Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of antioxidant defense enzymes and lipid peroxidation (LPO) was studied in the liver and blood of 126 patients with hepatobiliary diseases. The activity of superoxide dismutase (SOD) and catalase in the liver appeared inhibited and relevant interactions impaired. Catalase/peroxidase value in hepatic cirrhosis proved minimal. In response to hepatotropic drugs red cell SOD decreased, while glutathione and ceruloplasmin levels became elevated. Blood LPO values were adequate indicators of the disease progression. It is shown that deficient antioxidant defense of the liver in chronic affections contributes to oxygen radical formation which promotes pathological processes in the liver.
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PMID:[The clinical significance of the enzymatic system utilizing active forms of oxygen in chronic liver diseases]. 801 35

The clinicopathologic relevance of the hepatic expression of Lewis Y (Le(y)), a carbohydrate antigen, and its plasma levels was studied in benign and malignant liver diseases. Tissue and plasma antigens, respectively, were determined with an avidin-biotin-peroxidase complex method and a radioimmunoassay using monoclonal antibody AH6. Normal liver cells and bile ductules did not express Le(y). In the inflammatory tissues, the liver cells and proliferated bile ductules expressed Le(y). The strongest expression by the liver cells was observed in chronic active hepatitis with severe activity and that by the ductules in liver cirrhosis. Only 1 of 16 hepatocellular carcinomas expressed Le(y). The plasma levels of Le(y) increased significantly but nonspecifically in chronic persistent hepatitis, chronic active hepatitis, liver cirrhosis, and hepatocellular carcinomas. It was concluded that (1) Le(y) is an inflammation-associated but not a cancer-associated antigen; (2) the more the tissue damage advances, the more the antigen is expressed; and (3) hepatic and plasma Le(y) are, however, nonspecific markers of necroinflammatory liver diseases.
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PMID:Hepatic neoexpression and increased plasma levels of Lewis Y, a carbohydrate antigen, in chronic inflammatory liver diseases. 804 85

Plasma myeloperoxidase levels in patients with cirrhosis were compared with those in patients with chronic hepatitis and healthy controls by means of a specific radioimmunoassay for myeloperoxidase. The mean concentration of plasma myeloperoxidase in cirrhotic patients (309.1 +/- 17.2 ng/ml, n = 41) was markedly higher than that in chronic hepatitis patients (222.6 +/- 17.2 ng/ml, n = 21) (p < 0.01) and normal controls (219.5 +/- 5.7 ng/ml, n = 50) (p < 0.01). Plasma myeloperoxidase showed good negative correlations with neutrocyte count (r = -0.32, p < 0.01), thrombocyte count (r = -0.40, p < 0.01), red blood cell count (r = -0.32, p < 0.01), serum albumin (r = -0.35, p < 0.01), and cholinesterase (r = -0.32, p < 0.02) and positive correlations with serum alkaline phosphatase (r = 0.49; p < 0.01) and lactate dehydrogenase (r = 0.31, p < 0.01) in patients with cirrhosis or chronic hepatitis. Among lactate dehydrogenase isozymes, a good positive correlation was seen between plasma myeloperoxidase and lactate dehydrogenase-2 (r = 0.40, p < 0.01) and lactate dehydrogenase-1 (r = 0.03, p < 0.02). Plasma myeloperoxidase was significantly higher in the cirrhotic and chronic hepatitis patients with splenomegaly (341.1 +/- 19.4 ng/ml, n = 31) than in those without splenomegaly (217.4 +/- 12.2 ng/ml, n = 29) (p < 0.01). We also examined the difference between plasma levels of myeloperoxidase in the portal and peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High plasma concentration of myeloperoxidase in cirrhosis: a possible marker of hypersplenism. 824 62

To evaluate the diagnostic significance of neutrophil cytoplasmic antibodies in chronic liver diseases, we assessed the prevalence of neutrophil cytoplasmic antibodies in autoimmune liver diseases, in particular in primary sclerosing cholangitis, autoimmune chronic active hepatitis and primary biliary cirrhosis, and we also determined the specificity of perinuclear-pattern neutrophil cytoplasmic antibodies for these autoimmune liver diseases by testing sera from patients with nonautoimmune chronic liver diseases. Neutrophil cytoplasmic antibodies were detected in 79% of sera from patients with primary sclerosing cholangitis (n = 24), in 88% of sera from patients with autoimmune chronic active hepatitis (n = 24) and in 28% of sera from patients with primary biliary cirrhosis (n = 25). The presence of neutrophil cytoplasmic antibodies in these diseases correlated significantly (p < 0.008) with the presence of cirrhosis. Neutrophil cytoplasmic antibodies were not detected in nonautoimmune liver diseases. All neutrophil cytoplasmic antibody-positive sera produced a perinuclear fluorescence pattern on ethanol-fixed granulocytes. On neutrophils fixed with paraformaldehyde, a granular cytoplasmic immunofluorescence pattern was observed, demonstrating the cytoplasmic nature of the antigen or antigens involved. Further characterization studies showed that neutrophil cytoplasmic antibodies in autoimmune liver diseases are not directed against myeloperoxidase, proteinase 3 or elastase, the neutrophil cytoplasmic antibody specificities associated with necrotizing vasculitis, glomerulonephritis or both. On Western blots neutrophil cytoplasmic antibodies in autoimmune liver diseases showed reactivity with either lactoferrin, a 67/66-kD protein combination or a 40-kD polypeptide. Reactivity with either of these proteins was observed in sera from patients with primary sclerosing cholangitis (38%), autoimmune chronic active hepatitis (17%) and primary biliary cirrhosis (20%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence and characterization of neutrophil cytoplasmic antibodies in autoimmune liver diseases. 844 14

We have assessed the effect of the oral ingestion of thioacetamide on small intestine structure and function. Thioacetamide-treated rats showed diminished mucosa weight; protein, DNA, and RNA content; and leucine aminopeptidase activity as compared to controls in both jejunum and ileum. In the jejunum, there was a reduction in the activities of alkaline phosphatase, ATPase, glucose-6-phosphatase, and myeloperoxidase, whereas in the ileum, maltase, lactase, and gamma-glutamyltranspeptidase were reduced. In both jejunum and ileum we found enlarged intercellular spaces, dark epithelial enterocytes, and lymphocyte infiltration. Enterocytes showed lobulated nuclei, deranged mitochondria with loss of their cristae, dilated rough endoplasmic reticulum containing dense material, and vesiculation of the smooth endoplasmic reticulum and the Golgi apparatus. Smooth muscle cells of the intestine exhibited ultrastructural alterations. These findings indicate that chronic oral intake of thioacetamide mimics not only hepatic alterations but also small intestine alterations normally associated with human cirrhosis.
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PMID:Hepatotoxic agent thioacetamide induces biochemical and histological alterations in rat small intestine. 928 39

We developed a new, highly sensitive enzymatic method for quantifying creatine in erythrocytes, which comprises creatine amidinohydrolase, sarcosine oxidase, and peroxidase. In the present method, an N-methylcarbamoyl derivative of methylene blue, 10-N-methylcarbamoyl-3,7-bis(dimethylamino)phenothiazine (MCDP), was used as a sensitive chromogenic compound. Potassium ferrocyanide was used to prevent nonspecific oxidation of MCDP. The enzymatic method exhibited good analytical performance: precision, within-run CVs <1.0% and between-day CVs <2.0%; average analytical recovery, 99.3% +/- 1.8%; detection limit, 1.0 micromol/L in hemolysate; and linearity, at least up to 500 micromol/L as creatine concentration in hemolysate. Excellent agreement was observed between the present method (y) and HPLC (x), y = 1.029x - 0.002 micromol/g hemoglobin, r = 0.9998, S(y/x) = 0.053 micromol/g hemoglobin (n = 110). No significant interference was produced by various compounds, including guanidino compounds, amino acids, and reducing materials. The reference intervals (mean +/- 2 SD) for erythrocyte creatine obtained from 60 males and 60 females were (in micromol/g hemoglobin) 1.18 +/- 0.52 (0.66-1.70) for males and 1.35 +/- 0.49 (0.86-1.84) for females. Using this method, we documented changes in erythrocyte creatine in patients with various hemolytic conditions, including hemolytic anemia, liver cirrhosis, renal insufficiency, and chronic renal failure treated with hemodialysis with or without the administration of erythropoietin. We conclude that the use of MCDP allows sensitive measurement of erythrocyte creatine and that MCDP with potassium ferrocyanide can improve the sensitivity of assays that use peroxidase for detection of H2O2.
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PMID:Sensitive enzymatic assay for erythrocyte creatine with production of methylene blue. 966 28

Anti-neutrophil cytoplasmic antibodies (ANCA) are autoantibodies directed against cytoplasmic constituents of neutrophil granulocytes. Antibodies with specificity for proteinase 3 and myeloperoxidase are seromarkers for systemic vasculitides. ANCA with specificity for lactoferrin were described in patients with several idiopathic inflammatory diseases, such as the inflammatory bowel diseases and rheumatoid arthritis. However, the clinical significance of anti-lactoferrin autoantibodies is still unclear. In this study, we determined the clinical significance of anti-lactoferrin autoantibodies in sera from large groups of patients with ulcerative colitis (UC), Crohn's disease (CD), and primary sclerosing cholangitis (PSC). Antibodies to human lactoferrin were detected by ELISA and by immunoblotting, using an extract of sonicated neutrophils as antigen source. Autoantibodies to lactoferrin were found in 29% of patients with UC, 13% of patients with CD, and 22% of patients with PSC. In inflammatory bowel diseases, the presence of anti-lactoferrin antibodies was not related to treatment, disease activity, duration of disease, or disease extent. In PSC, the presence of autoantibodies to lactoferrin did not correlate with duration of disease or the presence of cirrhosis. However, patients with PSC and coexistent UC had significantly more frequently antibodies to lactoferrin than PSC patients without IBD. In conclusion, autoantibodies to lactoferrin are a common feature of inflammatory bowel diseases and PSC. However, the clinical significance of those autoantibodies is limited as they lack sensitivity and specificity for those disorders. Future research should address the pathophysiological role of anti-lactoferrin ANCA and the influence of anti-lactoferrin ANCA binding on the functional properties of the lactoferrin molecule.
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PMID:Prevalence and clinical significance of anti-lactoferrin autoantibodies in inflammatory bowel diseases and primary sclerosing cholangitis. 978 75

The activity of the enzymatic activity of the preparations of IgG1, IgG2 and IgG4, isolated from the blood of patients with acute virus hepatitis B and chronic viral hepatitis C resulting in cirrhosis, was studied. The blood samples were found to have DNAase activity significantly exceeding that of immunoglobulins isolated from the blood sera of healthy donors, as well as peroxidase, oxidase and esterase activities, whose level did not significantly differ from those of the donor blood sera. The interaction of IgG preparations with the cations of different metals was studied. The study revealed that the addition of CuSO4 solution at the final concentration of 4.7 x 10(-5) M to the blood samples led to a significant increase in activity in comparison with the initial one (on the average, 7.8 +/- 2.97 times) in all 14 samples. The activity thus observed was partially inhibited by the addition of the solution of staphylococcal protein A. As noted in the course of this study, high DNAase and peroxidase activities of Ig were most frequently observed in patients with cirrhosis of the liver. The difference in the levels of IgG activity between patients with cirrhosis of the liver and patients with virus hepatitis, but no signs of cirrhosis, is not significant.
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PMID:[The enzymatic activity of IgG preparations in viral hepatitis]. 978 8

The chronic alcoholic patient is usually immunosuppressed, but the significance of this phenomenon in terms of bile duct injury is unclear. The immunoreactivity of the bile duct cells was examined in a series of 69 frozen liver biopsy specimens obtained from patients with alcoholic liver disease, comprising 29 cases of cirrhosis, 26 of alcoholic hepatitis, 10 cases of alcoholic fatty liver, and 4 specimens from normal livers. Liver diseases such as primary biliary cirrhosis and human hepatic allograft rejection, known to have an autoimmune basis, share the characteristic feature of damage to the bile duct epithelial cells. In both instances the damage seems to be immune mediated, but the nature of the antigens involved is not established. We used the avidin-biotin-peroxidase complex method to test in alcoholic liver disease for the expression of a battery of surface antigen markers that have been incriminated in tissue injury and are usually present in lymphoid cells but also expressed by epithelium. In this study we investigated the expression of the following molecules: HLA class I (ABC) and class II (HLA-DR, HLA-DP, HLA-DQ), CD29, CD45RA, CD45RO, CD56, interleukin 1 (IL-I), IL-2, IL-4, interferon (IFN-gamma), tumor necrosis factor beta, and transforming growth factor beta1 (TGF-beta1). The bile duct epithelial cells strongly expressed HLA-ABC in all cases, CD56 in 47 of 55, IL-4 in 15 of 41, TGF-beta1 in 14 of 25, and CD29 in 4 of 25 cases. The other markers including IFN-gamma, HLA-DR, HLA-DP, and HLA-DQ were not expressed by bile duct cells. The expression of HLA class I agrees with previous observations while the absence of class II expression does not. The expression by the bile duct epithelium of CD56 confirms our own previous report. A new observation is the finding of molecules such as IL-4, TGF-beta1, and CD29 strongly expressed in the bile ducts cells. The presence of these molecules, taken together with the lack of IFN-gamma expression, contradicts previous speculations that attributed to IFN-gamma a role in the induction of major histocompatibility antigens and adhesion molecules in immune-mediated alcoholic liver disease.
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PMID:The antigenic heterogeneity of the bile duct epithelium in alcoholic liver disease. VA Cooperative Study Group 275. 1023 99

Oxidative damage to tissue proteins has been implicated in the pathogenesis of liver disease, but the mechanisms that promote oxidation in vivo are unclear. Hydrogen peroxide is transformed into an array of potentially damaging reactants by the heme protein myeloperoxidase. This proinflammatory enzyme is expressed by circulating neutrophils and monocytes but is generally thought to be absent from tissue macrophages. To determine whether myeloperoxidase is present in Kupffer cells, the fixed-tissue macrophages of liver, Western blot analysis, and immunohistochemistry were performed. Two different antibodies monospecific for myeloperoxidase identified a 60-kd protein, the predicted molecular mass of myeloperoxidase, in human liver extracts. Immunostaining detected the enzyme in sinusoidal lining cells of normal and diseased human livers. Immunofluorescence confocal microscopy demonstrated co-localization of myeloperoxidase and CD68, a monocyte/macrophage marker, in sinusoidal lining cells. Numerous myeloperoxidase-expressing cells were also evident in the fibrous septa of cirrhotic livers. Immunostaining with an antibody to proteins modified by hypochlorous acid, a characteristic product of the enzyme, indicated that myeloperoxidase is enzymatically active in cases of acute liver injury and cirrhosis. These findings identify myeloperoxidase as a component of human Kupffer cells. Oxidative damage resulting from the action of myeloperoxidase may contribute to acute liver injury and hepatic fibrogenesis.
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PMID:Immunohistochemical detection of myeloperoxidase and its oxidation products in Kupffer cells of human liver. 1173 58


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