UMLS:C0019158 - FACTA Search

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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indian childhood cirrhosis (ICC), endemic Tyrolean infantile cirrhosis (ETIC) and idiopathic copper toxicosis (ICT), are clinically and pathologically indistinguishable liver disorders of infants and young children linked with exogenous copper and with increasing evidence for a genetic predisposition. North Ronaldsay sheep are a primitive breed which have adapted to a copper impoverished environment (<5 ppm) and display an abnormal sensitivity to copper poisoning when transferred to a copper replete (11 ppm) habitat. The aetiological parallels prompted a study of copper-associated liver disease in North Ronaldsay sheep (RCT) to see if the pathology could contribute to the understanding of the childhood disorder. A retrospective study was performed in which the livers of 22 mainland-bred North Ronaldsay sheep were compared with three island-bred sheep and categorized for liver copper content and pathomorphology. It was found that all the mainland sheep had accumulated liver copper (>300 microg/g), in contrast to the island sheep, although 10 sheep with increased liver copper (mean 600 SD 270 microg/g) showed no evidence of liver damage. A further 10 sheep with liver copper (mean 1276 SD 508 microg/g) exhibited periportal to panlobular histochemical copper retention, a periportal and/or panlobular pericellular fibrosis, a mixed inflammatory infiltrate and cholangioplasia. Steatosis was absent and regeneration was in abeyance. Finally, two sheep (liver copper >2000 microg/g) had a more active hepatitis with a florid pericellular, panlobular fibrosis and cirrhosis. Electron microscopy identified large numbers of collagen-producing hepatic stellate (Ito) cells in periportal regions. The pathological findings were sufficiently reminiscent of ICC, ETIC and ICT to warrant further exploration of RCT as a putative animal model. The North Ronaldsay sheep liver may be a useful tool for the investigation of copper-induced fibrogenesis.
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PMID:Copper-associated liver disease in North Ronaldsay sheep: a possible animal model for non-Wilsonian hepatic copper toxicosis of infancy and childhood. 1159 8

An 81-year-old male patient developed hepatic fibrosis with ascites and esophageal varices 4 years after oral administration of UFT(R) as postoperative adjuvant therapy for lung cancer. Although serum transaminase levels remained normal during follow-up periods, ascites developed 3 years after the treatment, and disappeared rapidly after the cessation of UFT(R), but recurred by accidental readministration of UFT(R). Serum markers for hepatitis viruses, various auto antibodies and a history of alcoholic abuse were all negative. Liver biopsy showed mild to moderate hepatic fibrosis without hepatocellular necrosis. Serum levels of N-terminal propeptide of type III procollagen, 7S fragment of type IV collagen and hyaluronic acid were elevated at diagnosis and decreased after the discontinuation of UFT(R). Esophageal varices were also improved. These findings suggest that hepatic fibrosis can be induced by oral administration of UFT(R) and that serum fibrogenesis/fibrosis markers are useful for early diagnosis of UFT(R)-induced hepatic fibrosis.
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PMID:A case with hepatic fibrosis showing ascites and esophageal varices induced by oral UFT(R) administration. 1181 56

Lamivudine was administrated to six patients with acute exacerbation of hepatitis B who were undergoing immunosuppressive therapy. All patients had chronic hepatitis B and were receiving immunosuppressive therapy for other primary diseases (hematologic malignancies, collagen diseases, renal transplantation) when the hepatitis flared up. Only one patient tested positive for the hepatitis B virus e (HBe) antigen. All patients had normal ALT levels and were anti-HBe-positive before immunosuppressive therapy. The patients were treated with 150 mg of lamivudine daily. Lamivudine was well tolerated and showed no effect on the primary disease. In all patients, hepatitis B virus (HBV) DNA levels decreased in response to lamivudine administration. Four patients recovered from exacerbation, but two patients died from complications. Molecular analysis revealed that, regardless of whether patients had the wild HBV genotype or mutations within the core promoter or precore HBV regions, the effectiveness of lamivudine therapy was the same. These results demonstrated that lamivudine is very effective for treating acute exacerbation of chronic hepatitis B that occurs while a patient is undergoing immunosuppressive therapy, regardless of the phenotype of the virus.
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PMID:Lamivudine treatment for acute exacerbation of hepatitis B in patients undergoing immunosuppressive therapy. 1188 19

The contents of serum Type IV collagen and laminin were detected by radioimmunoassay and the diameters of portal veins were measured by B-mode ultrasound in 102 patients with different type of viral hepatitis. The results show that an increase of levels of Type IV collagen and laminin was found in patients with chronic severe hepatitis and fulminant hepatitis. The levels of Type IV collagen and laminin were obviously increased in the patients who have the diameter of portal vein > or = 12 mm compared with the patients who have the diameter of protal < 12 mm. There was a positive correlation between the levels of Type IV collagen, laminin and the diameters of portal vein.
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PMID:[Correlative study on the level of serum type IV collagen, laminin and the diameters of portal veins in patients with viral hepatitis]. 1201 6

Liver fibrosis is a prepathological state wherein damaged liver tissues in chronic liver diseases, such as hepatitis, are not repaired to normal tissues, but converted to fibrous tissue. 5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione (oltipraz), a cancer chemopreventive agent, is effective against a wide variety of chemical carcinogens. Recently, we reported that oltipraz inhibits liver fibrogenesis (Kang et al., 2002). In the present study, the effects of oltipraz in combination with dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene dioxybiphenyl-2,2'-dicarboxylate (DDB) on dimethylnitrosamine (DMN)-induced liver fibrogenesis were assessed in rats. Oltipraz (30 mg/kg body weight, p.o., 3 times per week for 4 weeks) was found to inhibit the increases in plasma ALT, AST and bilirubin by DMN, whereas DDB (30 mg/kg body weight, p.o., 3 times per week for 4 weeks) attenuated the increases in the plasma ALT and bilirubin. The lowered plasma protein and albumin contents in DMN-treated rats were completely restored by oltipraz, but not by DDB. DDB decreases liver cell injury and inflammation through inhibition of nuclear factor-kB. DMN increased the accumulation of liver collagen, as indicated by the increase in the 4-hydroxyproline content in liver homogenates, which was reduced by treatment with oltipraz, but not by DDB. Given the differential effect between oltipraz and DDB, the potential enhancement of antifibrotic efficacy by the drugs was assessed in the animal model. Despite the minimal effect of DDB on DMN-induced fibrogenesis, DDB (5-25 mg/kg), administered together with oltipraz (25-5 mg/kg), showed an additive protective effect against hepatotoxicity and fibrosis induced by DMN, which was shown by the blood chemistry parameters and histopathological analysis. The adequate composition ratio of oltipraz to DDB was 5:1. These results provide information on the pharmaceutical composition, comprising of oltipraz and DDB as the active components, for the treatment and/or prevention of liver fibrosis and cirrhosis.
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PMID:The anti-fibrogenic effect of a pharmaceutical composition of [5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione] (oltipraz) and dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene dioxybiphenyl-2,2'-dicarboxylate (DDB). 1243 1

Liver fibrosis represents a major medical problem with significant morbidity and mortality. Worldwide hepatitis viral infections represent the major cause liver fibrosis; however, within the United States chronic ethanol consumption is the leading cause of hepatic fibrosis. Other known stimuli for liver fibrosis include helminthic infection, iron or copper overload and biliary obstruction. Fibrosis can be classified as a wound healing response to a variety of chronic stimuli that is characterized by an excessive deposition of extracellular matrix proteins of which type I collagen predominates. This excess deposition of extracellular matrix proteins disrupts the normal architecture of the liver resulting in pathophysiological damage to the organ. If left untreated fibrosis can progress to liver cirrhosis ultimately leading to organ failure and death if left untreated. This review will discuss the molecular events leading to liver fibrosis. The discussion will include collagen gene regulation and proliferative signals that contribute to the amplification of the hepatic stellate cell, the primary fibrogenic cell type that resides in the liver.
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PMID:Liver fibrosis: signals leading to the amplification of the fibrogenic hepatic stellate cell. 1245 23

We investigated the incidence of recurrence after resection of small hepatocellular carcinomas (HCC) in patients infected with hepatitis C virus (HCV) to determine the appropriate surgical management of these patients. Sixty-one patients with anti-HCV antibody who underwent curative liver resection for small HCC (<or= 2.0 cm in greatest diameter) were categorized into two groups. Group 1 consisted of 27 patients with serum concentrations of type IV collagen 7S domain (7S collagen), a marker for hepatic fibrosis, < 8 ng/ml. Group 2 consisted of 34 patients with serum concentrations of 7S collagen >or= 8 ng/ml. Serum concentration of 7S collagen correlated with the severity of active hepatitis and the degree of fibrosis in the noncancerous hepatic tissue, both of which are related to risk potential of hepatocarcinogenesis. Serum concentration of total bilirubin, aspartate aminotransferase activity, indocyanine green retention rate at 15 minutes, the proportion of patients who were Child-Pugh class B, and the proportion of patients with severe active hepatitis or cirrhosis (determined by histologic examination) were significantly higher in group 2 than in group 1. Platelet count was significantly lower in group 2. Tumor-free survival rates were not different between the groups. In group 1, nonanatomic resection was a risk factor for recurrence by univariate and multivariate analyses (odds ratio = 3.45, p = 0.040). In group 2, nonanatomic resection was not a risk factor for recurrence. In patients with small HCV-related HCC, anatomic resection is recommended when the serum concentration of 7S collagen is low (< 8 ng/ml) because the potential of hepatocarcinogenesis may be low even after the operation.
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PMID:Appropriate surgical management of small hepatocellular carcinomas in patients infected with hepatitis C virus. 1265 89

Chronic hepatitis C virus (HCV) infection results in the development of liver fibrosis and cirrhosis in 20 to 25% of patients. The main task of the physician when examining a patient with a verified HCV infection is to identify the activity of inflammatory and necrotic processes in the liver, as well as the stage of fibrosis, and the reversibility of detected changes. Along with other clinical and laboratory parameters, this plays a major role in forecasting the course of hepatitis, as well as determines the therapeutic approach in each specific case. Liver biopsy remains the best way to assess the severity of chronic hepatitis C. The risk of developing cirrhosis depends on the stage (degree of fibrosis) and the grade (degree of inflammation and necrosis) observed in the initial liver biopsy. Non-invasive diagnostic approaches attempt to evaluate the serum markers of fibrogenesis. Biochemical markers of fibrosis scoring include thrombocyte counts, the prothrombin time, ratio of alaninaminotransferase (ALT) and aspartataminotransferase (AST) levels, the level of g-glutamyl transferase and the quantity of blood serum albumin. Another set of markers is based on the detection of molecular junctions that activate fibrosis, or participate in the generation of the liver extracellular matrix. The most applicable include hyaluronic acid (HA), type IV collagen (IV-C), N-terminal propeptide of type III procollagen (PIIIP), metalloproteinases (MMP), inhibitors of metalloproteinases (TIMP), and growth-transforming factor betta (GTFbeta). The review discusses the clinical significance of each of the criteria and possibility of their combination in the non-invasive monitoring of liver fibrosis.
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PMID:Invasive and non-invasive monitoring of hepatitis C virus-induced liver fibrosis: alternatives or complements? 1276 63

The special features of liver sinusoidal endothelium (LSE) are crucial for normal liver physiology. Cirrhotic livers, especially in primary biliary cirrhosis (PBC), are characterized by transformation of the LSE into a continuous, vascular type. The transformation is important for disease progression and explains some of the pathological hallmarks of the cirrhotic liver. Here, we investigated the presence of liver sinusoidal endothelial cell (LSEC)-reactive autoantibodies (Abs) in the sera of patients with autoimmune liver diseases, and assessed the ability of these Abs to transform LSE into vascular endothelium. Compared to healthy individuals (9%), significantly higher numbers of patients with PBC (59%; P < 0.001) and autoimmune hepatitis (AIH) (32%; P < 0.05) had Abs against LSECs. Incubation of primary LSEC cultures with F(ab')(2) fragments of anti-LSEC Abs isolated from sera of patients with PBC and AIH, induced 1) cell surface expression of vascular endothelium-associated markers, CD31, and factor VIII-related antigen; 2) significant production of fibronectin, laminin and collagen type IV; 3) loss of fenestrae, formation of tight junctions and Weibel-Palade bodies. Deposition of immunoglobulins on LSECs were found in liver biopsies of AIH and PBC patients. Thus, anti-LSEC autoAbs transform LSE into a vascular type and may therefore play an important role in the development of hepatocellular failure and portal hypertension in PBC and AIH patients.
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PMID:Capillarization of hepatic sinusoid by liver endothelial cell-reactive autoantibodies in patients with cirrhosis and chronic hepatitis. 1450 37

The extracellular matrix (ECM) expression is subject to distinct changes during ontogeny, and the natural course of liver fibrosis in neonates is thought to differ from that in adults. We compared the expression and distribution of main ECM components between neonatal and adult liver fibrosis. Liver biopsies from infants with neonatal cholestasis and fibrosis were compared to adult biopsies exhibiting an equivalent stage of fibrosis. All biopsies were examined by immunohistochemistry (indirect ABC method) for the ECM proteins, collagens I, III, IV, and VI, laminin, and fibronectin. Infants (aged 1-8 months) with neonatal hepatitis (n = 3), extrahepatic biliary atresia (EHBA) (n = 5), and normal histology (n = 2) were compared with 9 adults (aged 17-70 years) with chronic hepatitis (n = 3), primary biliary cirrhosis (PBC) (n = 4), and normal histology (n = 2). Collagens I, III, and IV and fibronectin were significantly increased in neonatal hepatitis with mild fibrosis (score < or = 4) compared to adults with an equivalent fibrosis stage. This increase was particularly notable in perisinusoidal spaces. Laminin expression was increased in portal and perisinusoidal spaces both in neonatal hepatitis and extrahepatic biliary atresia with mild fibrosis. In infants with moderate to severe fibrosis (score > or = 6), only collagen I was increased in comparison to adults, whereas collagen VI expression was identical in all groups, irrespective of the degree of fibrosis. Expression of matrix proteins was not different in infants and adults without fibrosis. The increased perisinusoidal deposition of certain ECM components in infants with active hepatitis and mild fibrosis may point to an underlying difference in the mechanism or stimulus of fibrogenesis in neonates as compared to adults.
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PMID:Divergent patterns of extracellular matrix protein expression in neonatal versus adult liver fibrosis. 1469 30

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