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)

Since 1970, the types of glomerulopathy encountered in patients with cirrhosis of the liver have been accurately determined. In alcoholic cirrhosis IgA glomerulonephritis is frequent, usually non-proliferative and latent, sometimes membranoproliferative. Defective elimination of circulating immune complexes made up of bacterial or food antigens and IgA antibodies is thought to play a part in the pathogenesis of this type of glomerulonephritis. Extramembranous or membranoproliferative glomerulonephritis, occasionally containing the viral antigen, may complicate post-hepatitis cirrhosis, in which case an antiviral treatment might be effective against the renal disease.
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PMID:[The glomerulopathies of cirrhosis of the liver]. 252 8

An investigation was conducted to clarify the relationships of IgA to the human liver. Immunocytochemical studies were performed on biopsy specimens from patients with cirrhosis and chronic hepatitis without any apparent history of alcohol abuse. The results showed that 1) a large amount of IgA is associated with the sinusoidal surface of hepatocytes, endothelial cells and Kupffer cells, 2) this IgA contains J chain and can form a complex with secretory component, and 3) this mainly belongs to the IgA1 subclass, 4) IgA in vesicles within hepatocytes and Kupffer cells is always associated with acid phosphatase activity, and 5) IgA containing vesicles within ductular epithelial cells always lack such enzyme activity. We conclude that 1) the IgA bound to the surface of hepatocytes, sinus endothelial cells and Kupffer cells is polymeric IgA1 uncomplexed with SC, and 2) this IgA occasionally enters these cells, and may be degraded in the lysosomes. 3) Polymeric IgA combines with SC in the ductular epithelium and may be secreted into bile. These findings suggest that J chain-linked polymeric IgA bound to the surface of hepatocytes and Kupffer cells has a certain pathological significance in liver diseases and might be involved in the clearance of excess IgA from the circulation.
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PMID:Studies on the relationships of IgA to human liver. IgA deposition in non-alcoholic liver diseases. 260 62

Circulating autoantibodies are often observed in liver disorders, especially in those thought to have an autoimmune etiology-such as primary biliary cirrhosis (PBC) and chronic active hepatitis (CAH). The pathophysiologic role of these antibodies, however, remains obscure. The present study was performed to evaluate the incidence and diagnostic value of different antinuclear antibodies in chronic liver diseases, and to assess whether the antibodies are a non-specific expression of the hypergammaglobulinemia observed in these disorders. We measured six different antinuclear and closely related antibodies (against ssDNA, dsDNA, Poly (I), Poly (dT), RNA and cardiolipin) and their IgG, IgA and IgM isotypes in the sera of 86 patients with autoimmune, as well as other chronic liver diseases--namely, PBC, CAH, alcoholic (AC) and cryptogenic cirrhosis (CC). Antibodies against all the various nuclear antigens were detected in all diseases studied. The incidence ranged from 4% (anti-cardiolipin-IgG in CC) to 74% (anti-Poly (dT)-IgM in PBC). Although the antibody profiles differed among the various disease entities, they were not distinct enough to be of any clinical diagnostic value. In alcoholic cirrhosis antibody levels correlated with corresponding immunoglobulin isotype levels (notably IgA), suggesting a non-specific expression of hypergammaglobulinemia. In the other liver diseases such a correlation was lacking, favoring the existence of an underlying specific antigenic stimulation, or some other more specific immune dysfunction.
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PMID:Antinuclear autoantibodies in chronic liver diseases. 262 Sep 1

In alcoholic cirrhosis, high levels of serum IgA make a prominent contribution to hyperglobulinaemia. Kinetic studies indicate that this predominantly reflects enhanced IgA synthesis rather than catabolism. Increase IgA synthesis might reflect increased antigenic load, diminished T-cell suppression, or T-cell independent B-cell stimulation (for example by lipopolysaccharide). To investigate this we studied T-cell control of IgA production by peripheral blood cells. Six patients with alcoholic cirrhosis were compared with six normal individuals. Serum IgA levels were significantly higher in the patients (6.6 mg/ml, SD 2.8 cf 1.7 mg/ml, SD 1.2). Seven day unstimulated cultures of peripheral blood mononuclear cells yielded supernatant IgA concentrations of 1,025 ng/ml (SD 600) in patients and 363 ng/ml (SD 222) in controls. T-cell control of IgA synthesis was explored by rosetting out T-cells, and reconstituting cultures at varying T:non-T cell ratios. Similarly shaped curves relating IgA per million non-T cells to the T:non-T cell ratio were found, with maximum IgA production at a T:non-T ratio of 8:2 in each group. IgA production at this ratio was 6.4 micrograms/ml/million non-T cells (SD 3.2) in cirrhosis of 3.2 (SD 1.0) in controls. T-cell control of IgA production thus appears normal, though set at a higher level, implying enhanced T-cell independent drive to IgA production in alcoholic cirrhosis.
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PMID:Regulation of peripheral blood B-cell IgA production in alcoholic cirrhosis. 264 70

A case of multiple myeloma (Bence Jones, lambda) associated with alcoholic liver cirrhosis is reported. A 56-year-old Japanese male died of hepatic failure and hypercalcemia. Autopsy revealed alcoholic liver cirrhosis and plasma cell myeloma. Immunoelectrophoretic analysis of his reserved serum disclosed the presence of M component of lambda Bence Jones protein. IgA and lambda light chain were demonstrated in the cytoplasm of the myeloma cells. Complications such as generalized amyloidosis, metastatic calcification, myeloma kidney and hemorrhagic pancreatitis were noted. The coexistence of multiple myeloma and liver cirrhosis has rarely been reported. On the basis of a review of the reported cases, a possible association between both diseases was discussed.
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PMID:Multiple myeloma in alcoholic liver cirrhosis. 265 75

Renal and hepatic samples were obtained from 121 forensic autopsies. In 64% of 107 individuals with evidence of alcohol abuse (AA), mesangial changes of mild cellular increase, deposits of IgA and IgM, and electron-dense deposits were found, with significantly higher incidence than seen in 14 controls. This mesangial glomerulonephritis (mesGN) was not limited to subjects with cirrhosis but was also observed in individuals with noncirrhotic alcoholic liver disease. Therefore, AA could be relevant in a larger number of mesGN patients than formerly suspected. When cases were separated by ethnicity, the incidence and severity of alcoholic liver disease were found to be essentially the same in American Indians, Hispanics, and Anglos. At the same time, mesGN in individuals with evidence of AA was more frequent in American Indians (87%) than in Caucasians (47%) (P less than 0.0001), with no statistically significant differences between Hispanics and Anglos. The possibility of ethnic influences on the predisposition to alcohol abuse-related mesGN is raised, although the importance of different patterns of alcohol ingestion cannot be ruled out.
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PMID:Frequent association of mesangial glomerulonephritis and alcohol abuse: a study of 3 ethnic groups. 272 26

Serum inhibition of complement-derived leukocyte chemotaxis was examined in alcoholic liver disease with or without cirrhosis. Chemotactic inhibitory activity (CIA) was detected with higher frequency and degree in alcoholic liver disease, especially with liver cirrhosis compared with normal subjects and non-alcoholic liver cirrhosis. CIA was found in anti-IgA adsorbed fractions in the sera of patients with alcoholic liver cirrhosis. Serum concentrations of IgA1 and IgA2 in alcoholic liver disease were statistically higher than in non-alcoholic liver cirrhosis. However, no correlation between CIA and the concentrations of IgA subclasses was demonstrated in alcoholic liver disease. This serum inhibitor may partly explain the high susceptibility to bacterial infection in alcoholic liver disease.
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PMID:Serum inhibition of complement derived leukocyte chemotaxis and levels of immunoglobulin A subclass in alcoholic liver disease. 274 44

Sera of 78 patients with different chronic liver diseases were examined for the presence of anti-histone activity using an enzyme-linked immunosorbent assay. Eighteen patients had primary biliary cirrhosis (PBC), 20 had chronic active hepatitis, and 40 had cirrhosis. Anti-histone antibodies were detected in 34 patients (43.6%), distributed among all liver disease entities studied. When antibodies of specific isotypes (IgG, IgM, and IgA) were measured, even higher frequencies were noted--50% for IgG and 53.8% for IgA. Antibodies to histone subfractions H1, H2a, H2b, H3, and H4 were also observed in all liver disorders investigated (in 22-32% of patients)--H1 and H3 being the prominent fractions involved. Of the various disease entities examined PBC was the one disclosing the highest frequency of anti-histone antibodies.
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PMID:Autoantibodies to histones and their subfractions in chronic liver diseases. 278 64

Among 108 individuals with chronic asymptomatic hepatitis B virus infection, liver biopsies and serological investigation were performed simultaneously to determine the correlations of anti-HBc with the infection level of the liver pathology. The results showed that the prevalence of IgA and IgM anti-HBc, and the titers of IgA, IgM, and total anti-HBc, correlated with the liver damage. IgA anti-HBc was most prominent, being present in the whole group of patients with chronic active hepatitis with cirrhosis, and was absent in the whole group of asymptomatic carriers with normal histology. There were no linkages of IgA and IgM anti-HBc with the infectivity; in addition, the titer of total anti-HBc correlated inversely with the viral replication.
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PMID:Significance of various classes of anti-HBc in individuals with chronic asymptomatic HBV infection. 291 27

Using immobilized anti-C3 antibody and an enzyme immunoassay, sera from 26 patients (eight with systemic lupus erythematosus (SLE), four with Hashimoto's thyroiditis, eight haemophiliacs and six with post-hepatitis cirrhosis) containing high levels of circulating immune complexes (IC) were selected. The IC were precipitated with 2.5% polyethylene glycol, washed, treated with acid buffer, neutralized and tested using an enzyme immunoassay in parallel with the original sera for antibody activity against a panel of antigens: human myosin and thyroglobulin, mouse actin and tubulin, calf thymus DNA and trinitrophenyl coupled to bovine serum albumin (TNP/BSA). It was found that all the isolated IC may contain IgG, IgA and IgM antibodies reacting with actin tubulin and TNP/BSA and also, depending upon the disease, antibodies reacting with some of the other antigens of the panel. By comparison to the antibodies present in the original sera, higher titers of antibodies were found in the isolated IC while some antibody specificities not detected in a given serum were occasionally noted in the isolated IC. The antibodies present in the IC seem to possess characteristics similar to those of polyreactive human natural autoantibodies. It is concluded that natural autoantibodies participate actively in the formation of IC found in pathological sera.
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PMID:Enzyme immunoassay analysis of antibody specificities present in the circulating immune complexes of selected pathological sera. 305 7


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