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)

Hepatocellular diseases, such as hepatitis, cirrhosis, or hepatic neoplasm, are associated with impaired metabolism of certain drugs, including aminopyrine, whereas cholestasis produced variable effects on aminopyrine metabolism. Reasons for the variable effects of cholestasis on hepatic aminopyrine metabolism were sought by performing in patients with hyperbilirubinemia the aminopyrine breath test (ABT), which consists of measurements of 14CO2 in breath 2 hr after oral administration of [14C]aminopyrine. Hyperbilirubinemia (total serum bilirubin less than 1.2 mg/100 ml) in these patients was due to hepatocellular disease or cholestasis. The ABT, defined as the percentage of the administered dose of 14C excreted in breath for 2 hr after [14C]aminopyrine administration, was 6.2 +/- 0.8% (mean +/- SD) in 107 control patients with normal total serum bilirubin. The ABT was severely abnormal (less than 3.1%) in 54 of 77 hyperbilirubinemic patients (70%) with hepatocellular disease and normal (greater than 4.5%) in only 5 of these patients (6%). In contrast, the ABT was severely abnormal in only 1 of 40 cases of cholestasis with hyperbilirubinemia and normal in 70% of these patients. Thus, aminopyrine metabolism is normal in most cases of hyperbilirubinemia due to cholestasis and is only rarely severely abnormal in these patients. On the other hand, severe abnormality in aminopyrine metabolism occurs in the majority of patients with hyperbilirubinemia due to hepatocellular disease. It therefore appears that the ABT may be useful in hyperbilirubinemia to distinguish patients with hyperbilirubinemia due to cholestasis form most patients with hyperbilirubinemia due to hepatocellular disease.
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PMID:Aminopyrine metabolism in the presence of hyperbilirubinemia due to cholestasis or hepatocellular disease. Combined use of laboratory tests to study disease-induced alterations in drug disposition. 87 Feb 74

A patient with alcoholic cirrhosis who developed fatal ischemic hepatitis induced by hemorrhagic shock, due to the spontaneous rupture of a hepatocellular carcinoma, is reported. This was the first manifestation of the hepatic neoplasm. To our knowledge, this is the first case report of ischemic hepatitis of this origin.
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PMID:Ischemic hepatitis secondary to the spontaneous rupture of a hepatocellular carcinoma in a patient with cirrhosis. 874 Aug 50

Aberrant promoter methylation is a fundamental mechanism of inactivation of tumor suppressor genes in cancer. The Ras association domain family 1A gene (RASSF1A) is frequently epigenetically silenced in several types of human solid tumors. In this study, we have investigated the expression and methylation status of the RASSF1A gene in hepatocellular carcinoma (HCC). In two HCC cell lines (HepG2 and Hep3B) RASSF1A was inactivated and treatment of these cell lines with a DNA methylation inhibitor reactivated the transcription of RASSF1A. The methylation status of the RASSF1A promoter region was analysed in 26 primary liver tissues including HCC, hepatocellular adenoma (HCA), liver fibrosis, hepatocirrhosis. Out of 15, 14 (93%) HCC were methylated at the RASSF1A CpG island and hypermethylation was independent of hepatitis virus infection. RASSF1A was also methylated in two out of two fibrosis and in three (75%) out of four cirrhosis; the latter carries an increased risk of developing HCC. Additionally, we analysed the methylation status of p16(INK4a) and other cancer-related genes in the same liver tumors. Aberrant methylation in the HCC samples was detected in 71% of samples for p16, 25% for TIMP3, 17% for PTEN, 13% for CDH1, and 7% for RARbeta2. In conclusion, our results demonstrate that RASSF1A and p16(INK4a) inactivation by methylation are frequent events in hepatocellular carcinoma, but not in HCA, which is in contrast to HCC without cirrhosis, viral hepatitis, storage diseases, or genetic background. Therefore, this study gives additional evidence against a progression of adenoma to carcinoma in the liver. Thus, RASSF1A hypermethylation could be useful as a marker of malignancy and to distinguish between the distinct forms of highly differentiated liver neoplasm.
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PMID:Frequent epigenetic inactivation of the RASSF1A gene in hepatocellular carcinoma. 1266 Aug 22

Hepatocellular carcinoma with osteoclast-like giant cells is extremely rare, and only six cases have been previously reported. Its histogenesis is at the moment controversial. The authors report a case of hepatocellular carcinoma with osteoclast-like giant cells found in a 74-year-old woman. The patient came with a dull pain in the right upper abdominal quadrants due to a liver neoplasm described at CT scan. A wedge resection of the fifth hepatic segment with appendectomy, omentectomy, and debulking of the major peritoneal implants was performed. Histologically, the diagnosis of hepatocellular carcinoma with high grade differentiation associated with giant osteoclast-like cells was done without any evidence of hepatitis or cirrhosis in the surrounding hepatic parenchyma. Immunohistochemistry was positive for CD10 and CD68 and in situ hybridization revealed the expression of receptor activator of nuclear factor-kappa B (RANK) in the giant cells and receptor activator of nuclear factor-kappa B ligand (RANKL) in the tumor cells.
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PMID:Hepatocellular carcinoma with osteoclast-like giant cells: report of the seventh case in the literature. 2579 39