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 extractable and nonextractable collagen and glycosaminoglycuronans (GAG) were estimated and characterized in 32 dried, defatted human livers obtained at necropsy. 10 had normal livers. 22 of the 32 livers were from patients who drank in excess: 5 had fatty livers, 7 had alcholic hepatitis, and 10 had cirrhosis. Livers with alcoholic hepatitis or cirrhosis had significantly increased total and 1 N NaCl-extractable collagen. Only alcoholic hepatitis livers had significantly increased Tris-buffer-extractable GAG, but the amino acid composition of these GAG (proteoglycans) was no different from that of normal livers. The major fraction of these GAG had isoelectric pH (pI) </= 3.1 in all livers. Livers with alcoholic hepatitis or cirrhosis had significantly increased nonextractable GAG. The major GAG fraction of all livers was chondroitin-4 or -6-SO(4). Alcoholic hepatitis livers had a significant increase of hyaluronic acid and an unidentified hyaluronidase-resistant GAG. Fatty livers showed no differences from normal ones. The data indicates that alcoholic hepatitis is associated with a significantly increased fibroblast activity, but fatty livers of alcoholics are not. The changes in histologically "inactive" micronodular cirrhosis of alcoholic patients indicate continued activity of fibroblasts in the connective tissue of these cirrhotic livers.
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PMID:Natural history of alcoholic hepatitis. IV. Glycosaminoglycuronans and collagen in the hepatic connective tissue. 427 Jun 46

Antithrombin III is of potential value for replacement therapy in patients with acquired or congenital deficiencies. Pasteurization of the purified inhibitor for 10 h at 60 degrees C can reduce the risk of transfusion hepatitis. Addition of appropriate stabilizers can largely prevent the loss of antithrombin activity which otherwise occurs during pasteurization. Studies of the mechanism of denaturation and stabilization have been facilitated by the use of 8-anilino-1-naphthalene sulfonate which binds weakly to the inhibitor and whose fluorescence undergoes a sigmoidal response to increasing temperature. The extent of the increase in 8-anilino-1-naphthalene sulfonate fluorescence correlates roughly with the loss of antithrombin activity and with the extent of protein aggregation as determined by high pressure liquid chromatography. The midpoint, Td, of the thermal denaturation curve increases by 13 degrees C and 19 degrees C in the presence of 0.5 M and 1.0 M sodium citrate, respectively. Phosphate, sulfate, and EDTA are also strong stabilizers while the chaotropic anions, iodide and thiocyanate are potent destabilizers. Heparin at 10 mg/ml increases Td by 7 degrees C, presumably through a direct binding mechanism; chondroitin sulfate and hyaluronic acid have no effect. Samples pasteurized for 10 h at 60 degrees C in the presence of 0.5 M and 1.0 M citrate retain essentially full activity but exhibit evidence of minor alterations in their interaction with heparin.
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PMID:Thermal denaturation of antithrombin III. Stabilization by heparin and lyotropic anions. 729 49

We have established reference ranges for the concentrations of hyaluronic acid in serum from 397 infants and children and measured serum hyaluronic acid at presentation and 1 year follow-up in 37 infants who presented with hepatobiliary disease in the first 6 months of life. In health, hyaluronic acid concentrations fell progressively from median (10-90 percentile) values of 93 micrograms/l (49-153) at 1-3 months of age to 20 micrograms/l (9-40) at 2-3 years and 16 micrograms/l (6-32) at 4-18 years. In patients at presentation, the hyaluronic acid concentration was raised in 11 of 15 with biliary atresia, 6 of 11 with alpha-1 antitrypsin deficiency and 6 of 11 with cryptogenic hepatitis of infancy. One year later, the 9 patients who developed progressive liver disease showed 2-6-fold increases in hyaluronic acid concentration while no increase was observed in the 28 with undetectable or mild disease. Increases in serum hyaluronic acid concentration appeared to be a better indicator of progressive liver disease in infancy than standard laboratory tests.
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PMID:Serum hyaluronic acid in healthy infants and children and its value as a marker of progressive hepatobiliary disease starting in infancy. 851 66

It has been reported that serum hyaluronate [hyaluronic acid (HA)] concentrations are increased in liver diseases, especially in alcoholic liver disease (ALD). However, the characteristics of serum HA concentration in patients with ALD have not been studied. In this study, first, we measured serum HA concentrations in patients with different stages of both ALD and non-ALD to clarify the characteristics of serum HA concentration in patients with ALD. Second, we measured serum HA concentrations in patients with ALD sequentially after abstinence. We also measured serum HA concentrations in patients with chronic type C hepatitis before and after treatment with interferon. Finally, we analyzed the relationship between serum HA concentrations and the contents of type IV collagen and laminin in the livers of both ALD and non-ALD patients. Serum HA concentrations in liver disease were higher than the cut-off value, and increased significantly (p < 0.001) in parallel with the progression of hepatic fibrosis in both ALD and non-ALD patients. Serum HA concentrations in patients actively drinking with ALD were significantly higher (p < 0.001) than those in non-ALD. After 4 weeks of abstinence, these concentrations fell to the levels of non-ALD. Although serum ALT levels were decreased in 80% of patients treated with interferon, serum HA concentrations were not changed or increased. A significant correlation between serum HA concentrations and hepatic type IV collagen and laminin content was present in ALD, but not in non-ALD. These results clearly suggest that the increase of serum HA concentrations in ALD may be associated with not only hepatic fibrosis, but also alcohol drinking.
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PMID:Characteristics of serum hyaluronate concentrations in patients with alcoholic liver disease. 943 36

We observed six cases of haemophiliacs with HIV-induced immunodeficiency who died from fatal liver failure despite the absence of evident cirrhosis. They all had the infection with hepatitis viruses (two patients with hepatitis B and D viruses and four patients with hepatitis C virus) and their CD4 counts were severely decreased. They were much younger than cirrhotic haemophiliacs without HIV. Their serum levels of hyaluronic acid and type IV collagen were lower than those in haemophiliacs with cirrhosis, and were normal. No patients had experienced symptoms or concomitant diseases characteristic of cirrhosis, such as ascites, jaundice, oesophageal/gastric varices or hepatocellular carcinoma, except for one case who had a history of mild ascites. The characteristics of this liver failure were different from liver failure resulting from cirrhosis caused by chronic hepatitis, which suggests liver failure that is specific to patients with immunodeficiency. This kind of liver failure can be a factor threatening survival in patients with HIV infection and with hepatitis virus co-infection in an immunodeficient state.
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PMID:Fatal liver failure in haemophiliacs with HIV-induced immunodeficiency: observation of six patients. 1021 59

Although intra-operative hyaluronic acid (HA) clearance has been reported to be a predictive parameter for early graft function after the implantation of a cadaveric hepatic graft, it has yet to be evaluated as a parameter in assessing graft function in living related liver transplantation. The aim of this study was to evaluate whether intra-operative HA clearance can be a predictive parameter of early graft function in living related liver transplant patients. Eight consecutive patients, who underwent a living related liver transplantation, were entered into the study. The HA clearance 180 min after reperfusion of the graft was evaluated. Significantly higher serum HA levels were found in the patients with fulminant hepatitis than in the patients with non-fulminant hepatitis before operation (P < 0.01), just before reperfusion (P < 0.01), and 180 min after reperfusion (P < 0.05). The HA clearance correlated with the peak total bilirubin within 5 postoperative days (P < 0.05) and the lactic acid one day after operation (P < 0.01). The intra-operative HA clearance serves as a sensitive parameter for assessing the postoperative graft function after the implantation of the new liver. Based on our findings, measuring the HA clearance was thus found to be clinically useful in the assessment of graft function in living related liver transplantation.
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PMID:Intra-operative hyaluronic acid clearance predicts postoperative graft function in living related liver transplantation. 1053 89

Serum levels of hyaluronic acid (HA) and tumor necrosis factor alpha (TNF alpha) in 94 patients with various liver diseases and 31 healthy controls were studied by RIA, Serum TNF alpha in hepatitis, liver cirrhosis (LC) and primary hepatic carcinoma (PHC) was higher than that of the control. Serum HA in chronic hepatitis, LC and PHC was higher than that in the control. The serum level of HA showed a positive correlation with the serum level of TNF alpha. It is considered that the increase of serum HA indicates an early fibrogenic tendency in patients with liver diseases. TNF alpha is involved in the formation of hepatic fibrosis.
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PMID:[The clinic significance of serum hyaluronate and tumor necrosis factor alpha levels in liver diseases]. 1068 11

Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.
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PMID:Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice. 1152 40

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

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


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