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)

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

Five enzymes were measured in 50 liver specimens (18 normal liver, 20 Reye liver, 12 diverse liver disorders other than Reye syndrome). The enzymes were: glutamic dehydrogenase (E.C. 1.4.1.3), monoamine oxidase (E.C. 1.4.3.4), lactate dehydrogenase (E.C. 1.1.1.27), D-glucose-6-phosphate dehydrogenase (E.C. 1.1.1.49), catalase (E.C. 1.11.1.6). The Reye syndrome group showed significant decreases in glutamic dehydrogenase (56%) and monoamine oxidase (70%) compared to normal control tissue and these changes were not characteristic of the non-Reye liver disorder group as a whole. Neither catalase nor lactate dehydrogenase appeared to be altered significantly in the Reye or in the abnormal control group compared with normal controls. Thus, only the prominent decreases in the mitochondrial enzyme activities appeared to be highly characteristic of Reye syndrome. Paradoxically, the means of the five hepatic enzymes and the admission levels of two serum enzymes indicative of liver damage (alanine and aspartate aminotransferase) were remarkably similar for both survivors and nonsurvivors of Reye syndrome.
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PMID:Quantitative evaluation of the extent of hepatic enzyme changes in Reye syndrome compared with normal liver or with non-Reye liver disorders: objective criteria for animal models. 396 10

Discriminant analysis was used to discriminate between Reye syndrome (RS) patients and non-RS cases based either on conventional blood chemistry data obtained upon admission, or on the activities of hepatic mitochondrial enzymes in biopsy or necropsy tissue. The control group for blood chemistry measurements contained children with upper respiratory tract infections, varicella, etc. who did not develop RS, as well as healthy children. Subjects with no liver disorder (e.g., accidental death, sudden infant death, etc.) or with non-RS liver disorders were used as controls for hepatic enzyme studies. Hepatic damage indicators (aspartate aminotransferase, AST; alanine aminotransferase, ALT; and bilirubin) correctly classified 86-96% of non-RS cases and 61-71% of RS. By contrast, AST and ALT had little prognostic value (63% overall correct). Ammonia effectively classified favorable outcome cases (95% correct) but not unfavorable (14% correct). However, when ammonia was included with stage of coma information 88% of the favorable and 85% of the unfavorable outcome cases were correctly classified. Discriminant analysis of hepatic enzymes (glutamate dehydrogenase and monoamine oxidase activity) for a RS and a non-RS group correctly classified 80% of non-RS and 95% of RS specimens. The function was suitable for the direct evaluation of RS-like mitochondrial enzyme changes in rat liver.
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PMID:Prognosis and diagnosis of Reye syndrome by discriminant analysis. 404 46

Detailed screening of the patients and staff in a unit specializing in liver disease was carried out over a year to ascertain whether transmission of the serum hepatitis virus was occurring and whether the situation was comparable in any way to that found in a Renal Haemodialysis Unit. Of the 154 patients with liver disease tested on admission, 6% were found to have Australia antigen in the serum and throughout the year there were rarely less than two patients in the ward at any one time with positive serum. No instances of clinical hepatitis were detected in the other patients following their stay in the ward or in their attendant medical, nursing and lay staff. Six staff members were found to have Australia antigen in their serum. In four of these, all nurses, it was present in the first sample tested and so the infection may have been acquired earlier. Temporary elevations in both plasma bilirubin and serum aspartate aminotransferase levels were found in another five staff members whose serum was negative for Australia antigen and who clinically were well. In a further eight and apparently healthy staff members, an isolated but persistent elevation of the plasma bilirubin was noted. In both groups these changes could represent the spread of subclinical infectious hepatitis and it is recommended that in units dealing with ;liver patients' not only should considerable care be taken during diagnostic and therapeutic procedures but the medical and nursing staff should be screened at regular intervals.
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PMID:Screening for transmission of hepatitis within a liver unit. 450 39

A randomised double-blind trial of (+)-cyanidanol-3(Catechin), 2 g/day versus placebo, was carried out in 40 patients with pre-cirrhotic alcohol-related liver disease over a three month period. Twenty received the active drug and 20 placebo; one non-compliant patient in the treatment group was withdrawn. Forty-one per cent (16/39) abstained from alcohol and showed significant improvements (P < 0.005) in mean values for serum aspartate transaminase, serum gamma glutamyl transpeptidase, and mean corpuscular volume. Ten of the 16 showed overall histological improvement on liver biopsy. Fifty-nine pr cent (23/39) continued to drink, though significantly reducing their mean daily alcohol intake (P < 0.001). No significant changes occurred in this group in mean serum enzyme values, though the mean value for mean corpuscular volume improved significantly (P < 0.01) and 16 of the 23 showed overall histological improvement. Changes occurred irrespective of treatment with Catechin which suggests that, over a three month period, this drug did not influence the course of alcohol-related liver disease.
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PMID:Treatment of alcohol-related liver disease with (+)-cyanidanol-3: a randomised double-blind trial. 610 1

The copper-chelating, immunological, and antifibrotic effects of D-penicillamine indicated that it might be suitable for the treatment of primary biliary cirrhosis (PBC). In a randomised clinical trail, 55 PBC patients received penicillamine (600 mg daily), and 32 received a placebo. Drug reactions developed in 16 patients on penicillamine. All deaths occurred in patients with stage 3 or 4 (late stage) liver histology on entry to the study. 5 (14%) of 37 penicillamine-treated patients and 10 (43%) of 23 placebo patients have died (p less than 0.01). Improvement in survival only became evident after 18 months. Survivors in the penicillamine group demonstrated a significant fall in serum aspartate transaminase, serum immunoglobulins, and liver copper concentrations. On follow-up liver biopsy 12-72 months (median 33) after joining the study, 21% of penicillamine-treated patients had less pronounced inflammation and piecemeal necrosis, whereas there had been no improvement in patients on placebo (p less than 0.02). Penicillamine did not retard the histological evolution of the liver disease from the early prefibrotic stages to the late fibrotic or cirrhotic stages. Both the copper-chelating and immunological effects of penicillamine are probably important in improving survival. The excellent prognosis of patients with PBC in its early histological stages, and the failure of penicillamine to prevent histological progression from early to late stages, suggests that penicillamine treatment should not be given to patients with PBC in the early (stage 1 or 2) histological phase of the disease. Penicillamine treatment is recommended in patients once liver biopsy has demonstrated histological results typical of late stage 3 or 4 PBC.
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PMID:D-penicillamine treatment improves survival in primary biliary cirrhosis. 611 2

Discriminant function analysis was used to determine the optimum combination of haematological and biochemical tests which gave the best discrimination between hospital patients with high and low alcohol intakes. We studied 265 patients with alcohol-related disease, 133 gastroenterology outpatients drinking less than 20 g of alcohol per day, and 104 patients with a variety of non-alcoholic liver disease. Values of mean cell volume (MCV), serum bilirubin, aspartate transaminase, serum alkaline phosphatase (AP) and gamma glutamyl transferase (gamma GT), serum albumin, serum globulin, and uric acid were determined in each patient. The best discrimination between the three groups of patients was provided by a combination of mean corpuscular volume, log10 gamma GT, and log10 serum alkaline phosphatase. In women, 92% of the high alcohol group, 100% of the low alcohol group, and 87% of the non-alcoholic liver disease were correctly allocated by the discriminant analysis. The corresponding figures for the men were 80%, 100%, and 71%. Thus, over 80% of patients with excessive alcohol intake were correctly allocated by the use of three simple laboratory tests.
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PMID:Biochemical and haematological indicators of excessive alcohol consumption. 611 77

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.
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PMID:Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase. 611 67

In hepatobiliary disease, the level of bile acids in the peripheral circulation is greatly increased due to impaired liver function. It has been suggested that serum bile acids are of greater value in confirming hepatobiliary dysfunction than the currently assayed conventional biochemical parameters. Fifty patients with confirmed liver disease were studied. Bile acid determinations and a battery of biochemical tests were performed on each patient. Although serum bile acid levels correlated well with liver disease, the combination of gamma-glutamyl transpeptidase or 5'nucleotidase with alkaline phosphatase in conjunction with alkaline phosphatase isoenzymes provided similar or better correlation. Also, the routinely assayed enzymes, such as gamma-glutamyl transpeptidase, alkaline phosphatase, and aspartate aminotransferase demonstrated excellent correlation with hepatobiliary dysfunction.
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PMID:A correlation of serum bile acid levels with conventional biochemical parameters in the assessment of hepatobiliary dysfunctions. 612 Jul 70

A randomised double-blind trial of thioctic acid (alpha-lipoic acid), 300 mg/day versus placebo was carried out in 40 patients with pre-cirrhotic alcohol-related liver disease over a six month period. Twenty patients received the active drug and 20 placebo. Twenty-two of the 40 patients (55%) abstained from alcohol and showed significant improvements (p less than 0.01) in mean values for serum aspartate transaminase, serum glutamyl transpeptidase, and mean corpuscular volume. Seventeen of the 22 (77%) showed overall histological improvement on liver biopsy. The remaining 18 patients (45%) continued to drink but significantly reduced their mean daily alcohol intake (p less than 0.001). No significant changes occurred in their laboratory indices, but five of the 18 (28%) showed overall histological improvement. Changes occurred irrespective of treatment with thioctic acid, which suggested that, over six months, this drug did not influence the course of alcohol-related liver disease.
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PMID:Treatment of alcohol-related liver disease with thioctic acid: a six month randomised double-blind trial. 612 79


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