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)

The concentrations of pyridoxal 5'-phosphate, and the holoenzyme activities and apoenzyme contents of alanine aminotransferase and aspartate aminotransferase in plasma were determined simultaneously in healthy individuals, patients with renal insufficiency with and without chronic haemodialysis and in patients with acute myocardial infarction. Plasma pyridoxal 5'-phosphate is significantly diminished in uraemic patients and in post-myocardial infarct sera, healthy females have lower pyridoxal 5'-phosphate levels (26.2 +/- 9.0 nmol/l) than healthy males (41.0 +/- 15.1 nmol/l). The stimulation in vitro of the activities of aspartate aminotransferase and alanine aminotransferase by addition of pyridoxal 5'-phosphate (0.1 mmol/l) was found to be independent of the endogenous coenzyme level. In sera of uraemic patients without chronic haemodialysis an inverse statistic correlation between pyridoxal 5'-phosphate-induced stimulation of aspartate aminotransferase activity and the concentrations of urea (r = -0.696) and creatinine (r = -0.715) was found. The respective correlations are much weaker for alanine aminotransferase. The apoenzyme fraction was highest in post-myocardial infarct sera. Follow up of these patients did not reveal any relationship between the fluctuations of pyridoxal 5'-phosphate levels and apoenzyme contents of both alanine aminotransferase and aspartate aminotransferase. The results permit the conclusion that the degree of in vitro stimulation of aminotransferases by pyridoxal 5'-phosphate can not be predicted from the endogenous coenzyme level.
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PMID:Plasma pyridoxal 5'-phosphate concentrations in relation to apo-aminotransferase levels in normal, uraemic, and post-myocardial infarct sera. 406 14

Sixty-four patients over the age of 40 years, undergoing elective surgery of at least one hour's duration, were randomized to treatment with either a thromboembolic deterrent ( TED ) stocking (Kendall Co.) or subcutaneous low-dose heparin 5 000 IU every 12 hours. Serum levels of alanine aminotransferase (S-ALAT), aspartate aminotransferase (S-ASAT), gamma-glutamyl transpeptidase (S-gamma-GT) and alkaline phosphatase (S-ALP) were measured. S-ALAT increased significantly on the 5th and 10th postoperative day, from 27 +/- 2 (x +/- SE) to 40 +/- 4 (p less than 0.01) and 55 +/- 7 U/l (p less than 0.001), respectively, in the heparin group and was significantly higher in the heparin than in the TED group both on the 5th (p less than 0.01) and 10th (p less than 0.05) postoperative day. S-ASAT and S-gamma-GT increased significantly during heparin treatment, but did not differ significantly from the values of the TED group. No change in S-ALP was registered in either group. It is concluded that prophylactic treatment with low-dose heparin induces a significant increase in S-aminotransferase levels, especially in S-ALAT. The phenomenon has profound differential diagnostic implications in conditions such as pulmonary embolism and acute myocardial infarction.
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PMID:Heparin-induced increase in serum levels of aminotranferases. A controlled clinical trial. 637 73

The course of plasma catalytic activities of total creatine kinase, creatine kinase isoenzyme MB, total, cytoplasmatic and mitochondrial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, glutamate dehydrogenase and concentrations of myoglobin, urea, acidic alpha 1-glycoprotein and creatinine were followed in 33 patients suffering from acute myocardial infarction. All patients were randomized in a double-blind, prospective study. One group (18 patients) was infused with streptokinase 1.5 X 10(6) units/90 minutes; the control group received routine continuous i.v. heparin treatment (1000 units/h). Ten hours after completion of the study protocol, treatment of both groups of patients was continued with heparin, 1000 units/h and Aspisol, 1 g/day2). Streptokinase treatment induced earlier wash-out and therefore earlier peak levels of several enzymes: total creatine kinase (11 hours), creatine kinase isoenzyme MB (6 hours), total and cytoplasmatic aspartate aminotransferase (6 hours) and lactate dehydrogenase (9 hours). Total creatine kinase peak catalytic activity and myoglobin peak concentration were higher in the group receiving thrombolytic therapy. A significantly different course of catalytic activity between both treatment groups was found for total creatine kinase and creatine kinase isoenzyme MB, total and cytosolic aspartate aminotransferase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. The course of mitochondrial aspartate aminotransferase catalytic activity was different only 12 hours after the beginning of treatment. The shift of several catalytic activities to an earlier peak level in plasma may indicate reperfusion of ischaemic myocardium due to thrombolytic therapy.
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PMID:Systemic short-term fibrinolysis with high-dose streptokinase in acute myocardial infarction: time course of biochemical parameters. 639 65

We examined sera from 159 patients with ischemic heart disease and hypertension and from 50 apparently healthy control subjects for content of trace elements, cholesterol, triglyceride, and enzymes. Concentrations of copper, cobalt, cholesterol, and triglyceride were increased in all patients, but calcium was decreased in patients with hypertension, acute myocardial ischemia, and acute myocardial infarction. Also accompanying acute myocardial infarction were decreased concentrations of zinc and iron but increases in nickel, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Magnesium concentration was lower in patients with acute myocardial ischemia. In acute myocardial infarction, the concentrations of copper, zinc, and iron were higher after 21-30 h (as compared with the values at 0-10 h), by which time concentrations of calcium, magnesium, cobalt, and alanine aminotransferase had decreased. The variation in concentration of trace elements in serum from cases of ischemic heart disease and hypertension corresponds to the severity of the disorder.
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PMID:Trace elements in serum from Pakistani patients with acute and chronic ischemic heart disease and hypertension. 671 25

A latex agglutination test for detection of elevated levels of myoglobin in serum has been studied, and its clinical value in diagnosis of acute myocardial infarction (AMI) has been evaluated on a retrospective material of fifty-five patients consecutively admitted to hospital on suspicion for AMI within 4 h after onset of symptoms. The analysis time was less than 10 min. There was no evidence of interference with other related proteins, as judged from analysis of sera with high content of aspartate and alanine aminotransferase, lactate dehydrogenase and creatine kinase, nor was the test sensitive to haemolysis. However, unspecific agglutination was seen with some sera containing a high concentration of rheumatoid factors. In sera with known concentrations of myoglobin, quantitated by a radioimmunoassay, the test was negative in all sera below 80 micrograms/l (n = 187), and positive in all sera above 140 micrograms/l (n = 209). In the range 80-140 micrograms/l the latex test could be either positive or negative (n = 105). The day-to-day reproducibility was high in the ranges below 80 micrograms/l and above 140 micrograms/l, but range 80-140 micrograms/l. In the diagnosis of AMI the predictive value of a positive result was 0.64, and the predictive value of a negative result was 1.0. The latex agglutination test is therefore clinically useful as an emergency test, and as a very early and sensitive indicator for AMI. Patients with a negative test result during the first 12 h after debut of symptoms can with great certainty be identified as not suffering from AMI, whereas patients with a positive test result should be monitored by further laboratory analyses.
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PMID:A rapid latex agglutination test for detection of elevated levels of myoglobin in serum and its value in the early diagnosis of acute myocardial infarction. 671 25

Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase (AST) were studied in the sera of 42 patients following acute myocardial infarction and compared to creatine kinase (CK), lactate dehydrogenase (LDH) and alanine aminotransferase (ALT). Mitochondrial AST( ASTm ) was detected in 93% (39/42) of patients. Maximum recorded ASTm activity was 59.5 +/- 8.8 U/l and was found 39.4 +/- 3.5 hours after the onset of symptoms (chest pain) of myocardial infarction. In contrast the maximum recorded cytoplasmic AST ( ASTc ) activity was greater (327 +/- 23 U/l) and it occurred earlier (33.5 +/- 2.2 hours) after onset of infarction compared to ASTm . ASTm correlated significantly (p less than 0.05) with ASTc , LDH and ALT but not with total CK or CK-MB. ASTc correlated significantly (p less than 0.05) with total CK, CK-MB and LDH but not ALT. Maximum recorded ASTm activity was significantly associated with the clinical assessment of left ventricular failure ( Killip classification) but not with ventricular arrhythmias. In a subset of 15 patients evaluated with invasive hemodynamic measurements of cardiac output and pulmonary capillary wedge pressure. ASTm correlated significantly (p less than 0.05) and better than CK-MB with the hemodynamic assessment of left ventricular dysfunction. Thus ASTSm can be readily identified in sera of patients after acute myocardial infarction and may be of value in the evaluation of patients with acute myocardial infarction.
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PMID:Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase in sera of patients after myocardial infarction. 672 62

Serum guanase activity was measured by a new method using direct colorimetric determination of ammonia in 25 patients with acute myocardial infarction, 21 dogs with experimental myocardial infarction and 6 CCl4-treated dogs, and compared with serum GOT and GPT activity. We found normal serum guanase activity in patients with acute myocardial infarction and in dogs with experimental myocardial infarction without liver damage, even when the serum GOT and GPT activities increased. On the other hand, serum guanase and transaminase activities were elevated significantly in the patients with acute myocardial infarction who had prominent symptoms of cardiac failure and congestion of the liver and CCl4-treated dogs. These findings suggested that the serum guanase activity was more specific than serum GOT and GPT activity as an indicator of liver damage and determination of serum guanase activity in the patients with acute myocardial infarction might be useful in assessing the presence of liver impairment.
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PMID:Clinical and experimental studies of the determination of serum guanase activity in acute myocardial infarction. 723 May 7

Ribonuclease (RNase) activity measured at pH 7.8 (the alkaline RNase) and pH 6.7 (the acid RNase) was estimated in serum of 54 patients with acute myocardial infarction (AMI). The estimations were performed on the first day of disease, then on the seven consecutive days and on the 14th day. A significant elevation in both alkaline and acid RNase activities on days 1--7 of AMI was found, compared with healthy control subjects. Elevation in both acid and alkaline RNase activity began on the 1st day of AMI and continued to increase up to peak values on the 3rd day for acid RNase and the 5 the day for alkaline RNase. On the 14th day both alkaline and acid RNase activities came back to the range found in normal sera. Increase in serum acid and alkaline RNase activity in AMI showed a time pattern different from that of GOT and GPT aminotransferases. However, the relationship between the elevation of serum RNase activity and severity of the disease was obvious.
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PMID:Serum ribonuclease activity in acute myocardial infarction. 729 72

A new method was developed for assay of guanase activity by direct colorimetric determination of ammonia. In this method, dotite bicine buffer is used for preparation of a stable substrate solution and with a fixed concentration of substrate of sufficient strength serum guanase can be measured sensitively and reproducibly. This assay system could be used as a routine clinical laboratory test in the diagnosis of liver damage. GOT, GPT and guanase activities were found to be significantly elevated in patients with various liver disorders, and those with acute myocardial infarction with prominent congestion of the liver and also in CCl4- treated dogs. However, serum guanase activity was normal in patients with various other diseases, in those with acute myocardial infarction and in dogs with experimental myocardial infarction without liver damage, even when the serum GOT and GPT activities were increased. The GOT, GPT and guanase in the medium of rat hepato cytes culture with 5.0 mM CCl4 were elevated. These findings suggest that serum guanase activity is a more specific indicator of liver damage than serum GOT and GPT. The determination of serum guanase activity in patients without liver damage, even when their serum GOT and GPT levels elevated, might be useful as a screening test of liver damage.
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PMID:Clinical evaluation of measurement of serum guanase activity as a screening test of liver damage. 732 86

An elevation of serum aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) may be produced in patients treated with i.v. full-dose HEPARIN. We studied the influence of low-dose s.c. HEPARIN (5,000 IU X 2) in 34 patients with acute myocardial infarction (AMI) and in 7 with cerebrovascular accidents or calf thrombophlebitis. Twelve patients (all males) with AMI showed a secondary elevation of GOT and GPT at about the sixth or seventh day after the commencement of therapy that persisted throughout the period of treatment. Four patients (two males and two females) with cerebrovascular accidents or thrombophlebitis showed similar increases of GOT and GPT.
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PMID:Hypertransaminasemia with subcutaneous heparin therapy. 732 13


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