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)

To evaluate the diagnostic significance of tenascin, the extracellular matrix glycoprotein in chronic liver disease, serum tenascin levels were measured by a newly developed ELISA in 21 patients with chronic persistent hepatitis, in 55 with chronic active hepatitis, in 59 with liver cirrhosis, in 31 with hepatocellular carcinoma, in 26 with acute hepatitis and in 66 healthy subjects. The serum tenascin level was significantly elevated in the patients with chronic active hepatitis, liver cirrhosis, hepatocellular carcinoma, and acute hepatitis when compared with the healthy subjects (p < 0.001). The serum tenascin level also increased with increasing severity of chronic liver diseases. A significant correlation was observed between the serum tenascin levels and serum levels of various extracellular matrix proteins such as type III procollagen N-aminoterminal peptide (PIIIP), laminin and the 7S domain of type IV collagen (p < 0.001). A strong positive correlation was observed between the serum tenascin levels and histologic findings, particularly in the degree of hepatic fibrosis. This is the first report documenting serum tenascin level increases in patients with various chronic liver diseases. The measurement of the serum tenascin levels may provide additional information relevant to the study of connective tissue.
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PMID:Serum tenascin levels in chronic liver disease. 752 6

The serum levels of beta 1 integrin (microgram/ml) were significantly higher in the patients with chronic persistent hepatitis (2.59 +/- 0.04), chronic active hepatitis (3.45 +/- 0.13), cirrhosis (4.77 +/- 0.30) and hepatocellular carcinoma (4.71 +/- 0.49) than in normal subjects (2.11 +/- 0.08). Serum levels of beta 3 integrin (microgram/ml) were significantly higher in the patients with chronic active hepatitis (10.48 +/- 1.22), liver cirrhosis (13.55 +/- 1.54) and hepatocellular carcinoma (14.1 +/- 1.77) when compared with normal subjects (5.51 +/- 0.52). A positive correlation was found between serum levels of beta 1 and beta 3 integrins (p < 0.001). A strong positive correlation was observed between serum levels of beta 1 integrin and histologic features, particularly in the degree of hepatic fibrosis, while no correlation was found between serum levels of beta 3 integrin and hepatic fibrosis. Immunohistochemical studies revealed that the beta 1 integrin was present on the plasma membranes of hepatocytes and sinusoidal lining cells in the normal liver, and was increased in fibrotic areas, and on the plasma membranes of hepatocytes and sinusoidal lining cells of the chronic liver disease. However, no positive staining for beta 3 integrin was observed in fibrotic area. The serum level of beta 1 integrin in patients with chronic liver diseases may therefore be a useful marker of hepatic fibrosis.
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PMID:Serum levels of integrins in chronic liver diseases. 753 15

In Japanese blood donors, positivity for antibodies to hepatitis C virus (HCV) ranges from 0.2% in subjects under 20 to 3.9% in those over 50 years. It is estimated that at least 2.3 million Japanese have contracted HCV infection through contaminated blood. HCV carrier state was confirmed by polymerase chain reaction for HCV-RNA in subjects positive for antibodies to more than one viral protein (70% of cases). Subjects positive for core antibody alone, however, were found to be HCV-RNA negative with normal liver function, and are considered to have only a past history of HCV infection (30% of cases). Acute hepatitis C progresses to chronic infection in about 90% of cases. In comparison with hepatitis B, chronic hepatitis C leads more frequently to cirrhosis and liver cancer, and rarely remits spontaneously. In typical HCV infection, aminotransferase activities fluctuate markedly in the early stages, then become relatively stable for 10 years or more, with chronic persistent hepatitis shown by histological examination. Thereafter, aminotransferase activities may change dramatically, with progression to chronic active hepatitis and rapid development of cirrhosis and hepatocellular carcinoma. On average, it takes about 30 years for chronic hepatitis C to progress from initial infection to cirrhosis and cancer, but the disease progresses much more rapidly in elderly patients.
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PMID:Epidemiology and long term prognosis of hepatitis C virus infection in Japan. 768 12

Tumor necrosis factor alpha (TNF alpha) was measured with an enzyme-linked immunosorbent assay. TNF alpha levels in peripheral blood of patients with twenty-one cases of chronic persistent hepatitis (7.3 +/- 9.5 micrograms/L), fourty-two cases of chronic active hepatitis (15.4 +/- 31.1 micrograms/L), one hundred and six cases of liver cirrhosis (11.1 +/- 17.7 micrograms/L) and one hundred and ten cases of parimary hepatocellular carcinoma (10.9 +/- 13.3 micrograms/L) was significantly increased when compared with normal controls (4.3 +/- 2.9 micrograms/L) (P < 0.01). There was significant correlation between tumor necrosis factor alpha levels and ALT elevation and also between TNF alpha levels and bilirubin contents more than 100 mumol/L in chronic hepatitis patients. Tumor necrosis factor alpha levels was also significantly in HBV concomitant with HCV and/or HDV infection than in HBV infection alone. There was no correlation in tumor necrosis factor alpha levels and AFP concentrations. These findings show that tumor necrosis factor participates in the activity process of liver disease.
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PMID:[Tumor necrosis factor alpha levels in patients with chronic liver diseases and its relationship to pathogenesis]. 771 14

Several reports have been recently published concerning the identification of HBV variants due to rearrangements of the preS1/preS2 or core regions of the viral genome. To evaluate the frequency of the natural occurrence of such variants and whether the heterogeneity of these genomic regions correlates with the severity of the liver disease, we have examined the preS1/preS2 region and the entire core gene sequences of HBV DNA isolated from sera of 30 chronic HBV carriers, 7 with chronic persistent hepatitis, 10 with chronic active hepatitis, 7 with cirrhosis, and 6 with hepatocellular carcinoma. We found no significant rearrangement in any of the preS1 regions examined, while genomic modifications precluding the preS2 protein production were detected in 4 cases, 2 with cirrhosis and 2 with hepatocellular carcinoma. The analysis of the core gene showed the presence of various numbers of missense mutations in the core region of most cases, independent of the grade of liver disease. Moreover, in contrast with previous reports, neither mutation cluster region nor deletion was observed. On the contrary, HBV strains with the precore mutation at nucleotide position 1896, effecting the rise of HBeAg-defective viruses, were found in 26 of the 30 cases examined. In conclusion, our data show that the precore mutant is the only HBV genomic variant commonly selected during a chronic infection. Other HBV variants, due to genomic rearrangements outside the precore region, may exist and influence the outcome of the infection and the course of the liver disease, but the emergence of each of these variants seems to be an unusual and probably casual event.
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PMID:PreS and core gene heterogeneity in hepatitis B virus (HBV) genomes isolated from patients with long-lasting HBV chronic infection. 774 38

In the search for parameters that can indicate changes in the behaviour of liver tissue from normal to chronic to neoplastic disease, DNA content by FCM (ploidy and percent of 4N cells) and morphobiological characteristics were investigated in fresh liver specimens of 16 patients with normal liver, 21 with persistent hepatitis (CPH), 23 with chronic active hepatitis (CAH), 17 with cirrhosis, and 13 with hepatocellular carcinoma (HCC). Aneuploidy was mostly found in HCC specimens (54%), whereas the percentage of 4N peak decreased in chronic hepatitis and cirrhosis patients but increased to 11.09% in HCC samples (r = -0.02; p = 0.05). Finally, the binuclearity rate decreased gradually from normal to flogistic to HCC specimens. The 4N peak and the binuclearity rate were closely correlated in non-HCC (p = 0.0006, by T-test) but not in HCC samples. Only DNA ploidy and the binuclearity rate have been confirmed as being significantly and independently related to the histology of liver tissue by multivariate regression analysis.
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PMID:Flow cytometry DNA content and morphobiological characteristics in chronic and neoplastic human liver disease. 779 88

We investigated the serum level of macrophage colony stimulating factor in acute and chronic liver disease. Levels of macrophage colony stimulating factor (mean +/- SD, ng/ml) were significantly higher in acute hepatitis (5.67 +/- 1.01, p < 0.01) and chronic active hepatitis (3.34 +/- 1.19, p < 0.01) than in healthy volunteers (1.90 +/- 0.25), asymptomatic hepatitis B virus carriers (1.98 +/- 0.40), and chronic persistent hepatitis (2.34 +/- 0.43). Levels of macrophage colony stimulating factor showed a highly significant correlation with the serum alanine aminotransferase levels in acute hepatitis (p < 0.01, rs = 0.903) and in chronic active hepatis (p < 0.01, rs = 0.672). Levels of macrophage colony stimulating factor in patients with cirrhosis (cirrhosis; 3.11 +/- 0.93 and hepatocellular carcinoma; 3.30 +/- 0.74) were significantly higher than in patients with chronic persistent hepatitis although the alanine aminotransferase levels were not significantly different. In cirrhosis, levels of macrophage colony stimulating factor correlated positively with the serum alanine aminotransferase levels (p < 0.05), total bilirubin levels (p < 0.05), and indocyanine green clearance (p < 0.05). An immunohistochemical study showed an increased number of macrophage colony stimulating factor positive mononuclear cells in portal areas in acute hepatitis. Our findings suggest that; (a) the serum levels of macrophage colony stimulating factor represent ongoing hepatocellular necrosis in acute and chronic liver disease, (b) the source of the increase in the serum macrophage colony stimulating factor levels in hepatic inflammation may be, in part, its production by infiltrating mononuclear cells in the liver, and (c) cirrhosis also causes elevated serum levels of macrophage colony stimulating factor.
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PMID:Serum levels of macrophage colony stimulating factor (M-CSF) in liver disease. 781 98

The spectrum of histological changes in needle biopsies of the liver tissue was analysed in 43 patients with chronic liver disease who were positive for hepatitis B surface antigen (HBsAg) in their sera. Majority of the patients were around 40 years and there was a male predominance. According to histopathological pattern, there were 18 (41.8%) cases of chronic active hepatitis, 16 (37.2%) cases of inactive cirrhosis, 3 (6.9%) cases of chronic persistent hepatitis and 2 (4.7%) cases of chronic lobular hepatitis and hepatoma each. Two (4.7%) cases could not be exactly categorised into any particular histological entity. The inflammation, hepatic cell necrosis and fibrosis were more marked in cases of chronic active hepatitis without past history of jaundice. Micronodular cirrhosis was the most common histological pattern in the study. Shikata orcein stain for detection of HBsAg in the hepatocytes was positive in 8 (18.6%) cases only.
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PMID:Hepatic histology in chronic liver disease in hepatitis B surface antigen positive cases. 782 48

The major cause of liver diseases world-wide are the infectious hepatitis A-E which are due for different viruses. Most of the cases are clinically asymptomatic and without jaundice with a high rate of cure. The diagnosis and the differentiation of the various clinical syndromes are based mainly on serological markers of the involved antigen-antibody-systems. For insurance purposes the chronic hepatitis B, C and D are of great importance. Where chronic persistent hepatitis has a nearly normal life expectancy, chronic active hepatitis which may develop into cirrhosis and/or hepatocellular carcinoma has an increased mortality.
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PMID:[Viral hepatitis. Insurance medicine observations]. 782 66

Hepatitis C virus genotype and the amounts of circulating HCV RNA are the most important factors in determining the efficacy of interferon therapy for chronic hepatitis C. To clarify the correlation of these two factors to the progression of liver disease, we classified 148 Japanese patients with type C chronic liver disease into genotypes and also measured their HCV RNA titers (logarithmic transformed copy number/ml serum) by competitive reverse transcription-polymerase chain reaction. We found type II in 23 (76.7%) of 30 patients with chronic persistent hepatitis, 34 (79.1%) of 43 with chronic active hepatitis, 29 (72.5%) of 40 with cirrhosis and 30 (85.7%) of 35 with hepatocellular carcinoma. Thus, there was no significant difference in the prevalence of type II among the various stages of chronic liver disease. We also found the RNA titer to be significantly higher in patients with chronic active hepatitis (8.0 +/- 0.8) than in those with chronic persistent hepatitis (7.0 +/- 1.0, p < 0.001), and also those with cirrhosis (7.6 +/- 0.8, p < 0.05) or hepatocellular carcinoma (7.7 +/- 0.8, p < 0.05). When the titers were compared among genotypes, there was no significant difference between type II and III at any stage (type II vs. type III: chronic persistent hepatitis, 7.2 +/- 1.0 vs. 6.7 +/- 0.8; chronic active hepatitis, 8.1 +/- 0.7 vs. 7.8 +/- 1.0; cirrhosis, 7.7 +/- 0.8 vs. 7.8 +/- 0.7; hepatocellular carcinoma, 7.7 +/- 0.8 vs. 7.8 +/- 0.5). In conclusion, although genotype affects interferon therapy efficacy, it seems to have little influence on serum RNA levels and the progression of type C chronic liver disease.
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PMID:Hepatitis C virus genotype and RNA titer in the progression of type C chronic liver disease. 783 20


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