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)

Serum gamma-glutamyl transpeptidase (gamma-GTP) was separated into four fractions by using wheat germ agglutinin (WGA) affinity electrophoresis. By two-dimensional analysis using gel filtration combining with affinity electrophoresis with WGA, anti-alpha 1-lipoprotein antiserum or anti-beta-lipoprotein antiserum, properties of each fraction were identified as a high molecular WGA affinity fraction (HM), a relatively high molecular beta-lipoprotein binding fraction (beta-LP), an intermediate molecular alpha-lipoprotein binding fraction (alpha-LP) and a low molecular fraction (LM). Quantitative alterations in each fraction of gamma-GTP in the serum of patients with various liver diseases and gall stones (GS) were also examined. In patients with hepatocellular carcinoma (HCC), the HM fraction was more increased compared with those in patients with non-alcoholic liver cirrhosis (LC) and chronic hepatitis (CH). The rate of HM fraction was correlated with total activity of serum gamma-GTP in HCC patients. In alcoholic liver disease (ALD), no remarkable differences of the rate of each gamma-GTP fraction were shown among alcoholic LC, alcoholic hepatitis, alcoholic CH and fatty liver patients. It was, however, shown that the rate of the LM fraction decreases and the HM fraction increases gradually in accordance with an increase in serum gamma-GTP activity in ALD. These data indicate that serum gamma-GTP isoenzymes can be separated clearly into four fractions by using WGA affinity electrophoresis, the HM fraction of serum gamma-GTP is relatively increased in HCC patients, and detection of the HM fraction may be useful to diagnose HCC, although it can be increased in ALD patients with high serum gamma-GTP activity.
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PMID:Separation and identification of serum gamma-glutamyl transpeptidase isoenzymes by wheat germ agglutinin affinity electrophoresis: a basic analysis and its clinical application to various liver diseases. 790 77

To aid understanding of markers of disease and predictors of outcome in alcohol-exposed systems, we undertook a literature survey of more than 700 articles to view the morphological characteristics and the clinical and experimental epidemiology of the Mallory body. Mallory bodies are filaments of intermediate diameter that contain intermediate filament components (e.g., cytokeratins) observable by conventional light microscopy or immunohistochemical methods, identical in structure regardless of initiating factors or putative pathogenesis. Although three morphological types can be identified under electron microscopy (with fibrillar structure parallel, random or absent), they remain stereotypical manifestations of hepatocyte injury. A summary of the conditions associated with Mallory bodies in the literature and their validity and potential etiological relationships is presented and discussed, including estimates on the combined light microscopic and immunohistochemical prevalences and kinetics. Emphasis is placed on proper confounder control (in particular, alcohol history), which is highly essential but often inadequate. These conditions include (mean prevalence of Mallory bodies in parentheses): Indian childhood cirrhosis (73%), alcoholic hepatitis (65%), alcoholic cirrhosis (51%), Wilson's disease (25%), primary biliary cirrhosis (24%), nonalcoholic cirrhosis (24%), hepatocellular carcinoma (23%), morbid obesity (8%) and intestinal bypass surgery (6%). Studies in alcoholic hepatitis strongly suggest a hit-and-run effect of alcohol, whereas other chronic liver diseases show evidence of gradual increase in prevalence of Mallory bodies with severity of hepatic pathology. Mallory bodies in cirrhosis do not imply alcoholic pathogenesis. Obesity, however, is associated with alcoholism and diabetes, and Mallory bodies are only present in diabetic patients if alcoholism or obesity complicates the condition. In addition, case studies on diseases in which Mallory bodies have been identified, along with pharmacological side effects and experimental induction of Mallory bodies by various antimitotic and oncogenic chemicals, are presented. Mallory bodies occur only sporadically in abetalipoproteinemia, von Gierke's disease and focal nodular hyperplasia and during hepatitis due to calcium antagonists or perhexiline maleate. Other conditions and clinical drug side effects are still putative. Finally, a variety of experimental drugs have been developed that cause Mallory body formation, but markedly different cell dynamics and metabolic pathways may raise questions about the relevance of such animal models for human Mallory body formation. In conclusion, the Mallory body is indicative but not pathognomonic of alcohol involvement. A discussion on theories of development and pathological significance transcending the clinical frameworks will be presented in a future paper.
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PMID:The Mallory body: morphological, clinical and experimental studies (Part 1 of a literature survey). 792 9

The most common causes of variceal bleeding are cirrhosis, schistosomiasis, and extrahepatic portal venous obstruction. The prognosis for an individual patient depends on the severity of the bleeding episode and the underlying liver function. Liver function is determined to a large extent by the underlying liver pathology. Patients with noncirrhotic portal hypertension or cirrhosis with good liver function have good short- and long-term prognoses. In patients with established cirrhosis, the presence of alcoholic hepatitis, hepatocellular carcinoma, or portal venous thrombosis may adversely affect prognosis. In addition to affecting prognosis, the underlying pathology may also influence choice of treatment. This point is particularly true for treatments such as shunt surgery, liver transplantation, or transjugular intrahepatic shunts.
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PMID:Relation between liver pathology and prognosis in patients with portal hypertension. 804 20

We undertook a retrospective study to determine the prevalence of hepatitis C virus (HCV) and hepatitis B virus (HBV) infection in 81 Caucasian patients with confirmed hepatocellular carcinoma (HCC). Besides HBV and HCV serological markers, HCV RNA and HBV DNA were detected in serum and liver tissue by polymerase chain reaction. Overall, HCV RNA was found in 20 cases (25%), HBV DNA in 21 patients (26%), and coinfection in 3 patients (3%). HCV RNA in liver tissue was not found without virus in serum, whereas HBV DNA was found in the liver tissue of one patient without viremia. In an additional analysis, 32 patients with HCC and alcoholic cirrhosis (HCC-AC) were compared to 35 cases with AC without HCC and 35 cases with alcoholic hepatitis. The prevalence of HCV RNA in HCC-AC (19%) was significantly higher than in the other groups (AC, 3%; alcoholic hepatitis, 0%). HBV DNA was present in 19% of HCC-AC as compared to 3% of AC and 0% of alcoholic hepatitis. We conclude that the form of HCC in 50% of the patients in a Western European country is related to chronic viral hepatitis. Our data obtained from a group of patients having alcoholic liver disease with or without HCC suggest that the prevalence of HCV RNA or HBV DNA in these populations increases with the severity of hepatic injury.
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PMID:Hepatitis C virus, alcoholic cirrhosis, and hepatocellular carcinoma. 806 79

The high prevalence of hepatitis C virus (HCV) markers in alcoholic liver cirrhosis (AL-LC) and hepatocellular carcinoma (HCC) suggests a close aetiopathogenic relationship between alcoholic liver disease (ALD) and HCV infection. In the present study, HCV markers in ALD were measured by the highly sensitive methods, and the changes of sequential HCV markers after abstinence in ALD patients were analysed in order to elucidate the effect of alcohol on HCV. Antibodies to HCV-related antigen were determined using the first or second generation test kit. HCV-RNA genomes encoding the NS-5 region were detected using the RT-PCR method. In the HCV-NS5 negative serum, HCV genomes of the 5'-noncoding region were detected using the two-stage PCR method. Titres of HCV-RNA were measured by multiple cyclic PCR and cDNA dot blotting. Typing of HCV genomes was carried out on the PCR product from the NS-5 region by slot blot hybridization using type-specific cDNA probes, or by restriction fragment length polymorphisms analysis. In alcoholic fibrosis and alcoholic hepatitis, the prevalence of HCV markers was low, suggesting that the main aetiological factor is alcohol but not HCV in these types of ALD. HCV markers were positive in the half of the patients with AL-LC, and in more than 80% of patients with AL-CH and AL-HCC, indicating that HCV infection closely relates to these types of ALD. The ratio of the K1 type to the K2 type of HCV genomes was 4:1 in all types of NANB liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between alcoholic liver disease and HCV infection. 814 26

National surveillance studies on alcoholic liver disease (ALD) in Japan were performed in 1978 and 1985, by a previous Japanese study group for ALD (Takeuchi group). In the present study, a subsequent nationwide surveillance study was performed from 1986 to 1991 and the results were compared with the previous two studies. In order to clarify the etiological relationships between hepatitis C virus (HCV) infection and ALD, an analysis was also done according to the new diagnostic criteria of ALD which was proposed by this group (Takada group). By the criteria of the Takeuchi group, the incidence of ALD was not significantly different during 1986 to 1991. However, the incidence of hepatocellular carcinoma (HCC) in alcoholic cirrhosis (AL-LC) clearly increased during this period. The analysis including the results of the previous study indicate that incidence of ALD reached a plateau in 1980 and then features of ALD in Japan entered a stable stage. However, HCC in AL-LC continued to show a linear increase from 1976 to 1991. Analysis with the new criteria of the Takada group was done in cases of 1990 and 1991. Approximately 2 out of 3 cases of ALD were caused by alcohol alone, and the remaining cases were caused by a combination of alcohol and HCV. Cases caused only by HCV were very rare. The main etiology in patients with alcoholic hepatitis and fibrosis was alcohol alone and that in chronic hepatitis of heavy drinkers was a combination of alcohol and HCV. In half of the patients with AL-LC, the etiology was alcohol alone and in the other half patients, it was a combination of both factors. In most patients with HCC, the etiology was a combination of alcohol and HCV, indicating that HCV infection may be important for the development of HCC in alcoholics.
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PMID:[A national surveillance study on alcoholic liver disease in Japan (1986-1991)]. 817 58

The characteristics of alcoholic liver disease (ALD) in Japanese patients were reviewed and compared with those in Western countries. From the study in Japanese cases, it became clear that alcoholic fibrosis and chronic hepatitis induced by alcohol were types of ALD other than the traditional 3 types. Liver injury in Japanese cases was clearly milder than that in American cases. In American cases, the injury may be fully developed, because of greater alcohol and fat intake. This may be one reason why the two above types of ALD have not been mentioned in the literature of Western countries. In Japanese patients, hepatitis C virus (HCV) infection is not related to alcoholic fibrosis and alcoholic hepatitis. On the other hand, the prevalence of HCV markers was high in chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC) patients. Alcoholic hepatitis and chronic hepatitis are the high risk groups for the development of cirrhosis and the chronic hepatitis group is at high risk for the development of HCC. Although the risk is low in alcoholic fibrosis, some patients also develop cirrhosis. About half of the cases of cirrhosis may develop from alcoholic hepatitis and alcoholic fibrosis, and the remaining half cases may develop from chronic hepatitis. Over 80% of HCC cases may develop from chronic hepatitis in Japan. Chronic alcoholism enhanced the development of HCV-related HCC. Recent increase of HCC in alcoholic cirrhosis in Japan may be related to the increase of alcohol consumption, the increase of blood transfusions, and longer survival of cirrhosis patients.
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PMID:Characteristic features of alcoholic liver disease in Japan: a review. 844 Apr 19

Ethane exhalation was measured in 42 control subjects, 52 patients with various non-alcoholic liver diseases, and 89 alcohol abusers who had been admitted to hospital for alcohol withdrawal and assessment of liver disease (six with normal liver tests, 10 with steatosis with or without fibrosis, six with alcoholic hepatitis, 29 with cirrhosis, 34 with both cirrhosis and alcoholic hepatitis, and four with both cirrhosis and a hepatocellular carcinoma). Ethane exhalation was similar in control subjects and in patients with non-alcoholic liver diseases, but was five times higher in alcohol abusers. Ethane exhalation in alcohol abusers was significantly, but very weakly, correlated with the daily ethanol intake before hospital admission, and the histological score for steatosis, but not with the inflammation or alcoholic hepatitis scores. Ethane exhalation was inversely correlated with the duration of abstinence before the test. In nine alcoholic patients, the exhalation of ethane was measured repeatedly, and showed slow improvement during abstinence. Ethane exhalation was significantly but weakly correlated with the Pugh's score in patients with alcoholic cirrhosis. It is concluded that the mean ethane exhalation is increased in alcohol abusers. One of the possible mechanisms may be the presence of oxidizable fat in the liver. The weak correlation with the Pugh's score is consistent with the contribution of many other factors in the progression to severe liver disease.
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PMID:Increased ethane exhalation, an in vivo index of lipid peroxidation, in alcohol-abusers. 847 92

To determine the incidence of hepatitis C virus (HCV) infection in patients with alcoholic liver disease (ALD), serum samples from 252 patients with ALD were tested for anti-HCV and HCV RNA. Serial sera of these patients were collected and stored under optimal conditions to allow exact quantification of HCV RNA. Fifteen patients who visited our hospital during the same period of time with chronic HCV infections served as controls. In those with ALD, anti-HCV and HCV RNA were positive in 55.5% and 41.2%, respectively. Patients with histologically diagnosed chronic hepatitis and hepatocellular carcinoma had much higher prevalence rates of HCV RNA (84% and 100%, respectively) compared to those with fatty liver (4.3%), hepatic fibrosis (10.1%) and alcoholic hepatitis (22.2%) (P < 0.01). Although no difference in serum HCV RNA levels was observed between the patients with both ALD and chronic HCV infection and those with chronic HCV infection alone, HCV RNA levels significantly (10-fold) dropped after abstinence in nearly half of the patients (P < 0.01). These data indicate that HCV infection in patients with ALD promotes progression of liver disease, and abstinence from alcohol is associated with a reduction in serum HCV RNA levels.
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PMID:Hepatitis C virus infection in patients with clinically diagnosed alcoholic liver diseases. 887 73

National surveys of alcoholic liver disease (ALD) in Japan were performed in 1978 and 1985 by a previous Japanese study group for ALD (the Takeuchi group). In the present study, a subsequent nationwide survey of ALD in Japan was conducted from 1986 to 1991 and the results compared with the previous studies. In order to clarify the aetiological relationship between hepatitis C virus (HCV) infection and ALD, results were also analysed according to new diagnostic criteria for ALD proposed by the current ALD study group (the Takada group). According to the diagnostic criteria of the Takeuchi group, the incidence of ALD did not differ significantly from 1986 to 1991. However, the incidence of hepatocellular carcinoma (HCC) in alcoholic cirrhosis (AL-LC) clearly increased during this period. The analysis, which included analysis of results from the previous studies, indicated that the incidence of ALD reached a plateau in 1980 and then stabilized. However, HCC in AL-LC continued to show a linear increase from 1976 to 1991. The new diagnostic criteria of the Takada group were used to analyse cases from 1990 and 1991. Approximately two out of every three cases of ALD were caused by alcohol alone, and the remainder were caused by a combination of alcohol and HCV. Cases caused only by HCV were very rare. The main aetiology in patients with alcoholic hepatitis and fibrosis was alcohol alone, and in the case of chronic hepatitis, in heavy drinkers, it was a combination of alcohol and HCV. In half the patients with AL-LC the aetiology was alcohol alone, and in the other half it was a combination of both alcohol and HCV. In the majority of patients with HCC, the aetiology was a combination of alcohol and HCV, indicating that HCV infection may be important in the development of HCC in alcoholics.
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PMID:National survey of alcoholic liver disease in Japan (1968-91). 896 25


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