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)

Out of 368 patients admitted to hospital for chest pain and suspected acute myocardial infarction, 267 were discharged within 24 hours on the basis of the clinical picture, electrocardiogram, and serum activities of aspartate transaminase, alpha-hydroxybutyrate dehydrogenase, and creatine phosphokinase. The patients were followed up for 28 days, during which 17 were readmitted, two of them twice and one three times. Two of the patients were readmitted with non-fatal acute myocardial infarction, and two died. The patients had been primarily divided into two groups: those admitted with presumably non-coronary chest pain (77 patients) formed group 1 and those with obvious coronary chest pain (190 patients) group 2. Both deaths occurred in patients in group 2 but the incidences of events during the follow-up period were otherwise similar in the two groups, and some patients in both groups may have had small acute myocardial infarctions when first admitted. The decision to keep in hospital or discharge a patient with chest pain of recent onset can be made within 24 hours of admission. To discharge the patient acute myocardial infarction need not necessarily be excluded and conventional tests are enough to enable a decision to be made.
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PMID:How long should patients with suspected myocardial infarction be under observation in hospital? 742 22

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43

Differential diagnosis of patients who present with chest pain remains problematical. It has been shown that 11.8-7% of patients with acute myocardial infarction (AMI) are sent home from the emergency department (ED). Audit of our own ED has shown the incidence of missed prognostically significant myocardial damage to be 6.7%. Diagnostic criteria for AMI have classically been based on the triad of history, ECG and measurement of cardiac enzymes. The choice of 'cardiac enzymes' has been dictated by the evolution of laboratory techniques, commencing with measurement of aspartate transaminase and progressing to measurement of creatine kinase (CK) and its MB isoenzyme (CK-MB). Measurement of CK-MB has been shown by both clinical studies and rigorous statistical analysis to represent the best test for the diagnosis of AMI. The advent of real time immunoassay together with advances in therapeutic options for management of acute coronary syndromes (ACS) has resulted in a paradigm shift in the approach to laboratory testing. Immunoassay for CK-MB (CK-MB mass measurement) is diagnostically superior to CK-MB activity measurement and is the test of choice for 'classical' AMI. Development of immunoassays for the cardiac troponins, i.e. cardiac troponin T (cTnT) and cardiac troponin I (cTnI), has enhanced diagnostic specificity. These measurements are completely specific for cardiac damage, allow quantitation of the extent of infarction and are diagnostically superior to CK-MB measurement. Applications of this specificity have included the differential diagnosis of CK elevation in arduous physical training, detection of myocardial damage after DC cardioversion and prediction of ejection fraction. Of more interest is the utility of these markers in management of patients presenting without clear electrocardiographic changes. Diagnosis and management of patients presenting with ST segment elevation has been clarified by large clinical trials of thrombolytic agents. In such patients, thrombolysis is the treatment of choice. Patients presenting with ST segment elevation represents the minority of patients with probable ACS 9.6% of all patients presenting to our hospital. The majority require risk stratification into high- and low-risk groups. It is here that cardiac troponins have a major role. The measurement of cTnT has been shown in a large number of studies to enable risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification which can be completed by 24 h from admission, as well as allowing a safe discharge policy from the ED. Measurements of cardiac troponins can also be used to predict prognosis in patients with other diagnostic categories. Patients with cardiac failure can be risk stratified according to cTnT status. cTnT status on admission allows subdivision into high- and low-risk groups in patients presenting with ST segment elevation. Certainly, cTnT measurement can be incorporated into a clinical decision-making strategy to assign patients to investigation and management pathways. There is evidence that cTnT may be useful to guide therapeutic options. The major issue is one of cost. In the U.K. model of managed care with undemanding diagnostic standards, the role of cTnT will be to enhance clinical decision-making strategies, to provide accurate diagnosis and to reduce lengths of stay. This can be shown to have potential for major improvements in cost efficiency. Improvements in diagnostic accuracy can reduce inappropriate long-term drug therapy. In systems with a more aggressive laboratory investigation strategy, rationalization of test numbers will provide an immediate cost reduction while improving quality. Finally, use of point-of-care testing (POCT) means that biochemical testing can be pe
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PMID:Troponin T or troponin I or CK-MB (or none?). 985 34

Assays of serum enzymes, such as aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and isoenzyme MB, are widely performed in the early phase of suspected ischemic myocardial injury. However, these enzymes are not restricted to cardiac muscle tissue and increases in their serum concentrations have been observed in non-cardiac conditions. The levels of CK, and especially those of the myocardial specific isoform (CK-MB), have served as essential components for clinical decision in emergency rooms for over 25 years. This standard diagnostic test is far from perfect in specificity and the time delay necessary for the detection of a rise in levels. The clinician needs specific and sensitive biological parameters that can be rapidly measured in serum immediately after ischemic damage. In the last years, several new serum markers of myocardial damage have been developed. Currently, an important place is reserved for some non-enzyme muscle constituents, such as myoglobin and troponin sub-units, which have better specificity and allow an earlier detection of myocardial damage. The immunoassay of human cardiac troponin is a specific and sensitive diagnostic method for acute and sub-acute myocardial damage. It is ideal for the detection of myocardial necrosis in complex clinical situations when the usual enzymatic markers may be ineffective. An important prognostic value of troponin levels, especially troponin T, is currently under investigation. Myoglobin is a protein with low molecular weight that is abnormally high in serum two hours after myocardial infarction. Despite their high sensitivity, the use of serum measurements in the emergency room is controversial because of their low specificity, requiring the exclusion of skeletal muscle damage. Sensitivity could be lost in patients with renal function damage. The measurement of CK-MB protein weight (CK-MBmass) is another marker that has been confirmed as more accurate than CK-MB activity assays, especially in patients presented within four hours after the onset of chest pain, but could be inaccurate in several circumstances. In this research article, the authors describe the most important parameters of enzymatic and non-enzymatic markers, the kinetics of serum release, the clinical applications and the problems.
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PMID:[Serum markers for ischemic myocardial damage]. 1066 Oct 20

Two patients, both women aged 31 and 73 years, were admitted with chest pain and coma, respectively. They had very high aspartate aminotransferase levels, accompanied by relatively low alanine aminotransferase levels. The second patient had developed acute liver failure and hepatic encephalopathy. Both patients were chronic alcohol abusers and had taken therapeutic doses of acetaminophen for a couple of days. The marked elevation of the aminotransferase levels and the rapid decline of these levels after discontinuing the use of acetaminophen and alcohol led to the diagnosis of acetaminophen hepatotoxicity. In chronic alcohol abusers, cytochrome P450 2E1 is induced and the amount of glutathione is depleted. This combination causes the formation of a relatively large amount of the radical N-acetyl-p-benzoquinone imine and a low potential to detoxify this metabolite, so that even small amounts of acetaminophen may cause liver damage. It is recommended that chronic alcohol abusers (more than four alcoholic beverages per day) use no more than 2 g acetaminophen per day.
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PMID:[Acetaminophen use by chronic alcohol abusers: a therapeutic dose may be too much for the liver]. 1192 19

We experienced a girl with polyarteritis nodosa (PN) diagnosed by myocardial biopsy. The symptoms began with high fever and skin rash. These symptoms and laboratory findings temporarily improved by oral prednisolone, however, she flared up with chest pain about 40 days after onset of the disease. Electrocardiogram indicated the elevation of ST-T levels and low voltage, and blood examination showed remarkable elevation of creatine phosphokinase (CK), white blood cell count (WBC), aspartate aminotransferase (AST) and lactic dehydrogenase (LDH) levels. We suspected systemic vasculitis and damage of coronary artery or/and heart muscle. Finally, she was diagnosed with classical polyarteritis nodosa by myocardial biopsy. Coronary angiography revealed no abnormalities. The combination therapy of cyclophosphamide pulses and plasma-exchange was very effective to suppress the disease activity.
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PMID:[A case of classical polyarteritis nodosa diagnosed by myocardial biopsy]. 1204 86

We experienced 4 cases of agranulocytosis due to anti-tuberculosis drugs (rifampicin [RFP], isoniazid [INH], ethambutol [EB], streptomycin [SM] or pyrazinamide [PZA]) among some 6,400 tuberculosis patients who underwent chemotherapy over the past 20 years from 1981 to 2002 in our hospital, and the incidence rate of agranulocytosis was estimated at 0.06%. The 4 cases of agranulocytosis were as follows. CASE 1: A 51-year-old woman with right chest pain and fever was admitted to our hospital on Jan 4, 2001. The white blood cell (WBC) count was 5,200/microliter. The tubercle bacilli were cultured in her sputum. The treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, allopurinol and teprenone was started on Jan 13. Pyrazinamide and allopurinol were stopped because of hyper-uric acidemia on Feb 7. Agranulocytosis and eosinophilia (WBC 1,300 [Neut 1%, Ly 57%, Eos 35%]) developed on Feb 13. All drugs were withdrawn and G-CSF drug nartograstim 100 micrograms was injected subcutaneously for 3 days. The WBC recovered to normal level and she was thereafter treated with INH, EB and Levofloxacin (LVFX) without any further trouble. Agranulocytosis in this case was supposed to be due to RFP. CASE 2: A 66-year-old man who had had nephrotic syndrome and hypothyroidism and has been treated with prednisolone 10 mg/day was admitted to our hospital on Aug 9, 2000 because of miliary tuberculosis. The tubercle bacilli were cultured in his sputum and the treatment with INH 0.3, RFP 0.45, and EB 0.75 g/day were started on Aug 10, but it was withdrawn on Aug 17 because of general skin eruption. After re-starting treatment with EB and INH on Aug 24, RFP was added in small dosage (0.05 g) on Oct 12, but agranulomatosis (WBC 2,300/microliter [Neut 2%]) developed on Nov 21, and all drugs were withdrawn again. The G-CSF drug filgrastim was used once subcutaneously, and WBC recovered immediately. He was thereafter treated with INH, EB, LVFX successfully. Agranulocytosis was supposed to be due to RFP. CASE 3: A 60-year-old woman without symptoms had abnormal chest roentgenograph, and consulted with our hospital on Aug 26, 2002. The broncho-alveolar lavage fluid was smear and culture-negative, but PCR-TB positive, and the case was diagnosed as pulmonary tuberculosis. Treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, alloprinol 300 mg and rebamipide 300 mg/day was started on Sept. 5, 2002. Late in September, she complained of appetite loss. The laboratory data on Oct 3 revealed WBC 900/microliter (Neut 1%, Ly 94%), aspartate aminotransferase (AST) 199 IU/l, and alanine aminotransferase (ALT) 253 IU/l, showing agranulocytosis and drug-induced hepatitis. The chemotherapy was immediately withdrawn and she was admitted to our hospital on the next day. Glycyrrhizin derivative (SNMC) 40 ml was injected for 5 days, and WBC recovered, and AST and ALT also became normal. CASE 4: A 60-year-old man was admitted to our hospital on March 11, 1981 because pulmonary tuberculosis had recurred. He had been treated with SM, PAS and INH in 1973 for pulmonary tuberculosis. On admission examination of blood count and blood chemistry were normal. Treatment with RFP, INH and SM was started on March 11. He stopped out from the hospital on April 17, but in a few days he returned back with sore throat, lower lip swelling and gingival bleeding. Blood cell count on April 24 showed pancytopenia with RBC 226, Hb 7.5, WBC 800 (Ly 96%, Eos 4%) and Plt 10,000/microliter. The bone-marrow showed NCC (nuceated cell count) of 5,500, and megakaryocyte 0. Thereafter ground glass appearance shadows were seen on the whole lung field, and he died May 26. Autopsy showed generalized aspergillosis. It was strongly suspected that either of RFP, INH or SM was responsible for his pancytopenia. We collected another 10 cases of agranulocytosis due to anti-tuberculosis drugs in the world wide literature, and found men/women ratio 5/8 (in one case gender was not known), the duration of chemotherapy before appearance of agranulocytosis 1-3 months, no change in the lymphocyte count of the peripheral blood, and the accompanying of another allergic signs such as skin eruption, blood eosinophilia or drug-induced hepatitis in some cases, and these findings suggest that the mechanism of agranulocytosis due to anti-tuberculosis drugs was allergic in nature.
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PMID:[Agranulocytosis due to anti-tuberculosis drugs including isoniazid (INH) and rifampicin (RFP)--a report of four cases and review of the literature]. 1467 45

We prospectively and blindly assessed the diagnostic and prognostic impact of implementation of the European Society of Cardiology/American College of Cardiology recommendations for redefinition of myocardial infarction (MI) in an unselected cohort of patients with suspected cardiac chest pain, with particular attention to prespecified clinical groups. All patients admitted to our institute with suspected cardiac chest pain were enrolled. Physicians provided usual care using serial electrocardiograms/creatine kinase (CK)/aspartate transaminase according to World Health Organization (WHO) criteria for MI, while blinded to additional measurements of cardiac troponin T (cTnT) and CK-MB mass. After discharge, diagnoses based on WHO and new criteria were compared, and major adverse cardiac events monitored for 6 months. Implementation of the new recommendations classified an additional 26.1% of patients as having MI compared with WHO criteria, and produced an overall diagnostic alteration in 11.5%. Two thirds of the additional patients with MI were previously diagnosed with unstable angina, whereas one third had "other cardiac" or "noncardiac" diagnoses. A similar MI cohort to the cTnT diagnosis was identified using a CK-MB mass discriminator value of 5 microg/L, but not 10 microg/L. The 6-month prognosis was similar in patients diagnosed with MI by new (cTnT) and WHO criteria, with the new criteria thus identifying a further high-risk cohort in the WHO negative group. In our cohort, the new Joint European Society of Cardiology/American College of Cardiology recommendations identify one fourth more patients as having MI. The 6-month prognosis of those patients reclassified as having MI was similar to those diagnosed with MI by both criteria.
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PMID:Impact of the recommendations for the redefinition of myocardial infarction on diagnosis and prognosis in an unselected United Kingdom cohort with suspected cardiac chest pain. 1505 Apr 81

For many years, cardiac markers have been used to assist cardiologists in the diagnosis and management of patients with cardiovascular disease. At first, enzyme activities of aspartate aminotransferase, lactate dehydrogenase and creatine kinase have been used in diagnosing patients with chest pain in order to differentiate those with acute myocardial infarction. In the field of cardiac markers, emphasis is currently put on the use of protein markers such as myoglobin, and cardiac troponin T or I. Troponins are very highly cardiac specific and their concentration in blood increase only from four to six hours after the onset of chest pain. Today we obligatorily use two markers, the first being the early one (myoglobin, isoform of creatine kinase), which is very sensitive and shows up in the circulation one to two hours after myocardial damage. Confirmation of myocardial damage can be obtained by definite markers (troponin I or T), which are highly specific of myocardial damage.
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PMID:[Biochemical markers in acute coronary syndrome]. 1520 94

Adult-onset glycogen storage disease type II (GSD-II), unlike the infantile form, is not normally associated with coexisting cardiovascular pathologies. In infantile onset GSD-II, cardiomyopathy is a common feature, and mutations in the genes for cardiac troponin T and I are likely to be involved. This case report describes a 39-year-old man with no classical risk factors for premature cardiac disease who presented with central chest pain and shortness of breath. Serum aspartate transaminase (AST) had been consistently elevated for 15 years. Adult GSD-II had been diagnosed two years previously by muscle biopsy. On presentation, there was an elevated serum creatine kinase and AST. Electrocardiography and echocardiography were both normal, and an acute coronary syndrome was ruled out. Cardiac Troponin T (cTnT) was found to be positive at 0.1 microg/L using a Cardiac Reader, subsequently confirmed on an Elecsys 1010 (both from Roche Diagnostics, Lewes, UK). cTnT may therefore be a useful biomarker in examining subclinical cardiac involvement in GSD-II patients.
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PMID:Evidence of cardiomyocyte necrosis in glycogen storage disease type II. 1727 99


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