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)

The most frequent hepatobiliary diseases in Vietnam are chronic hepatitis and cirrhosis, liver abscess, hepatobiliary ascaridiasis, angiocholitis, biliary lithiasis and primary liver cancer. The principal causes of chronic hepatitis and cirrhosis are HBV and HCV infections. Alcohol and chemicals (drugs, agricultural, industrial, war herbicides) also play an important role. Malaria causes hepatitis and fibrosis lesions, however no cirrhotic lesions were observed. There are two categories of liver abscess, amoebic and cholangitic, often caused by ascaridiasis. Treatment of amoebic abscesses is, at first, non-surgical for small abscesses, often combined with ultrasound guided abscess puncture. Cholangitis abscesses are more serious and often require surgical intervention. Among the gallstones, only 15% are of the gall-bladder, the majority are choledocho- and intrahepatic-lithiasis, composed largely of calcium bilirubinate and are frequently caused by Ascaris-related cholangitis and the nucleation of Ascaris eggs. Forty-seven per cent of acute cholecystitis are acalculous, showing a higher frequency than in Western countries. Primary liver cancer is one of the most frequent malignancies in Vietnam. More than 90% of liver cancers are hepatocellular carcinomas. The principal causes are HBV infection, followed by HCV infection, aflatoxin, alcohol and chemicals. Recent efforts aiming at earlier diagnosis, by selective screening in high-risk groups, have used clinical surveillance, abdominal sonography and AFP level determination. Promising results were obtained in prevention trials by reducing the high AFP level of cirrhotic patients using a vegetal drug, Gacavit, and by treatment with percutaneous ethanol injection therapy, as an alternative therapeutic measure for liver tumour resection.
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PMID:Some peculiarities of hepatobiliary diseases in Vietnam. 919 96

Properties of a hepatitis delta virus (HDV) RNA ribozyme system, which consists of three RNA oligomer strands (substrate 8-mer; enzyme 16-mer plus 35-mer) and contains a hybrid sequence of genomic and antigenomic RNA cores, are reported. Effects of Mg2+ concentration, divalent metal ion species, pH, and temperature on the cleavage activity were examined. The substrate cleavage activity increased with increasing Mg2+ concentration (0-100 mM). Ca2+ and Mn2+ ions were the most effective divalent cations and Mg2+ was less effective. The cleavage activity increased with increasing pH (5-7.5). The optimum temperature for the cleavage activity was 25-40 degrees C. The Mg2+ concentration, pH and temperature dependencies are different from those reported for the single-strand ribozymes (about 90-mer) although the divalent metal ion preference is very similar. Conformational change induced by Mg2+ ion titration was monitored by CD. The CD data and the activity-Mg2+ concentration data were analyzed by curve-fitting analysis using equations derived for multiple metal ion binding mechanisms. The data can be explained by a model in which three Mg2+ ions bind to one ribozyme unit.
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PMID:Properties of hepatitis delta virus ribozyme, which consists of three RNA oligomer strands. 935 86

The hepatic concentrations of copper, zinc, magnesium, calcium, and selenium were measured in LEC rats, which develop a spontaneous form of hepatitis at 3-4 months of age, and compared to trace metal concentrations in the LEA rat, its asymptomatic congenic strain. Consistent with results found by other groups, copper was found to accumulate within the liver of LEC rats to levels more than 50 times those measured in LEA rats. In addition, liver selenium concentration in LEC rats was found to be around 50% of that in LEA rats. The enzyme activity, and RNA for the selenium dependent enzyme, glutathione peroxidase, was also found to be reduced in LEC rat liver. These results indicate that hepatic selenium in the LEC rat is depleted and that, as a result of this, the capacity to protect cells from copper-induced free-radical damage is reduced.
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PMID:The LEC rat possesses reduced hepatic selenium, contributing to the severity of spontaneous hepatitis and sensitivity to carcinogenesis. 951 49

Determining the possible association of viral hepatitis infection and degree of pruritus is the primary concern of this study. Ninety-six adequately dialyzed CAPD patients (47 male and 49 female) and 526 normal controls (266 male and 260 female) were enrolled. Blood hemoglobin, ferritin, electrolytes, calcium, phosphate, albumin, urea, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase, and bilirubin were analyzed by routine methods. Serum HBsAg was examined, using a radioimmunoassay method and the anti-HCV, an enzyme immunoassay method. All cases were interviewed with a standardized questionnaire. The highest possible pruritus score (PS) was 22. The prevalences of HBsAg(+) and anti-HCV(+) were 14.6% and 17.7%, respectively. The mean PS in all 96 CAPD patients was 11.6 (range 7-22). The mean PS were 11.8 +/- 0.6 and 12.5 +/- 1.0 for patients infected with HBV and HCV, respectively. Both were significantly higher than that (10 +/- 0.9) of patients without hepatitis infection. AST and ALT were significantly higher in patients infected with viral hepatitis than those without. The other biochemical parameters were not significant. Thirty-seven (38.5%) of our 96 patients had mild pruritus (PS < or = 7) and 11 (15.9%) had severe pruritus (PS > or = 15). Of the 83.9% (26/31) patients with viral hepatitis, the grades of skin itching were moderate to severe; whereas those of the patients without viral hepatitis, 53.6% (37/69) belonged to the group of moderate to severe pruritus (p = 0.003, chi 2 test with Yates' correction). The authors recommended screening of viral hepatitis infection to be undertaken for uremic patients with unexplained skin itching.
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PMID:Viral hepatitis infection should be considered for evaluating uremic pruritus in continuous ambulatory peritoneal dialysis patients. 968 Nov 57

Recombinant human interferon alpha (alpha IFN) is the only treatment with proven benefit for chronic hepatitis C virus (HCV) infection. Nevertheless its use in some susceptible individuals has led to the development or aggravation of different autoimmune conditions. We report the case of a 20 year old woman on peritoneal dialysis with chronic lobular hepatitis secondary to HCV infection who developed de novo psoriasis 9 months after starting treatment with alpha-IFN. In addition to psoriasis, alpha-IFN prescription was also concurrent with an unexpected and refractory secondary hyperparathyroidism exacerbation initially characterized by a marked reduction of serum calcium levels and a consequential increase of PTH. Both complications disappeared after drug withdrawal. The clinical sequence makes an alpha-IFN-induced autoimmune side effect the most plausible hypothesis. The case is discussed and some possible etiopathogenic factors are briefly reviewed.
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PMID:Secondary hyperparathyroidism exacerbation: a rare side-effect of interferon-alpha? 1023 May 58

The natural substrate cleaved by the hepatitis delta virus (HDV) ribozyme contains a 3',5'-phosphodiester linkage at the cleavage site; however, a 2',5'-linked ribose-phosphate backbone can also be cleaved by both trans-acting and self-cleaving forms of the HDV ribozyme. With substrates containing either linkage, the HDV ribozyme generated 2',3'-cyclic phosphate and 5'-hydroxyl groups suggesting that the mechanisms of cleavage in both cases were by a nucleophilic attack on the phosphorus center by the adjacent hydroxyl group. Divalent metal ion was required for cleavage of either linkage. However, although the 3',5'-linkage was cleaved slightly faster in Ca2+ than in Mg2+, the 2',5'-linkage was cleaved in Mg2+ (or Mn2+) but not Ca2+. This dramatic difference in metal-ion specificity is strongly suggestive of a crucial metal-ion interaction at the active site. In contrast to the HDV ribozymes, cleavage at a 2',5'-phosphodiester bond was not efficiently catalyzed by the hammerhead ribozyme. The relaxed linkage specificity of the HDV ribozymes may be due in part to lack of a rigid binding site for sequences 5' to the cleavage site.
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PMID:Ribozyme cleavage of a 2,5-phosphodiester linkage: mechanism and a restricted divalent metal-ion requirement. 1049 15

Tumor necrosis factor (TNF) induces hepatitis when injected in human beings or in rodents. The molecular mechanism by which TNF induces hepatic distress remains largely unknown, although induction of apoptosis of hepatocytes appears to be an essential step. In order to increase the therapeutic value of TNF, we have studied the protective activity of several molecules and found that four chemically totally different substances confer significant protection in the model of TNF-induced lethal hepatitis in mice sensitized with D-(+)-galactosamine (GalN), but not in mice sensitized with actinomycin-D (ActD) or against anti-Fas-induced lethal hepatitis. Verapamil, a calcium-channel blocker, tannic acid, picotamide, a thromboxane A(2) receptor antagonist, and K76COOH, an inhibitor, amongst others, of complement, protected significantly against induction of lethality, release of the liver-specific enzyme alanine aminotransferase (ALT) and induction of apoptosis in the liver after TNF/GalN, except for K76COOH, which paradoxically increased ALT values after challenge, and which also protected against TNF/GalN in complement-deficient mice. The data suggest that activation of platelets and neutrophils, as well as induction of inflammation occur in the TNF/GalN model, but not in the TNF/ActD or anti-Fas models, in which direct induction of apoptosis of hepatocytes may be more relevant. The protective activity of the drugs may lead to an increase in therapeutic value of TNF.
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PMID:Tumor necrosis factor-induced lethal hepatitis: pharmacological intervention with verapamil, tannic acid, picotamide and K76COOH. 1067 38

The efficiency of some polysaccharides was investigated in mice with an experimental toxic hepatitis. Hepatitis was induced by the oral administration of 10% solution CCl4 in olive oil at a dosage of 3 ml/kg body weight every day during 7 days. After that tested substances were administrated every day 30-40 min before a feeding at a dosage of 150 mg/kg body weight during 14-21 days. Results showed that a calcium alginate, two low-methoxyl pectins (one with the degree of esterification about 50% and other with the degree of esterification less 5%), fucoidan, and chitozan, but not lambda-carrageenan and kappa-carrageenan, have beneficial affects on liver total lipid, glycogen, malondialdehyde, and diene conjugates as well as on blood total lipid and alanine aminotransferase activity in animals with experimental toxic hepatitis.
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PMID:[Effectiveness of dietary non-starch polysaccharides in experimental toxic hepatitis]. 1094

This report presents a 46-year-old man who was treated for hypertension with the angiotensin-converting-enzyme (ACE) inhibitor enalapril. After 3 years of continuous treatment he presented with jaundice and progressive liver failure that continued despite withdrawal of the medication. The patient was taking no other medication. All known causes of acute liver failure could be excluded indicating a drug-induced liver damage after long-term treatment with enalapril. Analysis of liver biopsies revealed a pathomorphological pattern comparable to than observed in severe halothane hepatitis. Serological studies including T-cell stimulation with enalapril and a broad spectrum of tests for autoimmunity including autoantibodies against calreticulin, the major Ca2+ and Zn2+ binding protein of the endoplasmic reticulum and suggested to be involved in the pathogenesis of halothane hepatitis were negative. Thus, the mechanism of enalapril-induced liver injury remains obscure. Liver failure progressed and finally led to orthotopic liver transplantation. To our knowledge, this is the longest duration of chronic treatment with an ACE inhibitor before liver failure occurred. In addition, liver failure progressed despite withdrawal of the medication. It is concluded that even after long-term treatment with an ACE inhibitor liver failure may be induced. Therefore, regular monitoring of liver enzymes should be considered.
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PMID:Acute liver failure due to enalapril. 1114 78

Simvastatin, a hydroxymethyl glutarate coenzyme A (HMG-CoA) reductase inhibitor, is a commonly used cholesterol lowering agent. The long-term safety profile of simvastatin, established over ten-years of clinical use, is excellent. Both rhabdomyolysis and hepatitis, however, are recognized toxic effects of this medication, and generally occur when the patients are taking more than 40 mg of simvastatin a day. Potent inhibitors of the cytochrome P450 3A4 (CYP3A4) enzyme increase the incidence of simvastatin toxicity. Calcium channel blockers are weak inhibitors of the CYP3A4 enzyme. Diltiazem is known to increase the serum concentration of simvastatin. Many patients who take both simvastatin and diltiazem require lower doses of simvastatin to achieve the recommended reduction in cholesterol. Since diltiazem is known to increase plasma levels of lovastatin, a similar phenomenon may occur with simvastatin. Our patient had been stable for three years on simvastatin therapy. His rhabdomyolysis and hepatitis coincided with the addition of diltiazem. This is the first report of the combined toxicities of rhabdomyolysis and hepatitis being induced by the addition of diltiazem to simvastatin therapy. This patient serves as a reminder to the clinician of the potential interaction of these two commonly used drugs.
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PMID:Simvastatin-diltiazem drug interaction resulting in rhabdomyolysis and hepatitis. 1155 Apr 1


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