Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutathione S-transferase (GST; EC 2.5.1.18), a sensitive marker of hepatocellular damage, was measured in patients on therapy for histologically proven, autoimmune chronic active hepatitis at various stages of the disease. GST levels were elevated in 65% of serum samples despite immuno-suppressive treatment compared with aspartate transaminase (AST) which was increased in only 23% of samples. In 55% of samples with normal AST concentrations, GST was elevated. No samples demonstrated abnormal transaminase with normal GST levels. It is concluded that continuing hepatocellular damage occurs in patients with autoimmune chronic active hepatitis on immuno-suppressive treatment.
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PMID:Glutathione S-transferase levels in autoimmune chronic active hepatitis: a more sensitive index of hepatocellular damage than aspartate transaminase. 337 Aug 35

We studied a consecutive series of 204 patients who were admitted to a hospital for addictive diseases during 40 months and who had a liver biopsy. Parenteral drug abusers (n = 34) were significantly younger than alcohol abusers (n = 23) or abusers of both (n = 147) and had lower levels of serum alkaline phosphatase, total bilirubin, and aspartate aminotransferase than the other two groups. Chronic active hepatitis and chronic persistent hepatitis were more frequent (p less than 0.001) in abusers of parenteral drugs alone, whereas cirrhosis was found most often (p less than 0.001) in abusers of both alcohol and parenteral drugs. Cirrhosis was present in 10 of 39 (26%) simultaneous abusers of alcohol and parenteral drugs compared with 58 of 96 (60%) alcohol-abusing former parenteral drug abusers (p less than 0.001). Methadone maintenance treatment was not associated with cirrhosis. Thus, methadone-maintained patients who abuse alcohol and develop cirrhosis should remain in methadone maintenance treatment and receive concomitant alcoholism treatment. Also, these data further support the hypothesis that abusers of both alcohol and parenteral drugs have an increased risk of developing cirrhosis.
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PMID:Chronic liver disease in abusers of alcohol and parenteral drugs: a report of 204 consecutive biopsy-proven cases. 354 73

The term chronic active hepatitis covers aetiologically different conditions with similar histological features. Autoimmune chronic active hepatitis - the type that was described originally - is the only type which responds well to prednisolone therapy. Autoimmune chronic active hepatitis can be differentiated from other types by serological and other markers. Treatment with prednisolone should be given for at least two years, with adjustment of dosage according to the serum levels of aspartate transaminase; maintenance does should be 8-12 mg a day. Azathioprine (50-100 mg a day) may be given concurrently as a corticosteroid-sparing agent. Prednisolone therapy in patients with autoimmune chronic active hepatitis enhances the quality of life and survival is prolonged greatly; currently the survival rate after 10 years for prednisolone-treated cases is at least 70%. Prednisolone is not effective in hepatitis B-associated chronic active hepatitis and may be deleterious. In cryptogenic chronic active hepatitis, in which markers of autoimmunity or hepatitis B viral infection are lacking, a trial of prednisolone therapy may be given for three months, and continued only if the indices of disease activity indicate a response. Corticosteroid agents have not proved of benefit in other liver diseases, including alcoholic hepatitis and acute liver failure, and a beneficial effect in primary biliary cirrhosis is yet to be established.
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PMID:Treatment of chronic active hepatitis and other liver diseases with corticosteroid agents. 356 Dec 94

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.
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PMID:Hyperadrenocorticism in a ferret. 365 2

The relationship between hepatitis B virus deoxyribonucleic acid in serum and histologic activity was determined in 11 patients with corticosteroid-treated severe chronic active hepatitis B who underwent clearance of hepatitis B e antigen. All patients cleared hepatitis B virus deoxyribonucleic acid from the serum, and clearance preceded the loss of hepatitis B e antigen by 9-49 mo (mean 24 +/- 4 mo). Seropositivity for hepatitis B virus deoxyribonucleic acid was always associated with histologic features of chronic active hepatitis. Resolution of histologic activity followed the loss of hepatitis B virus deoxyribonucleic acid from the serum and it preceded clearance of hepatitis B e antigen in all patients. A transient elevation of serum aspartate aminotransferase activity occurred in 5 patients at the time that absence of hepatitis B virus deoxyribonucleic acid in serum was first demonstrated, and it was followed by resolution of histologic activity. The serum level of hepatitis B virus deoxyribonucleic acid slowly decreased or remained unchanged in all but 1 patient during long-term corticosteroid therapy. We conclude that hepatitis B virus deoxyribonucleic acid in serum is associated with histologic activity in corticosteroid-treated patients with severe chronic active hepatitis B. Disappearance of hepatitis B virus deoxyribonucleic acid from the serum precedes the loss of histologic activity and clearance of hepatitis B e antigen. Serum hepatitis B virus deoxyribonucleic acid levels usually do not increase during long-term corticosteroid therapy.
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PMID:Hepatitis B virus deoxyribonucleic acid in serum during hepatitis B e antigen clearance in corticosteroid-treated severe chronic active hepatitis B. 367 39

A study was carried out to confirm the pathogenetic role of ethanol in the development of chronic active hepatitis (CAH) and to assess if previous or current superimposed hepatitis B virus (HBV) infection could be relevant to the course of alcoholic liver disease (ALD). We examined clinical and laboratory reports of 57 alcoholics with biopsy-proven CAH. Serum and/or tissue HBV markers and the presence or absence of cirrhosis were investigated. Alcohol was the only aetiological factor present in a small group of CAH, with or without histological findings suggestive of alcoholic damage. Age, sex and survival were similar among the subgroups of CAH with and without previous or current HBV infection and among the subgroups of CAH with and without associated histological alcoholic features. Among the laboratory data, the AST/ALT ratio was higher in CAH without previous or current HBV infection. The mean age was comparable in CAH patients with and without cirrhosis, whereas the cumulative 5-year survival was worse in CAH with cirrhosis (87% vs. 49%). These data suggest a difference in alcohol susceptibility in our subjects.
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PMID:Features of chronic hepatitis in alcoholics. A survey in Milan. 369 15

Corticosteroids, azathioprine and antiviral agents have a questionable effect on CAH B. Chloroquine, a lysosomotropic agent, was used to treat 7 patients with histologically confirmed CAH B. All were HBeAb positive. A working hypothesis considering cellular death in CAH B as the result of lysosomal enzyme liberation by activated Kupffer cells was the basis for treatment. In this model T lymphocytes have only an immunoregulatory role. Clinical and laboratory follow-up was done for 6-16 months (median 12 months). Serum chloroquine levels were recorded by a fluorimetric method. 150-450 mg of chloroquine base were administered according to bio-chemical disease activity. In all patients AST and ALT values returned to normal and there was a fall in serum delta GT and improvement of prothrombin time. an increase of globulins was noted. Inadvertent drug withdrawal resulted in aminotransferase increase in 3 patients with prompt restoration of normal values on readministration. One patient refused to continue the drug and died after two months. Variceal bleeding was the cause of death of a second patient. No side effects were noted. A repeat liver biopsy, a year later (4 patients) revealed inactive cirrhosis in all. Chloroquine administration is a safe treatment for patients with CAH B. Further studies are justified.
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PMID:Treatment of chronic active hepatitis B (CAH B) with chloroquine: a preliminary report. 375 92

To assess the spectrum of hepatic abnormalities in acquired immune deficiency syndrome (AIDS), we reviewed clinical, biochemical, and pathological material in 32 patients with AIDS. Eight-four percent of AIDS cases had a history of intravenous drug abuse. Ninety percent of AIDS patients has some liver biochemical abnormality at the first presentation of illness. During the course of AIDS, significant (p less than 0.05, paired Student's t test) rises in alkaline phosphatase and bilirubin occurred, without rises in aminotransferases. Mean abnormalities were mild, reflecting approximately 2-fold increases over baseline. Liver failure was not believed to contribute to the death of any AIDS patient. Pathological findings in AIDS included specific infectious diagnosis in 26%, granulomas in 16%, hemosiderosis in 26%, nonspecific abnormalities in 39%, cirrhosis in 23%, and chronic active hepatitis in 3%. AIDS cases were also compared to 10 selected age, sex, and epidemiologically similar non-AIDS patients. Although granulomas or infections were not seen in our comparison group, only the incidence of chronic active hepatitis was significantly different between the groups. If only those with intravenous drug abuse were studied, then none of 24 AIDS patients versus four of eight non-AIDS cases (p less than 0.005) had chronic active hepatitis. AIDS patients with specific hepatic infections tended to have a higher alkaline phosphatase and aspartate aminotransferase (p less than 0.05) than noninfected cases. However, substantial overlap existed, and no difference in hepatomegaly was noted. Ninety percent of AIDS patients were ingesting at least one potentially hepatotoxic drug. We conclude that AIDS patients have a high incidence of underlying hepatic abnormalities. However, clinical and biochemical abnormalities are similar in our selected liver biopsy patients with intravenous drug abuse with or without AIDS. As expected, AIDS patients have a higher incidence of hepatic granulomas and infections, but these patients were not clearly distinguishable from other AIDS cases. Histological examination showed a wide array of changes by light microscopy, but no specific lesion of AIDS was noted. The low incidence of chronic active hepatitis in this AIDS population may imply that the altered T lymphocyte function in AIDS could influence the course of liver disease in these patients.
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PMID:The liver in acquired immune deficiency syndrome: emphasis on patients with intravenous drug abuse. 382 29

One hundred and thirteen patients with histologically confirmed oral lichen planus, from three stomatology clinics, were examined for evidence of liver disease. No patient had clinical evidence of liver disease. Nine patients (7.9%) had a raised serum concentration of a single enzyme; 6 patients had raised gamma-glutamyl transpeptidase, 2 had raised alkaline phosphatase, and 1 had raised aspartate transaminase levels. No patient had serum auto-antibodies suggestive of primary biliary cirrhosis or chronic active hepatitis. Most patients presenting with oral lichen planus are unlikely to have liver disease.
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PMID:Lichen planus and liver disease: how strong is the association? 392 77

Seven children with chronic active hepatitis (CAH) and one child with persistently abnormal results of liver function test due to hepatitis B virus (HBV) infection were treated with human leukocyte interferon (Hu-alpha-IFN). Five of them were positive for eAg and two of the three who were measured for DNA polymerase (DNAP) activity in sera showed moderate elevations of its levels. Hu-alpha-IFN was injected intramuscularly daily or once weekly at doses of 0.05-1 X 10(6) IU. The total dose per patient varied from 10.5-54 X 10(6) IU. After administration of Hu-alpha-IFN, rapid loss of eAg was observed in two of the five eAg patients, and DNAP activity reverted to normal ranges in the two patients with moderate elevations of its levels. One of the patients who lost eAg has retained normal serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels for more than 2 years after therapy with Hu-alpha-IFN. Serial hepatic biopsies were performed in only one patient. In the second biopsy, 3 months after therapy with Hu-alpha-IFN, infiltration of inflammatory cells in the portal region was improved compared with earlier findings. Immediate and/or prolonged adverse side effects were not observed during or after administration of Hu-alpha-IFN. For the present, we propose these six conditions for use of Hu-alpha-IFN in children with HBV infection. Children should: (a) be more than 1 year old; (b) have abnormal liver function for more than 6 months; (c) have a liver biopsy demonstrating CAH; (d) have moderate elevation of DNAP activity; (e) be eAg positive; and (f) be unresponsive to other treatments.
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PMID:Therapeutic effects of human leukocyte interferon on chronic active hepatitis B in children. 398 64


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