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)

HBsAg has been sought by light microscopy in liver specimens from patients with cirrhosis (79 cases) and hepatoma (99 cases). The study was carried out on fixed material using orcein staining, immunoperoxidase technique and indirect immunofluorescence. HBsAg was detected in the serum by radio-immunoassay (RIA) using Ausria II-125 in 38 patients with cirrhosis and in 36 with hepatoma. In the 38 seropositive cases of cirrhosis HBsAg-positive cells were observed in 31 (81.6%) by the orcein staining and in 32 (84.2%) by the peroxidase and immunofluorescence staining. Among the 36 seropositive patients with hepatoma, HBsAg was detected in the surrounding non-neoplastic part of the liver, cirrhotic or not, in 30 (83.3%) by orcein staining and in 34 (94.4%) by the immunoperoxidase method and immunofluorescence. Positive solitary-cells were seen occasionally in the tumor tissue in 16 cases using orcein, in 9 using peroxidase and in 7 by fluorescence, out of the 36 seropositive patients with hepatoma. The results of this study do not support the hypothesis of a direct oncogenic effect of HBsAg on the liver cells, since this antigen was detected mainly in the non-neoplastic part of the liver tissue and only occasionally in the tumor cells. Of the 63 cases of seronegative hepatoma, 3 showed some round orcein-positive inclusion bodies in the cytoplasm of the neoplastic and the non-neoplastic cells; these bodies were not stained by the two immunological methods.
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PMID:Detection of hepatitis B surface antigen in fixed tissues of patients with cirrhosis and hepatoma. 23 Jun 34

Electron microscopic findings made on microsomal fractions of rat liver after treatment with microsomal antibodies obtained from the blood of patients diagnosed as having chronic aggressive hepatitis and liver cirrhosis and after incubation with peroxidase-labelled antihuman IgG are described and presented in this paper. Interpretation of these findings as the substrate of an antibody reaction directed against membranes of the endoplasmic reticulum of hepatocytes is discussed.
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PMID:The immunoelectron-microscopical demonstration of antibodies against endoplasmic reticulum (microsomes) in chronic aggressive hepatitis and liver cirrhosis. 88 90

Peritoneal liver biopsy specimens from eight patients with hepatitis B associated cirrhosis, complicated by hepatocellular carcinoma, were studied for identification and localisation of myofibroblasts. The avidin-biotin peroxidase complex technique was used on paraffin wax sections, using monoclonal antibodies for actin and desmin, and ultrastructural examination was performed. Myofibroblasts were found in seven of the eight cirrhotic specimens and in all eight tumour specimens. They were identified in the fibrotic areas by the immunohistochemical technique, but ultrastructural examination disclosed their presence in the perisinusoidal space and between tumour cells.
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PMID:Myofibroblasts in hepatitis B related cirrhosis and hepatocellular carcinoma. 131 87

Immunohistochemical evaluation of Cu, Zn- and Mn-superoxide dismutase (SOD) activity in various viral liver diseases was performed by the peroxidase-conjugated antibody indirect method. Anti-human Cu, Zn-SOD (rabbit) and anti-human Mn-SOD (guinea-pig) derived and purified from SOD of human erythrocytes and placentas were used to determine SOD distribution in liver tissues. SOD in the liver tissues was detected in 68 inpatients of our unit. They consisted of 23 cases with chronic hepatitis caused by hepatitis B virus (13) and hepatitis C virus (10), 24 with liver cirrhosis caused by hepatitis B virus (5) and hepatitis C virus (19) (15: compensatory, 9: decompensatory) and 21 with hepatocellular carcinoma caused by hepatitis B virus (2) and hepatitis C virus (18) complicated of liver cirrhosis. In viral liver diseases, SODs in the liver tissues were distributed to hepatocytes mainly in the pattern of cytoplasmic diffusion. The incidence of immunohistochemical Cu, Zn-SOD and Mn-SOD were 47.8% and 56.5% in chronic hepatitis, 93.3% and 86.7% in compensated liver cirrhosis, 11.1% and 22.2% in decompensated liver cirrhosis, respectively. The aggression of viral liver disease was accompanied with the decrease of SOD concentration in the liver tissues. Hepatocellular carcinoma cells were negative for Mn-SOD in all cases, and weakly positive for Cu, Zn-SOD in 2 out of 21 cases. Comparatively strongly positive SOD findings were obtained from normal regions neighboring carcinomas. A close relationship between the depletion of SOD in liver tissues and carcinogenesis in viral liver diseases was observed.
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PMID:Relationship between superoxide dismutase (SOD) and viral liver diseases. 132 May 79

Phenotypic expression of sialylated Lewis(x) antigen by means of the monoclonal antiserum SNH3 was studied in 87 livers, which included normal and steatotic livers and livers with chronic persistent and chronic active hepatitis, alcoholic hepatitis, allograft rejection, focal nodular hyperplasia, hepatocellular carcinoma, cholangiocarcinoma, metastatic carcinoma, cirrhosis of various causes (autoimmune, alcoholic, viral, drug induced, Wilson's disease, and primary biliary cirrhosis). The biotin-streptavidin-peroxidase method was used on formaldehyde-fixed, paraffin-embedded sections. Sialylated Lewis(x) antigen was not demonstrated in normal livers. Hepatocellular expression in a diffuse or perinodular honeycomb pattern was seen in cirrhosis, irrespective of cause. Sialylated Lewis(x) antigen was also observed in hepatocytes around metastatic carcinoma in the absence of inflammation, cirrhosis, or regeneration. Some bile ductules, most likely ductular hepatocytes, but not bile ducts, expressed sialylated Lewis(x) antigen. Sialylated Lewis(x) antigen was seen diffusely in fibrolamellar hepatocellular carcinoma, focally in other hepatocellular carcinomas, and either focally or diffusely in cholangiocarcinomas.
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PMID:Expression of sialylated Lewis(x) antigen in chronic and neoplastic liver diseases. 135 99

To investigate the potential role of lysosomes in cirrhosis, we analyzed the activity of lysosomal enzymes in rats exposed long-term to phenobarbital and carbon tetrachloride. The activity of lysosomal enzymes was markedly increased in the homogenate of cirrhotic livers (e.g., arylsulfatase 9 +/- S.D.2 vs. 16 +/- 6 nmoles.min-1.mg-1 in control rats and cirrhotic rats, respectively; p less than 0.001). The corresponding plasma levels were also increased (7 +/- 1 vs. 12 +/- 3 nmoles.min-1.mg-1; p less than 0.01), whereas biliary excretion was diminished (16 +/- 7 vs. 7 +/- 2 pmol.min-1.gm liver-1; p less than 0.05) in cirrhotic rats. Stereological quantification of lysosomes visualized cytochemically revealed an increase of pericanalicular lysosomes averaging 1.5 +/- 0.4 around a canaliculus in controls and 3.7 +/- 1.0 in cirrhotic rats (p less than 0.01). Because this suggested a defect in the transcellular vesicular pathway, we investigated the biliary excretion of horseradish peroxidase and epidermal growth factor in perfused livers. Bile flow and total horseradish peroxidase excretion were similar in control rats and cirrhotic rats. However, the early peak of biliary horseradish peroxidase excretion--usually taken as evidence of paracellular transport--was increased in cirrhotic rats (13 +/- 7 vs. 57 +/- 22%; p less than 0.01), whereas the second peak--reflecting the transcellular vesicular pathway(s)--was markedly reduced (87 +/- 7 vs. 43 +/- 22%; p less than 0.001). A similar reduction in the biliary excretion of intact epidermal growth factor and of its degradation products was found. These results demonstrate an increased number of lysosomes in hepatocytes of cirrhotic livers; this appears to be the result of accumulation rather than proliferation, in view of the reduced transcellular vesicular movement of different markers into bile.
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PMID:Hepatic accumulation of lysosomes and defective transcytotic vesicular pathways in cirrhotic rat liver. 139 8

There have been many reports on renal lesions of alcoholic cirrhosis, but not on those of post-hepatitis cirrhosis (PHC) up to present. A clinical and pathological observation on PHC was carried out prospectively in 18 and retrospectively in 34 cases. Renal specimens were examined with light and electron microscopy and immunopathological methods (immunofluorescence and peroxidase anti-peroxidase). Clinically, recurrent gross hematuria was observed in 2 and wild urinary abnormality in 17 cases. One case developed renal failure and the remaining 32 cases had no clinical evidence of renal involvement. Light microscopy showed wild mesangial lesions in 44 cases and glomerular basement membrane (GBM) thickening with segmental splitting in 29 and diffuse splitting in 2 cases. Massive protein deposition was found in the GBM, mesangium (Ms) and tubular basement membrane as well as the epithelium and endothelium. Immunopathological examination showed massive deposition of various immunoglobulins and complements in GBM and Ms, with IgG dominant in 8, IgM dominant in 7, IgA dominant in 6 and "full house" in 11 cases. HBsAg was detectable in GBM and Ms in 5 cases (9.6%) and HBcAg in one. Focal interstitial fibrosis and lymphocytic infiltration were found in 15 (28.3%). Our data revealed that renal lesions of post-hepatitis cirrhosis are different from those of the so-called "cirrhotic glomerulonephritis" in certain aspects. They are characterized by definite GBM involvement and massive deposition of immunoglobulins and complements. Its pathogenesis may be more complicated than that of other types of liver cirrhosis.
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PMID:[Renal lesions of post-hepatitis cirrhosis]. 142 1

Formalin-fixed, paraffin-embedded specimens from 110 cases of chronic hepatitis and 108 cases of cirrhosis were stained for HBxAg by the avidin-biotin complex technique using specific antisera made against full-length HBxAg polypeptide or derived synthetic peptides. These tissues were also stained for the HBsAg and HBcAg by the peroxidase-anti-peroxidase method. Among patients with chronic hepatitis, 86% were HBsAg positive in liver cells, 60% were surface antigen positive and 32% were core antigen positive. Among patients with cirrhosis, 97% were HBsAg positive in liver cells, 72% were surface antigen positive and 17% were positive for core antigen. Staining specificity was demonstrated, in part, by using preimmune sera in the place of primary antibody, by blocking of the primary antibody with the appropriate antigen before assay and by testing uninfected liver controls. The persistence and high frequency of HBxAg in liver cells from patients with chronic liver disease suggest that it may play one or more important roles in the pathogenesis of chronic infection. It is possible that detection of HBxAg in the liver could be an additional new diagnostic marker for hepatitis B virus infection. However, the function(s) of HBxAg in the pathogenesis of the chronic liver disease, if any, remains to be explained.
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PMID:HBxAg in the liver from carrier patients with chronic hepatitis and cirrhosis. 171 39

An enzyme-linked immunosorbent assay was developed for the determination of antibodies against the putative capsid protein of hepatitis C virus (HCV). A 36-mer oligopeptide with a sequence of RRGPRLGVRATRKTSERSQPRGRRQPIPKVRRPEGR (CP9) was synthesized; it was selected on the translation product of the presumptive HCV core gene, because of a high local hydrophilicity and excellent conservation by different HCV strains. The synthetic peptide was immobilized on a solid-support to capture antibodies directed to CP9 (anti-CP9) in test sera, which were detected by Fab' fragments of monoclonal anti-human IgG/gamma labeled with horseradish peroxidase. The specificity of anti-CP9 was confirmed by absorption tests. Anti-CP9 was detected in 13 (68%) of 19 patients with sporadic acute non-A, non-B (NANB) hepatitis and in 15 (83%) of 18 patients with post-transfusion acute NANB hepatitis. In 7 cases of acute NANB hepatitis who were followed, anti-CP9 developed earlier than antibodies against HCV (anti-HCV) detectable by a commercial assay kit. Among patients with chronic NANB liver diseases, anti-CP9 was detected in 103 (77%) of 133 with chronic hepatitis, 70 (62%) of 113 with liver cirrhosis and 31 (76%) of 41 with hepatocellular carcinoma. Anti-CP9 and anti-HCV overlapped in 175 (54%) among 324 cases of acute or chronic NANB liver diseases; 58 (18%) were positive only for anti-CP9 while 49 (15%) were positive only for anti-HCV. HCV RNA was detected, by amplifying HCV cDNA with polymerase chain reaction, in 10 of 11 sera positive only for anti-CP9. Among sera from 606 blood donors, 21 were positive only for anti-CP9. HCV RNA was detected in 5 (24%) of them, all of which had A492 values greater than 0.600 in ELISA for anti-CP9. Based on these results, anti-CP9 would complement anti-HCV for the diagnosis of HCV infection and contribute toward further decreasing posttransfusion NANB hepatitis.
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PMID:Enzyme-linked immunosorbent assay for antibodies against the capsid protein of hepatitis C virus with a synthetic oligopeptide. 196 54

A one-step sandwich enzyme immunoassay (one step sandwich EIA) for human serum immunoreactive laminin was set up with a pair of monoclonal antibodies prepared against human placental laminin P1 fragment. The assay was characterized by carrying out two immunoreactions simultaneously, laminin P1 fragment reacting with both a monoclonal antibody as a solid phase and a horseradish peroxidase-labeled monoclonal antibody (Fab') against human laminin P1 fragment as conjugate. Sensitivity of the immunoassay was 0.01 ng/well (0.5 microgram/l), and linearity was obtained between 0.01-20 ng/well (0.5-1,000 micrograms/l). The levels of laminin in sera from normal individuals and patients with liver cirrhosis, hepatocellular carcinoma and primary biliary cirrhosis were 103 +/- 15 micrograms/l, 228 +/- 70 micrograms/l, 341 +/- 163 micrograms/l and 232 +/- 93 micrograms/l, respectively. Protein immunoblotting showed that the serum immunoreactive laminin measured by the assay was a fragment with rel mol mass of 200 kDa.
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PMID:One-step sandwich enzyme immunoassay for human laminin using monoclonal antibodies. 209 55


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