Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early and appropriate treatment of acute pancreatitis (AP) depends on early causal diagnosis. Published studies have shown favourable results following sphincterotomy performed within the 72 hours of onset of severe gallstone-associated AP. Among the various bio-clinical indices, the lipase/amylase (L/A) ratio, computed within 72 hours after onset, has been shown to discriminate between alcoholic and non alcoholic AP. Our study evaluates the data of biochemical disorders in 51 patients presenting with an episode of AP; these patients were divided into 3 groups: A: alcoholic AP, n = 15; B: biliary AP, n = 25; and C: post-ERCP AP, n = 11. These 3 groups were similar with respect to clinical severity of AP and CT scan. The time delays between onset of the symptoms and the biochemical assay were 1.9 +/- 0.3, 1.9 +/- 0.2 and 0.6 +/- 0.3 d (P < 0.01). AST, ALT, bilirubin, GGT and alkaline phosphatase were significantly (P < 0.05) greater in group B. Blamey's score was 0.5 +/- 0.2, 2.8 +/- 0.2 and 2.5 +/- 0.4 in groups A, B and C respectively. Serum amylase, serum lipase and L/A ratio were identical in groups A and B. The decrease in serum amylase after 48 hours was more important only in group B (56 +/- 8, 80 +/- 4, 47 +/- 3% respectively in groups A, B and C). L/A ratio was significantly greater in group C when compared with group A and B (1.7 +/- 0.4, 1.5 +/- 0.2 and 2.2 +/- 0.3 in groups A, B and C respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the identification of acute biliary and alcoholic pancreatitis by early pancreatic enzyme assay possible?]. 751 3

We have developed a new multienzyme control serum, Seraclear-HE, which was designed to function not only as an accuracy and precision control serum but also as an intermethod calibrator for unifying interlaboratory clinical enzyme data in terms of reference method values. Seraclear-HE contains as analytes the following enzymes of human origin only: aspartate aminotransferase (AST, EC 2.6.1.1) and lactate dehydrogenase (LD, EC 1.1.1.27) from erythrocytes; alanine aminotransferase (ALT, EC 2.6.1.2) from a hepatoma cell line; alkaline phosphatase (ALP, EC 3.1.3.1) from an amnion cell line; creatine kinase (CK, EC 2.7.3.2) from an embryo kidney cell line; gamma-glutamyltransferase (GGT, EC 2.3.2.2) from a macrophage cell line; and amylase (AMY, EC 3.2.1.1) from urine and saliva. The seven partly purified enzymes were lyophilized in partially delipidated human serum containing sucrose (50 g/L), pyridoxal 5'-phosphate (30 mmol/L), and other stabilizers. The material is stable for at least 2 years at temperatures < or = 10 degrees C. For two concentrations of this preparation, reference method values (mainly International Federation of Clinical Chemistry and Japan Society of Clinical Chemistry) obtained at both 30 degrees C and 37 degrees C are assigned.
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PMID:Multienzyme control serum (Seraclear-HE) containing human enzymes from established cell lines and other sources. 1: Preparation and properties. 753 43

Turner syndrome or the gonadal dysgenesis syndrome which is monosomic because of the lack of an X chromosome (45 X) is associated to a greater incidence of autoimmune, particularly thyroidal, disorders and inflammatory intestinal disease, but is rarely associated to hepatic disorders. A female patient with chronic asymptomatic intrahepatic cholestasis which, to our knowledge, is the first reported in Spain, is herein presented. The 40-year old patient with a 45 X karyotype, feminine phenotype was accidently found to have a chronic alteration in the hepatic profile. Hepatic biochemical tests revealed AST 59 U/L, ALT 90 U/L, GGT 201 U/L and alkaline phosphatase 320 U/L. Hepatic echography was normal. Percutaneous liver biopsy was performed demonstrating minimum changes consisting of sinusoidal dilatation and pigment accumulation in the hepatocyte biliary pole. Treatment with ursodeoxycholic acid 15 mg/kg/day was administered showing a marked decrease in the laboratory parameters during follow up. Different hypothesis which may explain the association between chronic asymptomatic intrahepatic cholestasis and Turner syndrome are discussed.
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PMID:[Chronic asymptomatic intrahepatic cholestasis associated with Turner's syndrome]. 907 98

A prospective study of 21 patients with the diagnosis of non-alcoholic steatohepatitis (NASH) was carried out. All patients had hepatomegaly and in 10 (48%) image studies were consistent with steatosis and/or fibrosis. Biochemically, there was increase of AST, ALT and cholesterol in 48%, of GGT in 52% and of alkaline phosphatase in 38%. 18 patients were obese, 2 of them diabetic, 2 others had a history of exposure to drugs (amiodarone and isopropilic alcohol) and the last one presented hypothyroidism. Liver biopsies were studied using a semiquantitative scale to evaluate the degree of steatosis, inflammation and fibrosis in a scale from 1 to 3. Results showed a medium score of 2.6 for steatosis, 1.5 for inflammation and 1.8 for fibrosis. Four patients had cirrhosis and Mallory bodies were found in 11 cases (52%). NASH is an oligosymptomatic disease that can be found in different clinical conditions, mainly obesity, and is more frequent in women. It is histologically indistinguishable from alcoholic steatohepatitis. It is frequently underdiagnosed clinically and must be taken into account as a possible cause of cryptogenetic cirrhosis.
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PMID:[Non alcoholic steatohepatitis]. 765 98

Overproportional GLDH-increase was found to be the most frequently appearing pathological enzyme pattern in canine practice. Thus it could be shown that GLDH deviates, in spite of its mitochondrial localization and greater molecular weight, more frequently and to a higher degree from its reference value than the parameters ALT, AST, AP, GGT and Bilirubin. The results of the study suggest that the liberation of the enzyme is less determined by the intensity than by the intralobular target of the liver insult. Therefore an increase in GLDH-activity should no longer be interpreted as the result of severe liver damage. On the contrary, the enzyme appeared to be the most sensitive indicator for the diagnosis of primary and secondary hepatopathies. The phenomenon of isolated GLDH-increase could be interpreted in almost every disease group as an appearance of the over-proportional increase and can therefore be understood as a serological expression of a slight, perivenous liver affection. Only with effusion patients the enzyme pattern should be regarded as an independent finding, because it has extrahepatic reasons. The induction of the enzyme in cases of diabetes mellitus is discussed.
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PMID:[Diagnostic value of glutamate dehydrogenase determination in the dog]. 771 55

Of 1,756 liver biopsies performed in the years 1987-1991, in 139 cases the patients exhibited both a nearly normal liver histology and elevated GGT values. After exclusion of patients with known causes for an elevated GGT 15 patients were selected, who over at least one year, were documented as having at least 3 measured GGT values with an average of over 40 U/l. In the follow-up of 1-15 years a typical constellation was detectable: longterm elevation of GGT (average 47-156 U/l, moreover a smaller degree of elevation of GLDH and GPT), minimal deviations from norm in liver histology (periportal fibrosis and/or fatty liver degeneration), and functional abdominal complaints. This triad occurred predominantly in middle-aged males, did not exhibit laboratory-chemical or histological signs of progression or regression tendencies and could be interpreted as a "functional" liver disorder with parelleles to M. Gilbert-Meulengracht.
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PMID:[Increased gamma-GT, minimal changes in liver histology, abdominal complaints--a functional liver liver disease]. 775 3

The beneficial effects of ursodeoxycholic acid (UDCA) in patients with primary biliary cirrhosis led to therapeutic trials with this bile acid for the treatment of PSC. In two prospective placebo-controlled trials, UDCA led to a significant improvement of AP, GGT, ALT, AST, and, in one study, also of serum bilirubin. In both studies liver histology improved significantly, mainly due to a decrease of cellular infiltrates in portal triads. Pruritus and fatigue improved in approximately one-third of the patients, but, compared to placebo, this effect was not significant. In a follow-up study after on average 3.1 years of UDCA treatment, 7/43 of the patients with stages I-IV disease developed a stenosis of the common bile duct which was effectively treated by endoscopic dilatations. Of 57 patients with PSC included since 1987 in the study, 14 dropped out and of these in 10 information on the outcome is available. In patients treated by UDCA and, whenever necessary, by endoscopic dilatations, the frequency of transplantations was significantly reduced in comparison to patients who dropped out of the study. Bile duct carcinoma developed in 5% of our patients. The data indicate that treatment of patients with PSC with UDCA and by endoscopic dilatations of common duct stenoses is promising. In patients with endstage disease, the only effective therapy is liver transplantation. Therefore, the early diagnosis of the disease seems very important.
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PMID:Ursodeoxycholic acid therapy in treatment of primary sclerosing cholangitis. 782 79

The rodent liver carcinogen and hepatic peroxisome proliferator methylclofenapate (MCP) has been evaluated for genetic toxicity in a range of in vitro and rodent genotoxicity assays. It gave a negative response in each of the following assays: mutagenicity to S. typhimurium and E. coli (+/- S9 mix, plate and pre-incubation assays), clastogenicity to cultured human lymphocytes and CHO cells (+/- S9 mix), a mouse bone marrow micronucleus assay (24h and 48h sampling), a rat liver assay for UDS in vivo (12h sampling), assays for lac I (Big Blue) and lac Z (Muta Mouse) mutations in the liver of transgenic mice, and an assay of the ability of MCP to modify the mutagenicity to the liver of dimethylnitrosamine in both transgenic mutation assays. The micronucleus and UDS assays were conducted using a single administration of MCP at its maximum tolerated dose, while the transgenic assays were conducted using nine daily administrations of MCP at its cancer bioassay dose level. These nine daily administrations were shown to double the weight of the liver of non-transgenic, Big Blue and Muta Mice, as well as leading to a dramatic proliferation of peroxisomes (electron microscopy) in the livers of each strain. These changed parameters had returned to control levels when the mutation analyses were conducted (10 days after the final dose of MCP). Despite the liver enlargement observed following MCP administration, no evidence of mitotic activity was observed in treated livers, although an increased number of cells were undergoing replicative DNA synthesis during the final 3 days of the 9 days of administration (BUdR assessment of S-phase). Liver biochemistry parameters (ALT, AST, AP, CK, GGT and albumin) were unaffected by the chronic (9 day) administration of MCP indicating an absence of hepatic toxicity. These combined observations favour a non-genotoxic mechanism of action for the hepatic carcinogenicity of MCP. The clastogenicity in vitro of the perixisome proliferator Wyeth 14,643 has been confirmed in CHO cells, but it is noted that this chemical is more soluble than is MCP. In particular, at the highest dose level at which MCP could be tested, Wy 14,643 was also non-clastogenic.
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PMID:Evaluation of the genetic toxicity of the peroxisome proliferator and carcinogen methyl clofenapate, including assays using Muta Mouse and Big Blue transgenic mice. 785 96

Rickettsia spp. infections produce hepatic damage with transaminases elevation and biological signs of cholostasis. Classical biochemical tests of hepatic function were analyzed and compared in 8 patients with Q Fever (QF) and 7 with Boutonneuse Mediterranean Fever (BMF). Liver enlargement was detected in 75% of the QF group of patients as compared with the 57% of the BMF group. Transaminases were raised in 75% of the patients of the QF group and in 85, 7% of the BMF patients. Only one patient in the QF group showed manifest clinical jaundice. Statistically significant differences were found between the values of AST, ALT, alkaline phosphatase and GGT, which were higher in the QF group. Liver involvement is more important in patients with QF than in FBM. There is a large percentage of clinically silent involvement in both diseases. Liver function tests should be carried out in infections by Rickettsia spp.
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PMID:[Liver involvement in Q fever and Mediterranean boutonneuse fever. Comparative study]. 787 63

The object of the study was to discover the changes in the plasma activities of hepatic enzymes in patients on anticonvulsant drugs. The plasma activities of aspartate transaminase (AST), alkaline phosphatase (ALP), alanine transaminase (ALT) and glutamyltransferase (GGT) were studied in 123 unselected patients on anticonvulsants. The results were compared with 123 control patients not on anticonvulsants matched for age and sex. Patients with known liver disease were excluded. The plasma activities of AST and ALP were similar in the two groups. ALT and GGT were raised in patients on anticonvulsants. No patient developed clinical evidence of liver disease. It was concluded that raised ALT and GGT are not in themselves indications to alter anticonvulsant therapy. Changes in AST and ALP would be more specific markers of liver dysfunction in patients on anticonvulsants.
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PMID:Plasma activities of hepatic enzymes in patients on anticonvulsant therapy. 790 70


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