Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrophobic bile acids have been shown to be hepatotoxic, whereas treatment with ursodeoxycholic acid, a hydrophilic bile acid, has improved liver function indices in patients with chronic liver disease. Taurine administration has also been suggested to be useful for chronic hepatitis, taurine-conjugated bile acids being more hydrophilic than glycine-conjugated bile acids. To determine if taurine and ursodeoxycholic acid are beneficial and if their effects are additive, a double-blind, randomized trial was designed comparing the effects of ursodeoxycholic acid, taurine, and a combination of the two on indices of liver injury in 24 patients with chronic hepatitis. They were assigned at random to two of the four following treatments: ursodeoxycholic acid (600 mg/day), taurine (1.5 g/day), ursodeoxycholic acid plus taurine (600 mg + 1.5 g/day) or placebo, given in two successive cycles of 2 mo each, according to a balanced incomplete-block design. Ursodeoxycholic acid became the predominant biliary bile acid when administered alone or in combination with taurine, and taurine conjugate levels increased during taurine administration. Ursodeoxycholic acid reduced aspartate aminotransferase (35%), alanine aminotransferase (33%), and gamma-glutamyl transpeptidase (41%), whereas taurine alone did not. The addition of taurine to ursodeoxycholic acid produced only minor changes in the effects of ursodeoxycholic acid alone. Results were confirmed by the administration of ursodeoxycholic acid, in a successive open phase of the study, to the entire patient population, which was large enough for different subsets of patients to be compared. Serum bile acids were measured at entry and during the open phase: primary bile acids did not change, whereas ursodeoxycholic acid levels increased from trace amounts to very high levels, especially in patients with more severe histological disease. It is concluded that ursodeoxycholic acid, but not taurine, improves enzymatic indices of liver injury in chronic hepatitis.
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PMID:Effects of ursodeoxycholic acid and taurine on serum liver enzymes and bile acids in chronic hepatitis. 196 71

Plasma tumour necrosis factor alpha (TNF) and in-vitro TNF production by peripheral blood mononuclear cells (PBMC) were studied in 22 HBsAg seropositive patients and compared with 23 normal and 10 disease controls. Plasma TNF and unstimulated TNF production correlated (Rs = 0.55, p = 0.012) and were significantly elevated in HBsAg and HBeAg seropositive patients (p less than 0.001, p = 0.006) compared with normal controls. TNF production was also elevated in these patients when PBMC were stimulated with interferon-gamma (p less than 0.05) or LPS (p = 0.035). Plasma TNF and TNF production in HBsAg anti-HBe seropositive subjects were not elevated. TNF production in unstimulated cells correlated with serum HBV DNA level (R = 0.53, p = 0.02) but not with serum aspartate transaminase (AST) or histological activity. It is concluded that PBMC are activated to produce TNF both spontaneously and in response to second stimuli in chronic hepatitis B virus infection and that this activity is related to the presence of viral replication.
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PMID:Increased production of tumour necrosis factor alpha in chronic hepatitis B virus infection. 205 Oct 3

Seventeen of 73 (23.3%) multiply transfused patients with thalassaemia major (age range, 1-39 years) tested positive for antibody to hepatitis C virus (anti-HCV). Eleven of the 24 patients regularly transfused in countries outside Britain were anti-HCV seropositive; only six of the 49 regularly transfused in Britain were seropositive. The incidence of anti-HBs and anti-HBc was similar to that of anti-HCV in both the British and foreign patients. The anti-HCV seropositive patients showed significantly higher plasma aspartate aminotransferase activities (AST), mean (SD) 10.2 (70.3) U/l, and serum ferritin concentrations, 4067 (2708) micrograms/l, than the anti-HCV seronegative patients (AST, 33.9 (15.6) U/l; serum ferritin 2051 (2092) U/l), respectively. Among the 36 patients who had earlier undergone liver biopsy 10 of 21 with histological features of chronic active hepatitis or cirrhosis, or both, were seropositive for anti-HCV whereas only one of 15 without histological evidence of chronic viral hepatitis was seropositive for anti-HCV. It is concluded that HCV is a major cause of chronic hepatitis in patients with thalassaemia major and is associated with raised AST activity and serum ferritin concentration compared with patients seronegative for anti-HCV.
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PMID:Antibody to hepatitis C virus in multiply transfused patients with thalassaemia major. 211 95

Evidence is accumulating that ursodeoxycholic acid (UDCA), an agent widely employed for gallstone dissolution, exerts therapeutic effects in chronic liver disease. UDCA is thought to act mainly by reducing the detergent properties of bile, making it less toxic for the liver cells. Confirming the results of preliminary observations double-blind, placebo-controlled trials have shown that UDCA significantly decreased serum concentrations of liver enzymes such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transferase in primary biliary cirrhosis and other cholestatic conditions, as well as in chronic active hepatitis. A substantial improvement in liver histology has also been detected in UDCA-treated patients with primary biliary cirrhosis. The effect of UDCA in chronic hepatitis is currently a matter of investigation.
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PMID:Treatment of chronic liver disease with ursodeoxycholic acid. 229 32

We have treated 17 patients with non-A, non-B chronic hepatitis by recombinant interferon alpha (0.3-9 megaunits for 4-28 weeks). In six patients, serum aminotransferase levels fell to normal or near-normal range during treatment. The mean levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in 17 patients fell from 156 +/- 80 (mean +/- SD) and 213 +/- 135 at the beginning of treatment to 94 +/- 49 and 112 +/- 71, respectively, at the end of treatment. In 12 patients, liver biopsies were performed before and after (or during) the treatment, and histological activity indices (HAI) were blindly examined by two independent observers. For comparison, we examined histological changes of pre- and posttreatment liver biopsies of 19 patients who were treated by recombinant interferon for chronic hepatitis B. Mean HAI scores improved from 10.0 to 5.4 after treatment in non-A, non-B chronic hepatitis. The most marked reduction was noted in scores of portal inflammation and hepatocellular degeneration and/or necrosis. No such reduction was observed in B-viral chronic hepatitis. These data indicated that rapid biochemical resolution by the treatment was related to histological improvement of the liver in our patients with non-A, non-B hepatitis.
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PMID:Histological changes of the liver by treatment of chronic non-A, non-B hepatitis with recombinant leukocyte interferon alpha. Comparison with histological changes in chronic hepatitis B. 249 64

To define an iron overload index independent of liver cell damage, the mean annual levels of alanine aspartate transaminase (ALAT) and serum ferritin and their ratios were determined. Ferritin/ALAT ratio values were compared between two groups of patients with acute or chronic hepatitis without iron overload, and one group of thalassaemic patients with iron overload. The two groups without iron overload exhibited ferritin/ALAT ratio values of 2 and 1.2 respectively; a ratio value higher than 10 was always observed in those patients with iron overload. The ferritin/ALAT ratio is correlated with the degree of iron overload. This ratio increases in regularly-transfused patients without chelation treatment. It generally remains stable or decreases after initiation of iron chelation therapy. The ferritin/ALAT ratio thus appears useful in the follow-up of patients subjected to a long-term transfusional treatment particularly when acute or chronic liver cell damage may interfere with iron overload by increasing serum ferritin values.
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PMID:Use of the ferritin/alanine aspartate transaminase ratio as an iron overload marker independent of liver cell damage. 261 15

Forty-one patients with chronic hepatitis were divided into an HBe antigen-positive group (n = 13) and an HBe antigen-negative group (n = 28) to clarify the relationship between the presence of HBe antigen and liver function. In the HBe antigen-positive group, the activities of serum alanine aminotransferase (p less than 0.01), aspartate aminotransferase (p less than 0.05) and guanase (p less than 0.01) were significantly higher than those in the HBe antigen-negative group. The correlation coefficient between the HBe antigen titer and guanase activity was 0.528, which was higher than the corresponding values for alanine aminotransferase and aspartate aminotransferase. The determination of guanase activity in serum may be useful for evaluating the clinical severity of HBe antigen-positive chronic hepatitis.
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PMID:[Activity of guanase in serum and liver function tests in HBe antigen-positive chronic hepatitis]. 261 68

46 male chronic hepatitis B virus (HBV) carriers with active viral replication were randomised, with stratification for histology and sexual preference, to receive six months' lymphoblastoid interferon or no therapy. After nine to eighteen months' follow-up, HBeAg was no longer detectable and anti-HBe was present in 6 of the 23 treated patients. HBsAg was not detectable in 5 of these patients and 3 had anti-HBs. All of the controls remained positive for HBeAg and HBsAg. Seroconversion from HBeAg to anti-HBe was preceded in all cases by a pronounced increase in serum aspartate aminotransferase levels of more than ten times the upper limit of normal at eight to twelve weeks; this response was exclusively associated with interferon therapy. These results suggest that loss of HBsAg and a hepatitis-like illness in the third month of therapy are direct effects of interferon treatment.
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PMID:Loss of HBsAg with interferon therapy in chronic hepatitis B virus infection. 288 73

Fourteen children with biopsy-proven membranous nephropathy associated with hepatitis B virus (HBV-MN) were evaluated biochemically and serologically and compared to 45 children with idiopathic nephrotic syndrome (INS). The mean ages of the two groups were similar (4.9 +/- 1.6 vs. 4.6 +/- 2.6 years). Serum albumin levels were similar in both groups, but serum cholesterol was significantly reduced in children with HBV-MN compared to INS. Serum C3 was also significantly depressed in children with HBV-MN compared to INS, but no differences in C4 levels were noted. Serum alanine transaminase as well as aspartate transaminase concentrations were significantly elevated in children with HBV-MN compared to those with INS, suggesting the presence of chronic hepatitis in children with HBV-MN. Hepatitis B surface and e antigens were present in serum of all children with HBV-MN, but only 54% had circulating HBV-DNA particles demonstrable in their serum. Serum C3 levels were higher in children with HBV-MN and circulating HBV-DNA, compared to those without circulating HBV-DNA. No other serological or biochemical differences occurred between these two groups. Glomerular deposition of IgG and C3 occurred in 91% of children with HBV-MN; but IgM deposition appeared to occur more frequently and with greater intensity in those children positive for circulating HBV-DNA. Antibody to delta antigen was negative in all children with HBV-MN. We conclude that biochemical and serological differences can be identified between HBV-MN and INS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical and serological characteristics of children with membranous nephropathy due to hepatitis B virus infection: correlation with hepatitis B e antigen, hepatitis B DNA and hepatitis D. 304 Dec 94

For patients with chronic hepatitis B e (HBe)-positive hepatitis, long-term results of pilot studies with lymphoblastoid interferon-alpha, acyclovir, or a combination, and of a randomized controlled trial of interferon/desciclovir combination therapy are presented. HBe seroconversion was observed in more than 40 percent of patients treated with combination therapy, 30 percent with interferon therapy, 18 percent with acyclovir, and 0 percent with no treatment. HBe reactivation occurred in two patients with cirrhosis. Hepatitis B surface seroconversion followed HBe seroconversion in 11 to 30 percent of treated patients. HBe seroconversion was significantly related to initial low levels of viral replication and to transient aminotransferase elevation during the second half of the interferon treatment of 16 weeks. Clinical improvement and persistent normalization of aspartate aminotransferase was observed in all patients with HBe seroconversion. Conversion to a state of virus latency (HBe negative) mostly occurred after therapy, suggesting that the specific immunologic host response had been brought about by the suppression of virus replication through antiviral agents. Recommendations for selection of patients for antiviral combination therapy are made on the basis of these long-term results.
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PMID:Long-term follow-up of antiviral combination therapy in chronic hepatitis B. 304 80


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