Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of hepatitis C virus and its subtypes on the clinical course of liver disease in alcoholics was assessed. Hepatitis C virus infection was confirmed by a reverse transcription and polymerase chain reaction method for the hepatitis C virus NS-5 region in the sera of alcoholics with various stages of histologically proven liver disease. The frequency of hepatitis C virus was significantly higher in alcoholics with chronic hepatitis (73%) than in those with liver fibrosis (18%), alcoholic hepatitis (17%), and fatty liver (0%). Hepatitis C virus subtypes, namely K1 and K2, were determined by dot-blot hybridization analysis of the polymerase chain reaction products with specific probes, and their frequencies were 68% and 32%, respectively. The proportion of patients whose serum transaminase levels returned to normal following 4 weeks of abstinence in hospital was significantly lower in alcoholics with hepatitis C virus viremia (glutamic oxaloacetic transaminase: 53.8%; glutamic pyruvic transaminase: 42.3%) than in those without viremia (glutamic oxaloacetic transaminase: 86.2%, p < 0.01; glutamic pyruvic transaminase: 89.7%, p < 0.01). When alcoholics with the K1 and K2 subtypes of hepatitis C virus were compared, normalization of transaminase levels was less frequent in alcoholics with K1 (glutamic oxaloacetic transaminase: 42.8%; glutamic pyruvic transaminase: 28.6%) than in those with K2 (glutamic oxaloacetic transaminase: 88.9%, p < 0.05; glutamic pyruvic transaminase: 77.8%, P < 0.05). These data indicate that hepatitis C virus infection is associated with a reduced rate of recovery of serum transminase levels following abstinence in subjects with alcoholic liver disease, more so in the K1 subtype than in the K2 subtype.
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PMID:Relationship between hepatitis C virus subtypes and clinical features of liver disease seen in alcoholics. 779 Jul

We evaluated hepatitis B virus DNA and hepatitis C virus RNA in sera from 110 HBsAg and IgM HBc antibody-negative heavy drinkers (50 cirrhosis, 13 chronic active hepatitis, 25 fatty liver with or without mild to moderate fibrosis, alcoholic hepatitis or both and 22 healthy alcoholic subjects) with polymerase chain reaction. Results of hepatitis C virus polymerase chain reaction were compared with those obtained with two tests (second generation recombinant immunoblot assay and enzyme-linked immunosorbent assay) used to detect hepatitis C virus antibodies. Hepatitis B virus DNA was found in three (2.7%) patients. Hepatitis C virus RNA was detected in 29 (29.8%) of the 97 subjects whose sera were well preserved for RNA extraction (42.5% cirrhosis, 83.3% chronic active hepatitis, 8% fatty liver and 0% healthy alcoholic subjects). Results obtained with second-generation recombinant immunoblot assay and enzyme-linked immunosorbent assay had a high degree of agreement with polymerase chain reaction as expected, the kappa indexes being 0.76 and 0.61, respectively. Nevertheless, five hepatitis C virus RNA-positive patients had negative recombinant immunoblot assay results, whereas all hepatitis C virus RNA-positive patients had positive or borderline enzyme-linked immunosorbent assay results. We conclude that, in Italian HBsAg-negative alcoholic patients, "inapparent" hepatitis B virus infection is rare. On the contrary, hepatitis C virus infection, as detected on hepatitis C virus polymerase chain reaction, is quite frequent, especially in patients who have cirrhosis and chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:"Inapparent" hepatitis B virus infection and hepatitis C virus replication in alcoholic subjects with and without liver disease. 811 81

Although mortality from alcoholic liver disease has declined in some Western countries in recent years, elsewhere it is increasing and overall it remains a major health problem. Deaths are predominantly seen in patients with alcoholic hepatitis or cirrhosis, and when they occur in patients with fatty liver are usually unrelated to liver disease. Progression to cirrhosis is correlated with the severity of fatty liver and particularly with the presence of alcoholic hepatitis. Mortality from cirrhosis is strongly correlated with per capita alcohol consumption. The decline in cirrhosis mortality rates seen recently is related in part to decreases in per capita consumption, but probably also to the growth of self-help organizations which facilitate abstinence from alcohol. Recent studies suggest there is not an invariable dose-response relationship between alcohol intake and the severity of liver disease and that alcohol has a permissive effect which allows other aetiological factors to operate. Factors that influence susceptibility to alcoholic liver disease include gender (women develop alcoholic cirrhosis more readily than men), concomitant hepatitis C infection and possibly hepatitis B infection. It is uncertain whether HLA status or immune mechanisms are implicated. The systematic use of screening tests for hazardous consumption combined with early intervention therapies offers a good prospect of reducing morbidity and mortality from alcoholic liver disease.
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PMID:Epidemiology of alcoholic liver disease. 821

The aim of this study was to evaluate selected diagnostic and clinical aspects of chronic hepatitis C (CH-C) in the group of 80 patients: 68 males aged 24-65 (mean 39.8 +/- 10,5) and 12 females aged 35-66 (mean 48.7 +/- 12.6). The epidemiological data allowed to divide the basic group into 3 subgroups: patients with transfusion-associated CH-C (subgroup I: 12 males, mean age 38 +/- 6.7 and 2 females aged 40 and 46), CH-C patients with parenteral hepatitis C virus exposure-other than blood transfusion (subgroup II: 25 males, mean age 40.6 +/- 8.2 and 5 females aged 43 +/- 15.1) and sporadic cases with unknown HCV exposure (subgroup III: 31 males, mean age 38.2 +/- 11.2 and 5 females, mean age 50.5 +/- 10.3). The duration of the disease (CH-C) was calculated from the incident of acute viral hepatitis or the first signs of liver damage caused by HCV to the confirmation of CH-C by liver biopsy. The following data were analyzed: a frequency of acute viral hepatitis with jaundice at the beginning of the disease, ALT flare-ups, mean highest activities of ALP and GGT, frequency of hypergammaglobulinaemia and sings of fatty liver in ultrasonographic finding (USG). In all patients but one anti-HCV antibodies (ELISA 2nd generation test by Abbott) were detected. In 64/80 subjects antibodies to HCV antigens: 5-1-1, C 100-3, C 33c and C 22 were determined by RIBA-2 test (Ortho). In 62/80 patients HCV-RNA in serum was determined by RT PCR. Liver biopsy was performed in 71/80 patients. Other co-existent liver diseases were excluded. The similarity between 3 subgroups was shown: similar percentage of males and females, similar patients mean age and the duration of the disease. It was shown that the acute beginning of the disease with jaundice has been observed twice as frequent in subgroups I and II compared with subgroup III. The same frequency of ALT flare-ups in all subgroups was observed (25-28.6%). No differences in mean highest ALP and GGT activities in 3 subgroups were observed. It was shown, however, that hypergammaglobulinaemia was detected more frequently in subgroup III (30.5%) compared with subgroup I (7.1%) and II (16.7%). The signs of fatty liver in ultrasonographic findings were also observed more frequently in subgroup III (30.5%) than in subgroup I (14.3%) or II (16.7%). In all patient but one, in which anti-HCV antibodies by ELISA test were detected, anti-C 33c and anti-C 22 antibodies by RIBA were present. HCV-RNA in serum was detected in 77.8% subjects from subgroup I. 73.9%-from subgroup II and 66.7%-from subgroup III. In all HCV-RNA positive patients anti-HCV antibodies were detected. The evidence of chronic active hepatitis confirmed by liver biopsy was shown in 63.6%, 67.8% and 71.8% of patients from subgroup I, II and III, respectively. In no case normal liver morphology was present. Authors concluded the distressing fact of the high incidence of chronic active hepatitis in patients unaware of HCV infection, without the incident of acute hepatitis at the beginning of the disease (over 1/3 of all described subjects). The differences of the clinical course of the disease between subgroups 1 + II and subgroup III suggest two different routes of HCV infection or the presence of two different HCV mutants in Polish population. Authors emphasise the necessity of HCV gene typing in CH-C patients, which might explain the surprisingly high incidence of chronic active hepatitis in the reported group. The use of the presented data for the general practitcioner making the diagnosis of crytogenetic liver disease is also accentuated.
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PMID:[Selected diagnostic and clinical aspects of chronic viral hepatitis type C]. 875 40

We have evaluated the diagnostic efficacies of ultrasonography and hepatitis C virus (HCV) antibody measurement to differentiate pathogenesis of liver dysfunction in the asymptomatic adults with elevated ALT value. Among 4256 visitors to PL Tokyo Health Control Center for their health examination, 463 cases (11%) showed abnormal liver function including elevation of ALT value. Ultrasonography and HCV antibody measurement using the second generation reagent had been applied to 362 cases in order to screen the etiology of liver dysfunction. The ultrasonography succeeded to establish the diagnosis of fatty liver in 137 cases (38%) and 41 cases (11%) demonstrated positive HCV antibody. There were 4 cases with positive HBs antigen, however, it was found that their abnormal liver function was attributed to other etiology such as fatty liver and alcoholic liver dysfunction rather than chronic type B hepatitis. HCV antibody-positive cases showed higher levels of total protein, ZTT, AST, ALT, and lower levels of albumin, A/G, total cholesterol, triglyceride, gamma-GT and cholinesterase value than other cases. HCV antibody titers were not correlated to hepatic parenchymal damage estimated by ALT or cholinesterase value. Only a little correlation was observed between HCV antibody titers and HCV-RNA amounts determined by the competitive reverse transcription-polymerase chain reaction (RT-PCR) method. These results indicate sufficient diagnostic efficacies of ultrasonography and HCV antibody measurement for a pathogenesis differentiation in the asymptomatic patients with liver dysfunction, and these examinations should be employed as the first-step screening tests for the etiology determination of liver diseases in the primary care medicine.
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PMID:[Pathogenesis-screening tests for liver dysfunction in the asymptomatic patients with elevated ALT values and their diagnostic efficacies in primary care medicine]. 885 69

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

A histopathological study was conducted on alcoholic liver fibrosis with fatty change (21 cases) and alcoholic liver fibrosis without fatty change (18 cases) in comparison with nutritional fatty liver (27 cases). The diagnoses of alcoholic liver fibrosis groups were clinically fulfilled according to the criteria established by the Alcohol and Liver Research Group (Chief: Professor Takeuchi) of the Ministry of Education of Japan. Histological diagnosis of alcoholic liver fibrosis with fatty change was based on moderate and/or greater fatty metamorphosis of the hepatic lobules, alcoholic liver fibrosis without fatty change on a lesser degree of fatty metamorphosis than alcoholic liver fibrosis with fatty change, and nutritional fatty liver on clinicopathological features. All 66 cases were negative for viral markers of hepatitis B surface antigen and anti-hepatitis C virus in serum. Intrasinusoidal neutrophil infiltrations were significant in cases of alcoholic liver fibrosis groups more often than in cases of nutritional fatty liver. The degree of intrasinusoidal neutrophil infiltration in cases of alcoholic liver fibrosis groups was higher in cases who had last consumed alcohol recently, compared with those with longer abstinence. In alcoholic liver fibrosis with fatty change and nutritional fatty liver groups, mild-to-moderate degrees of ceroid-lipofuscinosis were recognized, but both fatty change and ceroid-lipofuscinosis were decreased according to the deterioration of fibrotic changes in alcoholic liver fibrosis with fatty change cases. On the other hand, it is significant that the frequency of ceroid-lipofuscinosis in alcoholic liver fibrosis without the fatty change group was lower than those of the alcoholic liver fibrosis with fatty change and nutritional fatty liver groups. Distribution of ceroid-lipofuscinosis has a tendency to be recognized around the central zone (zone III) of alcoholic liver fibrosis with fatty change cases with mild fibrosis, as in nutritional fatty liver cases, and the ceroid-lipofuscinosis disperses with the progression of fibrosis. These results suggest that fibrosis and fatty droplet deposition lead to microvascular heterogeneity. Therefore, the degree and distribution of fatty droplets, ceroid-lipofuscinosis, and intrasinusoidal neutrophil infiltration differ, depending on the etiology of fatty liver, and are an important histopathological barometer in cases of alcoholic liver fibrosis with fatty change and alcoholic liver fibrosis without fatty change, thus indicating the degree of fibrosis and the period since last alcohol intake.
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PMID:Correlation between intrasinusoidal neutrophilic infiltration and ceroid-lipofuscinosis in alcoholic liver fibrosis with or without fatty change: clinicopathological comparison with nutritional fatty liver. 898 40

Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide, which finally leads to development of hepatocellular carcinoma. Chronic hepatitis C is characterized by several histological features in the liver which discriminate it from other forms of hepatitis: bile duct damage, lymphoid follicles and steatosis (fatty change). Little is known, however, about the role of HCV or its viral proteins in the pathogenesis of hepatitis. Recently, the core protein of HCV has been suggested to have a transcriptional regulatory function, and thereby to be involved in inducing phenotypic changes in hepatocytes. To clarify whether or not the HCV core protein has an effect on pathological phenotypes in the liver, two independent transgenic mouse lines carrying the HCV core gene were established. These mice developed progressive hepatic steatosis, indicating that the HCV core protein plays a direct role in the development of hepatic steatosis, which characterizes hepatitis C. This transgenic mouse system would be a good animal model for the study of pathogenesis in human HCV infection.
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PMID:Hepatitis C virus core protein induces hepatic steatosis in transgenic mice. 922 25

Recently, hepatitis GB virus C (HGBV-C) has been recovered from patients with non-A-E hepatitis. However, it has been unclear whether HGBV-C may be related to the development of alcoholic liver disease (ALD) or not. In this study, we determined HGBV-C RNA in sera from alcoholic patients without markers for hepatitis C and B viruses to evaluate the role of HGBV-C in ALD. Serum samples were obtained from 68 patients with ALD and 40 nonalcoholic patients with chronic type C liver disease. HGBV-C RNA was detected in only 3 of 68 (4.4%) patients with ALD, in 2 of 27 patients with hepatic fibrosis, and in 1 of 5 patients with chronic hepatitis. There was no HGBV-C RNA in sera from patients with fatty liver, alcoholic hepatitis, or cirrhosis. Serum levels of AST, ALT, and gamma-glutamyltranspeptidase in alcoholic patients with, as well as without, HGBV-C RNA decreased to normal levels after abstinence. In addition, an inflammatory change was not observed in liver biopsy specimens obtained from two HGBV-C-positive patients with alcoholic hepatic fibrosis. Our results clearly suggest that the prevalence of HGBV-C infection in patients with ALD is rare and that HGBV-C may not play an important role in the development of liver disease in alcoholics.
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PMID:Clinical significance of hepatitis GB virus C infection in alcoholic liver disease. 943 37

Hepatitis C virus (HCV) is the main cause of chronic hepatitis worldwide. Chronic hepatitis ultimately results in the development of hepatocellular carcinoma (HCC). However, the mechanism of hepatocarcinogenesis in chronic HCV infection is still unclear. The ability of the core protein of HCV to modulate gene transcription, cell proliferation and cell death may be involved in the pathogenesis of HCC. Here, we report the development of HCC in two independent lines of mice transgenic for the HCV core gene, which develop hepatic steatosis early in life as a histological feature characteristic of chronic hepatitis C. After the age of 16 months, mice of both lines developed hepatic tumors that first appeared as adenomas containing fat droplets in the cytoplasm. Then HCC, a more poorly-differentiated neoplasia, developed from within the adenomas, presenting in a 'nodule-in-nodule' manner without cytoplasmic fat droplets; this closely resembled the histopathological characteristics of the early stage of HCC in patients with chronic hepatitis C. These results indicate that the HCV core protein has a chief role in the development of HCC, and that these transgenic mice provide good animal models for determining the molecular events in hepatocarcinogenesis with HCV infection.
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PMID:The core protein of hepatitis C virus induces hepatocellular carcinoma in transgenic mice. 973 2


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