Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sublobular nodules of hepatocytes free of iron or exhibiting much less iron than the surrounding parenchyma, referred to in this study as iron-free-foci, are frequently found in the livers of patients with genetic hemochromatosis complicated by hepatocellular carcinoma. To test the hypothesis that such nodules are preneoplastic lesions, iron-free foci were sought in the initial liver biopsy specimens of 185 patients with untreated and uncomplicated genetic hemochromatosis. Iron-free foci were found in 14 (7.6%) patients, all men, aged from 38 to 76 yr, with heavy iron overload and with fibrosis or cirrhosis. Twelve patients with iron-free foci were followed for 0.9 to 15 yr (7 +/- 6 yr). In six (50%), HCC developed, compared with 2 (8%) from a control group consisting of 24 patients without IFF matched according to age, sex, degree of fibrosis, liver iron amount and follow-up duration. The mean number of iron-free foci per iron-free foci-positive specimen was 3.2 +/- 2.1. Ten patients had dysplastic aspects in their iron-free foci, and four had intrahepatocytic iron-positive inclusions at the periphery of iron-free foci. Proliferative cell nuclear antigen was positive in 75% of iron-free foci and in 24% +/- 21% of hepatocyte nuclei in iron-free foci. This study clearly demonstrates that iron-free foci are proliferative lesions and strongly suggests that such nodules are preneoplastic foci. Therefore the finding of IFF in the initial liver biopsy specimen from a patient with genetic hemochromatosis should lead to regular screening for hepatocellular carcinoma.
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PMID:Preneoplastic significance of hepatic iron-free foci in genetic hemochromatosis: a study of 185 patients. 790 16

To identify the preneoplastic lesions of hepatocellular carcinoma and the fine structure of preneoplastic hepatocytes, we studied proliferative conditions in cirrhosis of the liver. In all, 46 foci of cellular alteration (FCA), three regions of adenomatous hyperplasia (ADH), and 21 small hepatocellular carcinomas (sHCC) were studied by published criteria for sHCC and by the proliferative activity of the lesions as examined with monoclonal antibodies against DNA polymerase alpha and proliferating cell nuclear antigen. The four patients with FCA composed of basophilic hepatocytes were classified by the criteria as having sHCC; cells had features similar to those of sHCC. Two of these four patients with FCA were found to have HCC several years later. The number of hepatocytes stained for proliferating cell nuclear antigen was 72 and 81 per 1000 hepatocyte nuclei in the two patients who developed HCC. In one of the three patients with ADH, a sHCC was found 1 year later, and dysplastic hepatocytes from the region of ADH in this patient had features similar to those of HCC cells by light and electron microscopy. In this patient, the number of hepatocytes stained for DNA polymerase alpha was 452 per 1000 nuclei. Therefore, FCA and ADH might be preneoplastic lesions of sHCC in cirrhosis of the liver. Preneoplastic hepatocytes seem to be small cells with basophilic cytoplasm, with a large nucleus to cytoplasm ratio, finely indented nuclei with a smaller amount of condensed chromatin than normal, and poorly to moderately developed organelles.
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PMID:Detection of the preneoplastic lesions of small hepatocellular carcinoma in cirrhotic livers. 790 90

In this paper we report the results we obtained after chemoembolization in 46 patients with HCC in cirrhosis. Chemoembolization is performed by introducing, through an angiographic catheter placed after the origin of the gastroduodenal artery, 20 mg of Doxorubicin Chlorhydrate mixed with 20 ml of Lipiodol and with 10 ml of contrast agent followed by embolization with Spongostan. Chemoembolization results were assessed comparing site, size and local spread of the tumor, hepatic compromission (according to Child's classification) and number of chemoembolization maneuvers with survival in each patient. Overall survival rates are 95.7% at 6 months, 88.5% at 12 months, 60% at 18 months, 36.4% at 24 and 31.8% at 30 months. The best responses were obtained with lesions smaller than 5 cm (100% survival at 6 months, 91.7% at 12 months, 71.4% at 18 and 42.8% at 24 months). Other factors favoring good treatment response were a single lesion (92.9% at 6 months, 91.7% at 12 months, 71.4% at 18 and 42.8% at 24 months), at least 3 cycles of chemoembolization (100% at 6 months, 90% at 12 months, 85.7% at 18 and 42.8% at 24 months) and a low degree of hepatic compromission (Child A and B rather than Child C; in the latter group the survival rates were 75% a 6 months and 0% at 12 months). In conclusion, chemoembolization proves to be the treatment of choice in the HCC patients who cannot undergo surgery.
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PMID:[Survival in 46 patients with hepatocarcinoma treated by chemoembolization]. 793 27

Clinically, acute hepatitis C is an asymptomatic disease in up to 90% of cases. Transaminases fluctuate characteristically. Anti-HCV (RIBA-II) and HCV-RNA (PCR) are diagnostic early in the course of the disease. The risk of chronification is high, exceeding 50% of cases, irrespective of disease transmission (parenterally or sporadic). Alpha-interferon is applicated in pilot-studies to reduce the risk of chronification, with varying results. Chronic hepatitis C is an insidious disease. Again, most cases are asymptomatic. Bilirubin is normal. GPT-activity tends to fluctuate during the course. Anti-HCV and HCV-RNA can be detected in serum. About 20% of cases progress to cirrhosis (and HCC) after a long-lasting disease (20 to 30 years after infection). Alpha-Interferon therapy is successful in about 25% of patients.
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PMID:[Hepatitis C: clinical aspects, course and therapy]. 793 55

Viral causes of acute or chronic hepatitis are the hepatitis A virus [HAV], the hepatitis B virus [HBV], the hepatitis C virus [HCV], the hepatitis delta virus [HDV], and the hepatitis E virus [HEV]. These viruses haven been characterized in great detail and can be detected by specific and sensitive serological or molecular assays. While HAV and HEV cause only acute hepatitis, infection with HBV, HCV or HDV frequently takes a chronic course. With time chronic viral hepatitis can progress to liver cirrhosis and its clinical sequelae as well as to hepatocellular carcinoma [HCC]. Apart from prophylactic measures aimed at the prevention of these viral infections, for those chronically infected natural or recombinant alpha-interferon may be a therapeutic option with the potential to prevent the development of liver cirrhosis and HCC.
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PMID:[Viral hepatitis A to E--diagnosis, clinical aspects and therapy]. 794 Apr 9

We studied 21 cases of hepatocellular carcinoma with liver cirrhosis to investigate the influence of liver function on stereotactic microwave tissue coagulation therapy. The cases were divided into three groups by the operation. The first group received only hepatectomy, the second hepatectomy and coagulation therapy for any remaining tumor, and the third group received only coagulation therapy. In group one, the average value of ICG R15 increased from 26.6% to 33.8%. In group 2, the average value of ICG R15 increased from 18.9% to 32.1%. And in group 3, the initial ICG R15 was 26.1%; after four weeks, the ICG test was 25.4%. These results showed that coagulation therapy alone had less influence on hepatic function. We propose that the coagulation therapy should be selected for cases of HCC with liver cirrhosis which have a poor liver function.
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PMID:[Influence of liver function on stereotactic microwave tissue coagulation therapy for hepatocellular carcinoma]. 794 43

Herein, we present the diagnostic efficacy of various imaging diagnostic techniques for small liver cancer(HCC) and HCC occurrence predictability by ultrasonography during the follow-up period of chronic liver diseases. During the recent 4 years, 78 nodules of small liver cancer measuring 2 cm or less in diameter were found in 50 patients with liver cirrhosis. In this study, the tumor size was divided into 2 groups; 1.5 cm or less in maximal diameter (group A) and 1.6 to 2 cm (group B). The tumor detectability of ultrasound (US), computed tomography (CT), magnetic resonance imaging (MRI), angiography and lipiodol CT in group A vs group B was 96% vs 97%, 68% vs 88%, 65% vs 94%, 12% vs 78% and 38% vs 89%, respectively. Therefore, angiography and lipiodol CT were not effective for detection of small HCCs smaller than 1.5 cm. Recently, helical CT scanning has been induced in the diagnosis of HCCs and the tumor detectability was enhanced to 82% even in group A. Additionally, helical-dynamic CT has some advantages in evaluating vascularity, especially arterial feeding which is a specific finding to HCCs. In comparison with contrast-enhanced US using CO2-microbubbles, helical-dynamic CT had equivalent accuracy in diagnosing hypervascular tumors, while hypovascular masses were observed in about 30% of group A. With respect to prediction of HCC occurrence in cirrhotic liver, sonographic evaluation of liver parenchyma seemed to be an important parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Integrated diagnosis of small hepatocellular carcinoma with imaging diagnosis]. 799 12

The western HCC registry comprised data from 322 patients who underwent hepatic resection for HCC over a 50-year period. The majority of patients had lesions > 4 cm and were symptomatic at presentation. Lesions were mostly unicentric. Cirrhosis was not a prevalent problem, unlike the East. In the most recent decade, 1980-1989, we noted a significant decrease in operative mortality from 19% to 10% overall, and 15% to 4% in the noncirrhotic group. We identified four variables that resulted in poorer postresectional outcome: cirrhosis, regional nodal disease, multicentric disease, and tumor-free resectional margin < 1 cm. Although these factors are associated with a poorer outcome after resection, whether they should serve as contraindications to surgery should be determined by individual surgeons, taking into account the patient's overall status, concomitant risk factors, and treatment objectives.
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PMID:Hepatoma registry of the Western world. Repeat Hepatic Resection Registry. 803 52

The expression of intercellular adhesion molecule-1 (ICAM-1) was investigated in frozen sections obtained from 40 resected liver specimens of patients with hepatocellular carcinoma using immunoperoxidase techniques and immunoelectron microscopy. ICAM-1 was expressed in 80% of the HCC specimens on the membrane of cancer cells. In noncancerous regions characterized by cirrhosis in 28 cases and chronic hepatitis in 12 cases, ICAM-1 was rarely expressed on hepatocytes but was expressed mainly on the endothelium of portal vessels and sinusoidal lining cells. These results suggest that expression of ICAM-1 in hepatocellular carcinoma may be induced by malignant transformation of hepatocytes.
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PMID:Expression of intercellular adhesion molecule-1 in hepatocellular carcinoma. 810 90

To examine the significance of mutation of the p53 tumour suppressor gene in the development of human hepatocellular carcinoma in a high-prevalence area for hepatitis B viral infection but a low-exposure area for aflatoxin B1, the spectrum of p53 gene mutations was examined in 21 tumour samples from Hong Kong Chinese patients, all of whom were HBsAg positive. DNA sequencing covering exons 5 to 9 of the p53 gene and Hae III restriction enzyme digestion for preliminary assessment of mutation at codon 249 were performed. Immunohistochemical staining with anti-p53 monoclonal antibodies was done on both tumour and nontumour liver tissues. Six tumours (28.6%) showed a p53 mutation and all were point mutations. Of the six point mutations, two (9.5%) were at codon 249 and both were G to T transversions (AGG-->ATG and AGG-->AGT transversions). The remaining point mutations were transversions scattered at codon 172 (exon 5), 214 (exon 6), 273 (exon 8) and 330 (exon 9). Mutated p53 protein was detected in five of these six cases with demonstrable point mutations by DNA sequencing, in contrast to none detected in all of the 15 cases without demonstrable point mutations. The presence of p53 mutations, including those at codon 249, did not show a significant association with tumour size, sex, age, tumour invasiveness in terms of liver invasion, microsatellites and venous permeation, cirrhosis and encapsulation, but tumours with low cellular differentiation tended to have a higher incidence (71%) of point mutations than those with high cellular differentiation (8%). In conclusion, both the overall p53 mutation rate and that a codon 249 in HCC in Hong Kong Chinese are lower than those reported in tumours from China and sub-Saharan Africa. The low mutation rate at codon 249 is compatible with a low aflatoxin exposure. A special type of p53 mutation has not been found to be associated with hepatitis B viral infection. Mutations of p53 gene tends to occur in tumours with low cellular differentiation, suggesting a late occurrence in the event of tumour progression.
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PMID:p53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chinese. 810 45


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