 MG/100ML. The plasma concentration of LP-X was significantly correlated to the plasma activity of alkaline phosphatases and serum bilirubin, but seemed to be superior to these two parameters in the differentiation between intrahepatic and extrahepatic cholestasis. Plasma levels of LP-X above 400 mg/100 ml are highly indicative of extrahepatic biliary obstruction.
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PMID:Quantitative determination of the abnormal lipoprotein of cholestasis, LP-X, in liver disease. 16 86

Extrahepatic and intrahepatic biliary obstruction of different etiology were studied in 62 patients, who were investigated for the presence of lipoprotein X (Lp-X). It was found present in 19 of 20 cholestasis by lithiasis, in all three primary biliary cirrhosis patients, in 2 of 4 cirrhosis, in 5 of 13 hepatitis, in all three benign recurrent intrahepatic cholestasis and in 1 of 2 recurrent juandice of pregnancy. It was found in a Dubin Johnson. Lp-X disappeared in 4 patients within two weeks after relief of the obstruction. It was found in patients with cholestatic hepatitis during the first week of jaundice. It was found in the first 48 hours in three patients with cholestasis by lithiasis. Lp-X does not help in differential diagnosis between extrahepatic and intrahepatic biliary obstruction, but the time of its appearance could contribute to it in some cases. A word of caution is raised in indicating surgery in a cholestatic patient without the presence of Lp-X.
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PMID:LP-X in cholestasis. 17 23

During the 11 1/2 year period ending 13 months ago, 93 consecutive patients were treated with orthotopic liver transplantation. Fifty-six of the recipients were 18 years old or younger, and the other 37 were adults. The most common indications for operation were biliary atresia, primary hepatic malignant tumor, chronic aggressive hepatitis and alcoholic cirrhosis. There has been a gradual improvement in results throughout the period of study, although to a satisfactory level. Twenty-seven of the 93 patients survived for at least one year after liver replacement with a maximum of six years, and 16 are still alive after 13 to 71 months. The 11 late deaths after one to six years were caused by chronic rejection, biliary obstruction, recurrence of hepatoma, systemic infection or hepatitis of the homograft. Rejection of the liver as judged by classical histopathologic criteria played a surprisingly small role in the heavy over-all mortality, accounting for less than 10 per cent of the deaths. Technical or mechanical problems, especially those of biliary duct reconstruction, were a far greater cause of failure, as were systemic infections. Six of the 37 adult recipients had lethal cerebrovascular accidents during, or just after, operation. When abnormalities of liver function developed in the postoperative period, the nearly automatic diagnosis of homograft rejection, in retrospect, proved to have been wrong in most instances. Further development of liver transplantation depends upon two kinds of progress. There must be reduction of operative and early postoperative accidents and complications by more discriminating patient selection, purely technical improvement and better standardization of biliary duct reconstruction. The second area will be in sharpening the criteria for the differnetial diagnosis of postoperative hepatic malfunction, including the liberal use of transhepatic cholangiography and needle biopsy. Only then can better decisions be made about changes in medication or about the need for secondary corrective surgical procedures.
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PMID:Orthotopic liver transplantation in ninety-three patients. 17 41

Many reports have demonstrated an elevation of circulating carcinoembryonic antigen (CEA) in the majority of patients with alcoholic liver disease and, less frequently, in patients with nonalcoholic liver disease. Several explanations for this finding have been proposed, eg, increased production or release of CEA by the damaged liver, decreased hepatic metabolism, or diminished excretion of CEA of extrahepatic origin. In an attempt to clarify the mechanism of CEA elevation in liver disease, we have compared the CEA plasma level as measured by radioimmunoassay with CEA demonstrable in liver tissue by the indirect fluorescent antibody technique in 7 patients without significant changes in the liver biopsy specimen, 23 patients with alcoholic liver disease, and 16 patients with miscellaneous liver diseases such as acute or chronic nonalcoholic hepatitis or extrahepatic biliary obstruction. The mean CEA plasma level in patients with alcoholic liver disease was significantly higher than in patients with nonalcoholic liver disease (8.8 +/- 9.5 vs 2.7 +/- 2.5 ng/ml; P less than 0.02). In normal liver tissue, CEA was observed in the apical cytoplasm and along the luminal surface of bile duct epithelial cells, suggesting that under normal conditions CEA accumulates in and is excreted by bile ducts. In patients with alcoholic hepatitis and/or cirrhosis there was marked bile ductular proliferation and prominent cytoplasmic CEA-specific staining and both were associated with elevated CEA plasma levels in more than 80% of cases. In the group of miscellaneous liver diseases, bile ductule counts and CEA-specific staining did not correlate with CEA plasma levels. These observations suggest that proliferating bile ductules contribute to elevated plasma CEA in alcoholic patients.
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PMID:Carcinoembryonic antigen in normal and diseased liver tissue. 35 25

Computed tomography (CT) and radionuclide examinations of the liver and pancreas in 50 patients were compared retrospectively to evaluate their value as diagnostic tests. CT was superior to 75Se-selenomethionine in evaluating pancreatic disease. Both 99mTc-sulfur colloid scans and CT scans were sensitive detectors of liver masses; however, there were more false positive 99mTc-sulfur colloid scans (16% compared to 4%). CT was superior in detecting biliary obstruction and ascites, in assessing diseases that involved the liver extrinsically, and in evaluating the status of adjacent organs. 99mTc-sulfur colloid scans were more sensitive in detection of diffuse non-neoplastic liver diseases (cirrhosis, hepatitis, and cholangitis). Simultaneous interpretation of CT and radionuclide scans was often more helpful than independent interpretation, and the two techniques are therefore complementary.
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PMID:Retrospective comparison of radionuclide scans and computed tomography of the liver and pancreas. 40 38

Human hepatic bile contains a glycoprotein (biliary glycoprotein I, BGP I) which cross-reacts with the carcinoembryonic antigen (CEA). A radioimmunoassay for BGP I was developed. The interference of CEA or 'non-specific cross-reacting antigen' (NCA) in the assay was small. The serum levels of BGP I were determined in healthy subjects, in patients with hepato-biliary diseases and in patients with various infectious or inflammatory disorders. Healthy individuals, including pregnant women, had a serum BGP I concentration of about 0.5-1 mg/l. Diseases of the liver or biliary tract (e.g. hepatitis A or B, cytomegalovirus hepatitis, obstructive jaundice or primary biliary cirrhosis) were associated with elevated serum levels of BGP I, as opposed to infectious diseases not affecting the liver mostly showing values within the normal range. Raised levels of serum BGP I activity may reflect biliary obstruction as a result of interference with normal BGP I secretion to the bile.
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PMID:Elevated serum levels of a biliary glycoprotein (BGP I) in patients with liver or biliary tract disease. 47 33

Liver biopsy was done at the time of operation in 125 consecutive upper abdominal procedures to assess the incidence of unsuspected or undiagnosed hepatic abnormalities. Specifically excluded were hepatic lesions unexpectedly identified at laparotomy. Sixty-seven percent of the liver biopsy specimens were abnormal, the most frequent findings being fatty metamorphosis, cholestasis, triaditis, fibrosis, inflammatory infiltrate, cholangitis, cirrhosis, and hepatitis. The most frequent operation performed was cholecystectomy. In 63 patients with chronic cholecystitis, there was a 51% incidence of abnormal liver histology, while in nine patients with acute cholecystitis, the incidence was 78%. In 83% of all other operations, abnormal liver biopsy specimens were identified. Bile leakage, hemorrhage, and infection did not occur in this series, despite inclusion of patients with severe biliary obstruction, abnormal clotting factors, and intra-abdominal sepsis. New techniques of histochemical enzyme analysis and electron microscopy are expected to enhance the clinical correlation of occult hepatic lesions. We conclude that liver biopsy in a safe, informative adjunct to all upper abdominal procedures.
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PMID:'Routine' liver biopsy in upper abdominal surgery. 88 45

Phenobarbital was administered to a patient with extrahepatic biliary obstruction who was initially thought to have cholestatic hepatitis. On two occasions, administration of the drug was associated with a decrease of jaundice, pruritus, and serum bile acid levels. This strongly suggests that phenobarbital may be effective not only in intrahepatic cholestasis, as reported earlier, but also in extrahepatic obstruction, and therefore cannot be used for the differention of these two types of cholestasis.
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PMID:Effect of phenobarbital in a case of extrahepatic cholestasis. 111 59


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