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)

A molar ratio of free branched-chain amino acids to tyrosine (BTR) was determined in the plasma of patients with liver diseases using a new enzymatic method. In addition, clinical significance of BTR was studied by comparing particularly with that of Fischer's ratio (a molar ratio of branched-chain amino acids to aromatic amino acids (tyrosine+phenylalanine], which was obtained by conventional HPLC (Amino acid autoanalyzer, Hitachi 835). Following results were obtained: 1) Enzymatically determined branched-chain amino acids and tyrosine showed significant correlations with respective results obtained by HPLC (r = 0.937, 0.972). 2) Significant correlation was also found between enzymatically determined BTR and Fischer's ratio obtained by HPLC. Changes of BTR in clinical courses were found to be in parallel with those of Fischer's ratio. 3) BTR as well as Fischer's ratio correlated significantly with ICG R15, KICG, prothrombin time (%) and serum albumin level. 4) BTRs in patients with decompensated liver cirrhosis or with fulminant hepatitis were significantly lower than those in patients with acute or chronic hepatitis. In conclusion, new enzymatic assay of branched-chain amino acids and tyrosine as described here is quite simple method, and is also considered to be very useful parameter of the clinical conditions of patients with liver diseases, particularly representing the severity of liver diseases and the protein nutritional status.
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PMID:[Enzymatic determination of a molar ratio of free branched-chain amino acids to tyrosine (BTR) and its clinical significance in plasma of patients with various liver diseases]. 258 54

Sera from 40 patients with a clinical diagnosis of halothane-associated hepatitis were tested for the presence of antibodies to the trifluoroacetate (TFA) halothane metabolite hapten using an ELISA assay, with TFA-albumin as the antigen. Positive results were obtained in 30% of cases of which 3/4 with encephalopathy were positive and 9/36 non-fulminant cases were positive. Antibody specificity to the TFA hapten was confirmed in each positive result by a 'hapten inhibition' experiment in which TFA albumin binding was blocked by preincubation of serum with TFA-lysine. Most probably this assay detects a relatively low affinity cross-reaction with the TFA hapten of antibodies in the patients' sera which are directed against specific TFA-labelled liver proteins. Anti-TFA-albumin antibodies were not detected in 28 normal subjects, 5 subjects with fulminant hepatic failure secondary to other causes, 6 subjects with a history of 2 or more exposures to halothane but with no evidence of liver disease and 28 patients with a variety of chronic liver diseases. It is concluded that ELISA testing using trifluoroacetylated rabbit serum albumin (TFA-RSA) as antigen is a quick and convenient assay for the confirmation of halothane-associated hepatitis in fulminant hepatic failure secondary to halothane, but is less sensitive when the illness follows a milder course.
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PMID:Detection of antibodies to a halothane metabolite hapten in sera from patients with halothane-associated hepatitis. 260 25

We have reported that a liver growth factor isolated from plasma of partially hepatectomized rats is an albumin-bilirubin complex. In this paper, we characterize the liver growth factor purified from subjects with hepatitis (h-LGF). This factor increases synthesis of DNA in a dose-dependent manner both in vivo in mouse hepatocytes, with a dose of maximal stimulation of 150 ng of h-LGF/mouse, and in vitro in rat liver cell culture, with maximal effect at 7.5 to 10 ng of h-LGF/ml. In vivo, h-LGF increases the mitotic index of mouse hepatocytes, its action being organ-specific, acting on liver, but not on spleen, kidney, lung or brain. In vitro, h-LGF stimulates the uptake of 22Na+ by hepatocytes. In addition, we carried out a study comparing it with human serum albumin in terms of absorbance, fluorescence, circular dichroism spectra, amino acid composition, tryptic maps and antigenic determinants (Ouchterlony immunodiffusion). All these tests suggested that human serum albumin is a constituent of h-LGF. Moreover, when albumin isolated from humans without hepatic pathology is incubated with bilirubin, the albumin-bilirubin complex formed mimics the activity of the human liver growth factor with respect to stimulation of DNA synthesis and the effects on the mitotic index of mouse hepatocytes in vivo. We propose that this human liver growth factor is an albumin-bilirubin complex.
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PMID:Liver growth factor purified from human plasma is an albumin-bilirubin complex. 261 47

Various thyroid parameters in liver disease which were morphologically diagnosed were measured, and their relationship to liver function was mainly studied. Serum T4 levels were elevated in acute hepatitis (AH), chronic persistent hepatitis (CPH) and chronic aggressive hepatitis (CAH) compared with in normal controls (C). Serum T3 levels were elevated in CAH and reduced in liver cirrhosis (LC). Serum reverse T3 (rT3) levels were elevated in AH and chronic liver diseases (CLD). T3/T4 ratios decreased in AH, CPH and CAH. RT3/T3 ratios increased in AH and CLD. Serum Free T3 (FT3) levels reduced in CLD in order of CPH, CAH and LC, and were low levels in AH with the same degree as LC. Moreover, serum FT3 levels revealed negative correlation with ICG-R15 and positive correlation with prothrombin time (PT) and serum albumin levels (Alb). Therefore serum FT3 level was considered to become a sensitive index of liver damage. Serum free T4 (FT4) levels did not change significantly in AH with high levels of transaminases and reduced in only LC. Therefore serum FT4 may become an index of severity of liver dysfunction. On the other hand, T3/T4 ratios and rT3/T3 ratios showed less correlation with liver function tests compared with free thyroid hormones.
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PMID:Studies on changes of thyroid hormones in various liver diseases: usefulness of free thyroid hormones as liver function test. 273 36

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

The sera of 16 individuals chronically infected with the hepatitis D virus were analyzed for hepatitis B virus (HBV) markers. The majority of these patients had a non-replicative form of viral type B hepatitis as indicated by negative tests for HBeAg and HBV-DNA. Pre-S-encoded proteins were detected in 13/16 sera. Sera that were negative for polymerized serum albumin did also not contain pre-S1-encoded proteins. The presence of pre-S-encoded proteins is probably predominantly associated with 22-nm HBsAg forms present in large amounts in sera of individuals with chronic type D hepatitis.
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PMID:Expression of Pre-S-encoded proteins in sera of individuals chronically infected with hepatitis D virus. 323 18

The effect of alpha-interferon treatment on serum levels of hepatitis B virus-encoded proteins was analyzed in eight patients with chronic type B hepatitis who participated in a pilot study of interferon therapy. Three individuals became HBsAg-negative, 4 lost HBeAg but remained HBsAg-positive and 1 remained positive for both HBsAg and HBeAg. Initiation of interferon treatment was rapidly followed by reduction or loss of hepatitis B virus DNA in the serum but by little immediate change in hepatitis B virus antigen levels. Changes in hepatitis B virus antigens were usually delayed. Loss of HBsAg from the serum was preceded by the sequential disappearance of pre-S-encoded proteins (pre-S1 and polymerized human serum albumin) and HBeAg. In patients who lost HBeAg but remained HBsAg-positive, serum levels of pre-S1 and polymerized human serum albumin usually, but did not always, decrease. The individual who remained HBsAg- and HBeAg-positive had unchanged serum levels of pre-S1, polymerized human serum albumin and HBsAg. These results suggest that alpha-interferon inhibits hepatitis B virus DNA replication but has little direct effect on synthesis of hepatitis B virus gene products.
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PMID:The effect of recombinant alpha-interferon treatment on serum levels of hepatitis B virus-encoded proteins in man. 361 48

A simple and sensitive ELISA was developed to characterize the interaction between polymerised human serum albumin (pHSA) and HBsAg, using pHSA-coated polyvinylmicrotitre plates as solid phase and anti-HBs-coupled HRPO as the conjugate. The interaction was found to be specific and dependent on the size of albumin polymer. pHSA-binding activity (pHSA-BA) was studied in both HBsAg-negative and HBsAg-positive sera from various liver diseases including acute viral hepatitis, fulminant hepatitis, cirrhosis of liver, chronic active hepatitis, and healthy HBsAg carriers. pHSA-BA was detected only in HBsAg-positive sera. Analysis of HBsAg-positive sera indicated pHSA-BA in high proportions of patients sera as compared to sera from healthy HBsAg carriers. pHSA-BA was detected both in the presence and absence of HBe markers, though the mean BA was relatively high in presence of HBeAg. The effect of human serum immunoglobulins (IgG, IgA, and IgM) on the BA was investigated and a correlation between pHSA-BA and HBsAg-IgM complex positivity in sera was established. Finally, the probable role of human serum IgM in facilitating the binding process was discussed.
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PMID:Studies on HBsAg binding with polymerised human serum albumin by ELISA. 361 Dec 89

Polystylene latex particles coated with serum albumin of various species, including non-primate serum albumin, were agglutinated by sera containing hepatitis B surface (HBs) antigen and hepatitis Be (HBe) antigen and by purified HBs antigen. Monomer and polymer albumin separated from human serum albumin preparations on latex particles were found to react with HBs antigen. Monomer from non-primate serum albumin preparations bound to latex particles was also found to have the ability to react with HBs antigen, but polymer of non-primate serum albumin did not. The mechanism of reaction between HBs antigen and the latex-bound serum albumin of various species is discussed.
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PMID:Interaction of hepatitis B surface antigen with serum albumin of various species on polystylene latex particles. 361 93

A guinea pig model of halothane hepatitis was used to explore the humoral immune response induced by multiple halothane exposures and the potential role this response might play in contributing to liver damage. Three different strains of guinea pigs (Strain 2, Amana, and Hartley) were exposed to 1% halothane under either 21 or 80% oxygen for 4 hr at 2-week intervals. In each strain, halothane induced the appearance of an antibody cross-reactive with trifluoroacetylated guinea pig serum albumin (TFA-GSA). Three of six Strain 2 guinea pigs demonstrated an association between antibody titer and serum glutamate pyruvate transaminase levels. However, the possible cause and effect relationship between these two factors requires more investigation. Hartley guinea pigs had a 4- to 11-fold higher level of anti-TFA antibody than the other two strains because of either a "higher responder" genetic background or exposure conditions that favored oxidative metabolism of halothane. Immunization of Amana guinea pigs with TFA-GSA evoked a specific anti-TFA antibody response. However, the presence of this antibody before halothane exposure did not potentiate the transient liver damage induced by exposure. Thus, these results demonstrate that in guinea pigs multiple exposures to halothane induce the formation of an antibody that recognizes a reactive intermediate of halothane formed during the anesthetic's metabolism.
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PMID:Generation of halothane-induced immune response in a guinea pig model of halothane hepatitis. 368 90


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