Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic non-A, non-B hepatitis (NANBH) is a common and often progressive liver disease. Based on current serological tests, hepatitis C virus (HCV) infection is responsible for most cases. Interferon-alpha (IFN) treatment at a dose of 3 x 10(6) units given three times per week for 24 weeks has been shown to be effective in normalizing serum alanine aminotransferase (ALT) levels and reducing hepatic inflammation in approximately 40% of these patients. The purpose of this study was to identify pretreatment characteristics in patients with chronic hepatitis C(CH-C) which would best predict a favourable response to IFN treatment (normalization of serum ALT). One hundred and sixty-three adult patients who had participated in a large multicentre treatment trial were included in the study group; 84 had been treated with 3 x 10(6) units of recombinant IFN-alpha-2b (rIFN) subcutaneously three times per week for 24 weeks and 79 patients had been treated with 1 x 10(6) units rIFN in the same dosage schedule. Forty-one pretreatment historical, clinical, laboratory and histological variables were evaluated. In addition, early biochemical improvement during treatment was evaluated as a predictor of ultimate response. Univariate analysis identified six variables (dose, dose m-2, weight, body surface area, ongoing ethanol use, white blood cell count and the presence of symptoms) as potential predictors of response (two-tailed, P < 0.15). By multivariate analysis, however, only the 3 x 10(6) dose of rIFN was independently predictive of response (P < 0.01). When the analysis of response was confined to those patients who received treatment with 3 x 10(6) units of rIFN, seven variables [body weight, surface area, dose m-2, current ethanol use, serum albumin and the presence of chronic persistent hepatitis (CPH) on entry liver biopsy] were more frequent in patients who responded to therapy. In a multivariate model, only CPH and body weight predicted an increased likelihood of response (P < 0.01). However, the model was not a sensitive predictor of response as only 18% of the study group had CPH on liver biopsy. A decrease in serum ALT levels within the first 12-16 weeks of rIFN treatment was found to be the strongest indicator of an ultimate response to treatment. Thus, assessment of early response to IFN treatment is the only practical means of predicting complete response and avoiding prolonged and unnecessary therapy in those with little chance of response.
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PMID:Clinical predictors of response to recombinant interferon-alpha treatment in patients with chronic non-A, non-B hepatitis (hepatitis C). The Hepatitis Interventional Therapy Group. 879 May 60

Chronic viral hepatitis is caused mainly by chronic infection with hepatitis viruses B (HBV), C (HCV), or delta (HDV). Persons chronically infected with one or more of these viruses may develop chronic progressive hepatitis, cirrhosis, and liver failure. In addition, chronic HBV and HCV infections are major causal risk factors for hepatocellular carcinoma. Alcohol consumption accelerates the development of chronic liver disease among HCV-infected individuals and may have similar effects on persons chronically infected with HBV alone or HBV and HDV, but the reported studies are inconsistent.
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PMID:The epidemiology of hepatitis viruses B, C, and D. 879 71

A positive association between the incidence of hepatocellular carcinoma and the consumption of alcoholic beverages has been reported from some countries. The possible mechanistic nature of the association remains unclear, however. The effects of alcohol, as ethanol and as ethanol in various complex mixtures in the many different alcoholic beverages, were compared with the effects of well-known genotoxic and nongenotoxic or epigenetic carcinogens in carcinogenesis. There is no convincing evidence that alcohol can initiate the long multistep process of development of hepatocellular carcinoma. Thus, it appears that alcohol cannot be considered as a complete carcinogen. The effects of alcohol were also compared with known promoting agents for liver cancer. Although the available data are less clear, nevertheless it appears that alcohol cannot be considered as a bona fide promoting agent for liver cancer development. The most likely roles of alcohol in the genesis of liver cancer are: (1) to induce a well-known precancerous liver lesion, cirrhosis, and (2) to modulate, in an as yet ill-defined manner, the process of cancer development with known human carcinogenic influences such as hepatitis due to hepatitis B and hepatitis C viruses. Alcohol is well known to induce several enzymes in the liver and, thus, could theoretically modulate one or more steps in the carcinogenic process. Because alcohol has been found to alter cell membranes in well-defined ways and cell membrane changes, especially in the liver endoplastic reticulum, appear to be common in the later steps in liver cancer development, it is suggested that one site of alcohol action might be in the modulation of the biophysical composition of the liver endoplasmic reticulum and plasma membrane, favoring the cellular evolution to neoplasia.
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PMID:Alcohol and other chemicals in the development of hepatocellular carcinoma. 879 78

Hepatocellular peroxisomes harbor one of the metabolic pathways for ethanol metabolism (i.e., catalase in the presence of H2O2-generating enzymes). We studied the morphometric characteristics of these organelles in 26 biopsy samples of patients with different alcohol-induced lesions (12 with steatosis, 5 with hepatitis, and 9 with cirrhosis) and compared the findings with those obtained in seven control livers. All 33 human liver biopsy samples were stained for catalase activity to facilitate peroxisomal identification. Morphometric analysis of the peroxisomes was performed on calibrated electron micrographs. The numerical density of the peroxisomes was significantly increased to 183%, whereas the mean peroxisomal diameter (dcircle) revealed a significant decrease to 89%. This resulted in a normal volume density of the peroxisomal compartment, whereas the surface density was significantly induced. Peroxisomal shape was not different between alcoholic and control livers. When alcoholic livers were divided into three subgroups according to histopathological findings, similar morphometric results were obtained when compared with control livers, although significantly was sometimes lost. No differences in peroxisomal characteristics were found among alcoholic subgroups. The mean peroxisomal diameter per human liver (alcoholic and control) was inversely correlated to the numerical density. It is concluded that the peroxisomal adaptation in human alcoholic liver is such as to create an efficient environment for a presumably increased peroxisomal metabolism.
Alcohol Clin Exp Res 1996 Aug
PMID:Morphometric characteristics of human hepatocellular peroxisomes in alcoholic liver disease. 886 67

Perinuclear antineutrophil cytoplasmic autoantibodies have been described in inflammatory bowel diseases and in primary sclerosing cholangitis. Because the data concerning their occurrence are conflicting, we have used indirect immunofluorescence on ethanol-fixed neutrophils to test the sera from a large population of 382 patients with various liver and digestive diseases: in particular, from 27 patients with primary sclerosing cholangitis, 105 patients with autoimmune chronic active hepatitis, 30 patients with primary biliary cirrhosis and 124 patients with inflammatory bowel disease. The prevalence of the perinuclear antineutrophil cytoplasmic autoantibodies was 37% in ulcerative colitis and 15% in Crohn's disease. They would not be helpful in the differential diagnosis between these two inflammatory bowel diseases. Within the group of autoimmune liver diseases, perinuclear antineutrophil cytoplasmic autoantibodies were detected in 44% of sera from patients with primary sclerosing cholangitis and in 36% of sera from patients with type I autoimmune active hepatitis, but not in primary biliary cirrhosis. When primary sclerosing cholangitis was associated with an inflammatory bowel disease, the prevalence of these autoantibodies was 60%. They were 88% specific for primary sclerosing cholangitis and 86% specific for type I autoimmune active hepatitis. Despite their moderate sensitivity and specificity in primary sclerosing cholangitis, they remain the only serologic marker of this autoimmune liver disease. Moreover, they turned out to be a more sensitive marker for inflammatory bowel disease with associated primary sclerosing cholangitis.
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PMID:Antineutrophil cytoplasmic autoantibodies in autoimmune liver and inflammatory bowel diseases. 886 75

The hepatoprotective effect of Alstonia scholaris R. Br. on liver injuries induced by carbon tetrachloride (CCl4). beta-D-galactosamine, acetaminophen and ethanol were investigated by means of serum-biochemical and histopathological examinations. Post treatment of A scholaris reduced dose-dependently the elevation of serum transaminases level and histopathological changes such as cell necrosis, inflammatory cell infiltration, which were caused by the single administration of 32 microliters/kg CCl4 or 600 mg/kg acetaminophen in mice. A. scholaris significantly lowered 288 mg/kg beta-D-galactosamine induced serum transaminases elevation in the serum-biochemical analysis in rats. A tendency was also shown to inhibit cell necrosis and inflammatory cell infiltration caused by beta-D-galactosamine in histopathological examination. All serological and histopathological effects of A. scholaris were compared with those of Bupleurum chinense, which has been reported previously as a treatment criteria of hepatitis.
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PMID:The protective effect of Alstonia scholaris R. Br. on hepatotoxin-induced acute liver damage. 887 72

The effect of ethanol on cells infected with mouse hepatitis virus (MHV) was investigated. After MHV infection of competent cells, NCTC1469, ethanol was added to the culture at various concentrations, and the viability of cells was measured using 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide. To examine the possible involvement of the ethanol metabolite, acetaldehyde, alcohol dehydrogenase activity was measured in NCTC1469 cells. Ethanol alone did not show cytotoxicity against NCTC1469 cells at concentrations from 0.125% to 2%. After infection with MHV, the viability of cells decreased, and this decrease was further enhanced, dose-dependently, by the addition of ethanol. The activity of alcohol dehydrogenase in the cells was below the detectable level. The same phenomena were also demonstrated in cells infected with influenza virus and Herpes simplex virus. These results demonstrate that ethanol enhances MHV-mediated cytotoxicity; this exacerbation of cytotoxicity by ethanol is suggested to be an effect common to cytopathic virus-infected cells.
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PMID:Effect of ethanol on mouse hepatitis virus-induced cytotoxicity. 888 34

A number of episodes of non-A, non-B hepatitis (NANB) have been associated in the recent past with the administration of intravenous immunoglobulin (IGIV). It now appears that hepatitis C virus (HCV) is the cause of NANB, although not all the factors leading to HCV transmission by IGIV are completely understood. Nevertheless, based on a retrospective analysis of two episodes of HCV transmitted by anti-Rh D immunoglobulin (anti-D), cold ethanol fractionation clearly is important in ensuring viral safety; both of these intravenous anti-D preparations were manufactured without benefit of this purification step. Other episodes of HCV transmission have been associated with IGIV produced using chromatography (particularly DEAE-Sephadex chromatography), which has been used after cold ethanol fractionation to further purify immunoglobulin G. DEAE-Sephadex chromatography may have only a marginal partitioning capacity, such that infective HCV virions are not further fractionated into waste fractions. All IGIV preparations associated with HCV transmission were formulated as lyophilized preparations, which may be important in stabilizing HCV before administration to patients. The role of anti-HCV screening in improving the viral safety of IGIV preparations remains unclear, but additional viral inactivation steps, such as solvent-detergent treatment or incubation at pH 4.0, probably are required for IGIV manufactured using chromatographic procedures.
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PMID:Intravenous immunoglobulin and hepatitis C virus: an overview of transmission episodes with emphasis on manufacturing data. 893 Apr 41

Recently it has been reported that Shosaiko-to (SHO), a traditional Chinese medicine used for treating gastritis and hepatitis, also has been found useful for treating gastric ulcers, although no pharmacological study has yet investigated the precise antiulcer properties of SHO. Herein, the authors report on the results of a rat study in which the effects of SHO on gastric ulcers, acid secretions and potential difference of gastric mucosa (PD) were studied. SHO (100, 250 or 500 mg /kg, p.o.) significantly inhibited the development of ethanol-induced gastric lesions in a dose-dependent manner. SHO (500 mg/kg, p.o.) significantly inhibited the development of aspirin-,indomethacin- or water-immersion-stress induced gastric lesions. Sucralfate (500 mg/kg, p.o.) inhibited both ethanol- and aspirin-induced gastric lesions, and cimetidine (10 mg/kg, p.o.) inhibited aspirin-, indomethacin- or stress-induced gastric lesions. SHO (10, 30 and 100 mg/kg, i.p.) also significantly inhibited pentagastrin- and 2-deoxy-D-glucose (2-DG)-induced gastric acid secretions in a dose-dependent manner, whereas cimetidine (1 mg/kg, i.p.) inhibited a pentagastrin-induced secretion and atropine (0.05 mg/kg, i.p.) inhibited pentagastrin- or 2-DG-induced acid secretions. SHO (250, 500 or 1000 mg/kg, i.g.) significantly inhibited ethanol-induced PD reduction. Sucralfate (500 mg/kg, i.g.) inhibited the reduction, and cimetidine (250 mg/kg, i.g.) didn't inhibit it. These results indicate that SHO not only possesses the capability of protecting the rat gastric mucosa as well as sucralfate, but also is able to inhibit gastric acid secretions like cimetidine or atropine.
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PMID:[Antiulcer properties of shosaiko-to]. 894 Jul 3

There is a growing body of evidence to suggest that cytokines may be involved in the aetiology of alcoholic hepatitis. To study the effects of chronic ethanol feeding on cytokine production we have maintained rats on the control and ethanol-containing forms of the Lieber-DeCarli liquid diet for six weeks. The animals were then given an i.v. injection of endotoxin to induce hepatitis. It was found that the ethanol-fed animals had biochemical and histological evidence of mild to severe liver damage whereas control-fed animals had minimal liver damage. When plasma levels of cytokines were measured, it was found that the ethanol-fed rats produced much higher levels of tumour necrosis factor and interleukin 6 bioactivity than the control-fed rats. However, elevated levels of interleukin 1 protein were not seen in the ethanol-fed animals.
Alcohol Alcohol Suppl 1994
PMID:The effect of chronic ethanol feeding on cytokines in a rat model of alcoholic liver disease. 897 67


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