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)

No doubt chronic liver diseases due to schistosomiasis and other causes as virus hepatitis are not uncommon among Egyptian patients. Besides, neoplastic changes in such patients are always seen. So, the aim of this work was to evaluate the estimation of hepatocytes DNA in chronic liver diseases as a diagnostic feature for early preneoplastic changes in different groups of patients. These groups included (a) chronic persistent hepatitis, (b) chronic active hepatitis, (c) liver cirrhosis due to schistosomiasis and other causes & (d) hepatocellular carcinoma. The results were evaluated histochemically and histopathologically. It was concluded that the cytophotometic evidence of hepatocytes DNA in chronic liver diseases is a promising mean in detecting early preneoplastic changes.
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PMID:Cytophotometric estimation of hepatocytes DNA in chronic liver diseases including schistosomiasis for detection of early preneoplastic changes. 784 29

The incidence of hepatocellular carcinoma (HCC) was prospectively studied in 251 chronic hepatitis patients, and was compared between the 127 cases of hepatitis B and 124 cases of hepatitis C. All patients were diagnosed by needle biopsy on entering the study, and the cases consisted of chronic persistent hepatitis (CPH), chronic active hepatitis (CAH)2a, and CAH2b (cirrhosis was not included). Of the cases of chronic hepatitis B, 5 cases of HCC (3.9%) were detected; among the chronic hepatitis C cases, 13 cases (10.4%) were detected. Thus, although the mean follow-up periods were in the same range, the incidence of hepatocellular carcinoma was 2.7 times higher in hepatitis C than in hepatitis B (chi 2 = 3.116, P < .05). Using the Kaplan-Meier method, the incidence of HCC was significantly higher in chronic hepatitis C (P = .0194, generalized Wilcoxon test). In hepatitis C, the incubation period until HCC was detected was shorter when the liver disease was more advanced. Such a tendency was not observed in hepatitis B. In the 13 cases of HCC occurring in chronic hepatitis C, noncirrhotic liver was seen in only 1 case (7.7%), whereas 2 of the 5 cases of HCC (40%) in chronic hepatitis B were noncirrhotic. The prevalence of hepatitis C virus (HCV) genotypes II and III was the same in the total followed cases and HCC cases.
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PMID:Incidence of hepatocellular carcinoma in chronic hepatitis B and C: a prospective study of 251 patients. 787 62

During the period 1982-1990, 544 patients with clinical evidence of liver disease were admitted to King Fahd University Hospital, Al-Khobar, Saudi Arabia. Besides routine laboratory and sonographic investigations, all were subjected to either a needle liver biopsy, laparoscopy or a laparotomy. The tissue diagnoses were as follows: liver cirrhosis 17.3%, periportal fibrosis 14.3%, metastatic cancer 12.9%, primary hepatoma (hepatocellular carcinoma: HCC) 12.1%, hepatic granuloma 11.2%, chronic active hepatitis 7.7%, chronic persistent hepatitis 2.2%, fatty liver 7.2%, hydatid liver disease 4.6% and others 2.8%. In 7.7% the histology was normal. These results will be discussed and compared with results reported in local and international literature.
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PMID:Pattern of chronic liver disease in the eastern province of Saudi Arabia. A hospital-based clinicopathological study. 789 3

To examine whether serum collagenase activity reflects the amount of hepatic collagenase in the fibrotic liver, we measured serum collagenase activity in 67 patients with chronic liver disease and in 26 healthy controls. Collagenase activity in serum was measured after reactivation by denaturing and dissociating the inhibitors with 3 M KSCN and 1 mM aminophenylmercuric acetate. Serum collagenase activity was 35% lower than control in chronic persistent hepatitis, 48% lower in chronic active hepatitis, 56% lower in liver cirrhosis and 68% lower in hepatocellular carcinoma. To interpret this finding of low serum collagenase activity, we measured serum concentration of TIMP (Tissue Inhibitor of Metallo-Proteinases). Serum TIMP concentration was increased as liver disease developed, and it was inversely correlated with serum collagenase activity. These results suggest that in this assay condition serum collagenase activity is influenced by TIMP, and thus may not reflect the amount of hepatic collagenase in patients with chronic liver disease.
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PMID:Serum collagenase activity in chronic liver diseases. 789 42

Expression of insulin-like growth factor II in two human hepatocellular carcinoma cell lines and in hepatitis B, cirrhosis and hepatocellular carcinoma in 419 cases were investigated, and its relationship with the expression of hepatitis B virus X gene was studied by means of immunohistochemical and electron microscopic techniques. The results demonstrated that hepatocellular carcinoma cells (SMMC 7721 and QGY 7703) in culture could express insulin-like growth factor II. Expression seemed to be regulated by cell density, which was suggested as the molecular basis of the contact inhibition of cell proliferation. In tissue sections, cells with high expression of insulin-like growth factor II were observed not only in hepatocellular carcinoma (93%) but also in 95% of the pericancerous liver tissues, 72% of cirrhotic livers, 64% of chronic active hepatitis and 37% of chronic persistent hepatitis. In most cases of hepatocellular carcinoma, insulin-like growth factor II was localized in the cytoplasm of the cancer cells. In the benign liver disorders, four types of cells that highly expressed insulin-like growth factor II were observed: (a) a kind of small liver cell we named the small polygonal liver cell; (b) multinuclear giant hepatocytes; (c) hepatocytes in most of hyperplastic and neoplastic nodules, small hepatocyte nodules and some of regenerative nodules; and (d) some proliferating ductular cells. Even more interestingly, insulin-like growth factor II expression was shown to be closely related to the expression of hepatitis B virus X gene product. We suggest that the activation of insulin-like growth factor II gene and its overexpression may be a crucial step in the processes of hepatitis B virus-associated hepatocarcinogenesis and that the X gene product may activate the insulin-like growth factor II gene through a transactivation mechanism. In addition, we studied the characteristics of small polygonal liver cells, and the roles they may play in the regeneration and carcinogenesis of hepatitis B virus-infected liver are discussed.
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PMID:Expression of insulin-like growth factor II in hepatitis B, cirrhosis and hepatocellular carcinoma: its relationship with hepatitis B virus antigen expression. 792 18

We examined the quasispecies of the hepatitis C virus genome in 28 patients with liver disease of varying severity. Nucleotide sequences of the hepatitis C virus genome spanning the region from the core to envelope were used to calculate the nucleotide diversity: 0.58% +/- 0.88% in 5 patients with acute hepatitis, 0.85% +/- 0.62% in 5 patients with chronic persistent hepatitis, 1.79% +/- 0.92% in 11 patients with chronic active hepatitis, 3.05% +/- 1.26% in 4 patients with cirrhosis and 2.71% +/- 1.47% in 3 patients with cirrhosis complicated by hepatocellular carcinoma. Thus the intrapatient variation in nucleotides increased significantly with severity of liver disease (p < 0.01), except in those cases of cirrhosis complicated by hepatocellular carcinoma. Multivariate analysis including the histology, duration of infection, age, sex, history of blood transfusion and serum level of ALT at diagnosis as variables showed that the histological finding was the strongest independent factor of the nucleotide diversity (p = 0.003). Serial analysis of the genome in three patients demonstrated that the intra-patient variation in nucleotides increased with the progression of liver disease. The magnitude of the intrapatient variation in nucleotides deduced from the observed changes in the patients was correlated with the mean serum levels of ALT. These findings suggest that the degree of diversity of HCV quasispecies is related to the progression of liver disease.
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PMID:Degree of diversity of hepatitis C virus quasispecies and progression of liver disease. 792 45

The proliferative activity of chronic liver diseases and hepatocellular carcinomas (HCCs) was studied by PCNA immunohistochemistry. Human liver tissues were obtained by surgical operation or needle biopsy, and PCNA was detected by immunohistochemistry. PCNA-labelling indices (PCNA-LIs) of methanol-fixed tissues corresponded with the incidence of S-phase cells previously reported, whereas paraformaldehyde-fixed tissues showed extremely high PCNA-LIs in all specimens. Therefore, methanol-fixed tissues were used for evaluation. The PCNA-LIs of the methanol-fixed tissues were: normal liver 0.78 +/- 0.38%, chronic persistent hepatitis 1.06 +/- 0.86%, chronic aggressive hepatitis 2A 1.01 +/- 0.50%, chronic aggressive hepatitis 2B 4.20 +/- 1.79%, inactive cirrhosis 0.81 +/- 0.49%, active cirrhosis 1.96 +/- 0.93%, HCC of Edmondson's type I 4.83 +/- 1.98%, type II 6.65 +/- 1.69%, and type III 38.7 +/- 30.6%. PCNA-positive cells showed little specific distribution; in periportal areas in chronic hepatitis, at the margins of pseudolobules in cirrhosis, and throughout the tumor in HCC. These findings indicated that proliferative activity increased during the progression of chronic hepatitis, but that it decreased at the stage of cirrhosis. In chronic liver diseases, the PCNA-LIs reflected hepatitis activity. HCC showed higher proliferative activity than liver cirrhosis, and the histological grade was correlated with the PCNA-LI.
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PMID:Evaluation of hepatic proliferative activity in chronic liver diseases and hepatocellular carcinomas by proliferating cell nuclear antigen (PCNA) immunohistochemical staining of methanol-fixed tissues. 795 55

This study was conducted to determine and compare serum trace metal levels in viral hepatitis-associated chronic liver disease. Of 98 patients aged 43 (+/- 13) [mean (+/- SD)] years, 83 (85%) were seropositive for hepatitis B surface antigen (HBsAg) and 15 (15%) were seropositive for anti-hepatitis C virus (HCV). Twenty-five patients had chronic persistent hepatitis, 32 chronic active hepatitis, 21 post-necrotic cirrhosis, and 20 hepatocellular carcinoma. Determination of fasting serum trace metal levels (zinc, copper, calcium, magnesium, and phosphorus) was performed after the patients had been on a 2-day diet containing 10-12 mg zinc/day. Compared to healthy volunteers (n = 30), serum zinc levels were significantly decreased in patients with chronic active hepatitis, cirrhosis, and hepatocellular carcinoma (P < or = 0.0001), and copper levels were significantly elevated only in patients with hepatocellular carcinoma (P < 0.0001). The overall serum levels of calcium, magnesium, and phosphorus were within normal ranges, and levels of calcium and magnesium correlated with serum zinc (P = 0.01-0.03). Serum zinc levels correlated with bilirubin, albumin, and cholesterol (P = 0.0004 < or = 0.0001), but not with daily urinary zinc excretion. Serum copper levels correlated with alkaline phosphatase and gamma-glutamyltransferase (P = 0.008-0.0001). These results suggested that changes in liver cell pathology compounded by functional impairment may alter the metabolism of trace metals, in particular, zinc and copper. The possible relationship of these changes to the pathogenesis of chronic liver disease is discussed.
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PMID:Serum trace metals in chronic viral hepatitis and hepatocellular carcinoma in Thailand. 800 May 10

Liver biopsy specimens of 65 cases of chronic viral hepatitis, including 29 cases of type B, 34 cases of type C, and two cases of non-A, non-B, non-C type, were immunohistochemically stained for proliferating cell nuclear antigen (PCNA) to evaluate the proliferative activity of hepatocytes. According to a histopathologic evaluation using the histology activity index (HAI) scoring system, chronic persistent hepatitis and chronic active hepatitis were clearly differentiated with no overlapping of the score. The labeling indices of PCNA of hepatocytes in chronic persistent hepatitis had a significant relationship with HAI scores (r = .54), suggestive of a contribution of lobular hepatocyte necrosis and/or portal inflammation to the regenerative rate of hepatocytes, but did not exceed 3.0%. On the other hand, 11 of 47 cases of chronic active hepatitis showed PCNA labeling indices higher than 3.5% without any significant relationship with the HAI scores. There was no significant difference, however, of distribution of HAI scores or PCNA labeling indices between hepatitis types B and C. Based on current concepts of the role of hepatocyte proliferation in the development of liver cirrhosis and hepatocellular carcinoma, the present results suggest that the high proliferative rate of hepatocytes subject to the persistent liver cell injury in chronic active hepatitis may be related to a reconstruction pattern of the liver in cases of progression to cirrhosis and development of hepatocellular carcinoma.
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PMID:Proliferative activity of hepatocytes in chronic viral hepatitis as revealed by immunohistochemistry for proliferating cell nuclear antigen. 810 May 54

Hepatitis C virus (HCV) frequently leads to chronic hepatitis, cirrhosis, and hepatocellular carcinoma, but the mechanism of liver injury is unknown. To determine whether replication of HCV is related to liver damage, we studied 17 liver biopsy specimens (six anti-HCV-positive chronic persistent hepatitis specimens, seven anti-HCV-positive chronic active hepatitis specimens, and four anti-HCV-negative controls) by reverse transcription followed by double polymerase chain reaction for the 5' nontranslated regions of the genomic and replicative strands of HCV. The histologic activity index as well as lymphoid aggregates in portal tracts, bile duct damage, and fatty change were assessed semiquantitatively. There was a statistically significant correlation between the presence of HCV RNA sequences in liver tissue and anti-HCV antibody in serum (P < .005). No correlation was detected between the histologic activity index or any individual histologic parameters and the presence of genomic or replicative strands of HCV. These findings suggest that a direct viropathic effect is less important than other mechanisms, such as the host immune response, in the pathogenesis of hepatocyte and bile duct injury in chronic hepatitis.
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PMID:Genomic and replicative hepatitis C virus RNA sequences and histologic activity in chronic hepatitis C. 811 15


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