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)

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

The time course of changes in serum proteins and other blood constituents after eccentric exercise of the forearm flexors by six nonweight-trained female subjects (age, 19.7 +/- 1.9 years) was investigated. Eccentric muscle actions are those in which the muscle lengthens as it exerts force, as when a person lowers a weight. Serum levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, myoglobin, as well as urea nitrogen, uric acid, creatinine, calcium, and phosphorus were examined before and for 6 days after exercise. Creatine kinase increased dramatically (peak value ranged from 6740 to 24,200 U/L) and aspartate aminotransferase, lactate dehydrogenase, alanine aminotransferase, and myoglobin followed the same time course as creatine kinase, but their peak values were lower. These proteins did not increase significantly until 48 hours after exercise and reached peak values 3 to 5 days after exercise. Alkaline phosphatase, gamma-glutamyl transpeptidase, uric acid, urea nitrogen, creatinine, calcium, and phosphorus showed no change. There is either a delay in muscle protein release by damaged muscle fibers, or the proteins are unable to leave the interstitial area for the 24 to 48 hour period after exercise. Because of the long delay, care should be taken when blood protein levels are interpreted in persons who have exercised strenuously (even if only for a short period of intense effort) several days before any diagnostic tests are performed.
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PMID:Time course of serum protein changes after strenuous exercise of the forearm flexors. 174 Jun 32

A 74-year-old male was admitted to hospital with acute rhabdomyolysis and myoglobinuria due to hypokalemia. The hypokalemia resulted from diuretic treatment. He had no family history of myopathy, and no diarrhea and vomiting. The neurological examination revealed painful quadriplegia. The blood pressure was 160/74 mm Hg. Laboratory examination showed hypokalemic and hypochloremic metabolic alkalosis (serum K 1.5 mEq/l, serum Cl 89 mEq/l, base excess + 20.9, HCO3- 44.9 mmol/l, pH 7.563) and marked elevations of serum CPK, LDH, GOT, GPT and myoglobin. Endocrinological and renal functions were normal. Muscle biopsy revealed marked necrosis with remarkable phagocytosis and vacuolar degeneration. The cessation of diuretics and intravenous infusion of potassium chloride resulted in a marked improvement in clinical and laboratory findings. The diuretics-induced hypokalemic myopathy is rare in the literature.
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PMID:Marked hypokalemic rhabdomyolysis with myoglobinuria due to diuretic treatment. 175 65

Biochemical evaluation of 60 patients with crush syndrome developing after the Armenian earthquake demonstrated informative value of some parameters: total blood protein, aspartate and alanine aminotransferase, myoglobin and middle-mass molecules. An aggravation of the disease accompanied acute renal failure and concomitant injuries. The above parameters proved valuable criteria in diagnosis of the clinical alterations.
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PMID:[Clinical-laboratory parallels in crush syndrome]. 178 87

A 77-year-old woman with a 9 years history of Parkinson's disease was admitted to our hospital because of high fever, disturbance of consciousness, increased muscular rigidity and abnormal involuntary movements. She was continuously treated with levodopa + carbidopa (Menesit) 300 mg and amantadine 150 mg every day until admission. On admission, the pulse rate was 102 per minute, blood pressure 90/40 mmHg, body temperature 40.9 degrees C, and bloody stool was noticed. On laboratory examination, erythrocyte sedimentation rate was 6 mm/h, thrombocytes 8.1 X 10(4)/microliters, fibrinogen 91 mg/dl, FDP 40 mg/ml, suggesting DIC. According to her biochemical examination, serum GOT (167 u), GPT (119 u), CPK (847 IU/l), BUN (53.9 mg/dl) and myoglobin (10,370 ng/ml) were increased. These laboratory data indicated that she was suffering from neuroleptic malignant syndrome (NMS) with disseminated intravascular coagulation (DIC). On diagnosis of NMS associated with DIC, she was treated with dantrolene and FUT-175. Dantrolene was effective on the elevated COK level and FUT-175 was effective on the DIC, and symptoms of NMS and DIC were completely improved after a period of 14 days. Patients with Parkinson's disease have been suspected to have a low incidence of DIC, and this may be the first case report on successful treatment of levodopa-induced NMS with DIC in the patient with Parkinson's disease.
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PMID:[Successful treatment of levodopa-induced neuroleptic malignant syndrome (NMS) with disseminated intravascular coagulation (DIC) in a patient with Parkinson's disease]. 204 8

An autopsy case of rhabdomyolysis following homicidal intoxication of paraphenylenediamine was reported and the toxicological mechanism of PPD against skeletal muscles was discussed. The case was a 44 years old, previously healthy male, drinking a beverage containing PPD, prepared for a homicidal use. Total intake of PPD was about 3 g (63 mg/kg). Principal clinical manifestation of the patient was muscle rigor with tenderness, initially developed in the lower extremities and subsequently extending to all over the skeletal muscles. Laboratory examinations disclosed high CPK (137,600), LDH (3895), GOT (3400) and GPT (545), and leukocytosis (26600), indicating massive skeletal muscle necrosis. ECG revealed mild depression of ST junction in the II and aVF leads. Urine showed dark brownish discoloration and diminished in volume subsequently. Scattered necrosis of muscular fibers was observed in a biopsy of the femoral muscles. The consciousness was rather clear during the course. The patient collapsed suddenly and soon died in the course of about 30 hours. Clinically, the cause of death was thought to be acute renal failure due to rhabdomyolysis. Afterwards PPD was detected in the urine obtained in the hospital. Autopsy confirmed the clinical diagnosis: Renal collecting ductules and distal tubules were occluded by dark brownish myoglobin casts and its epithelium massively necrotized; Skeletal muscles showed scatteredly coagulation necrosis and were partially associated with inflammatory cell infiltration.
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PMID:[Rhabdomyolysis due to paraphenylenediamine (hair dye)--report of an autopsy case]. 207 68

The serum myoglobin (MG) was assayed by the radio-immunological method in 30 patients, all victims of a recent myocardial infarction (MI) and in 30 tests subjects suffering (21 cases) or not (9 cases) from heart diseases, but none from myocardial infarction (MI). The blood samples have been collected on hospital admission of the patient, then every four hours during the first 48 hours and finally, every 12 hours from the 48th to 72nd hour. The normal value is less than 85 micrograms/l. The creatine-kinase (CK), the aspartate aminotransferase (ASAT), the alanine aminotransferase (ALAT) and the lactate dehydrogenase (LDH) were also assayed each time. In MI, there is a significant increase in the serum MG level (731 +/- 323 micrograms/l against 174 +/- 198 micrograms/l in the test subjects; p less than 0.001). The sensitivity of this assay reaches 97%, its specificity 80%, its positive predictive value 83% and its negative predictive value 96%. Starting from the beginning of the characteristic pain of infarction, the MG level exceeds the normal values after 3.3 +/- 1.6 hours, reaches its maximum after 9.3 +/- 3.7 hours and comes back to normal after 38 +/- 8.1 hours. On the other hand, the MG level does not enable any conclusion regarding either the transmural/not transmural nature, or the site, or the acuteness of the MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Value of the assay of serum myoglobin in recent myocardial infarction]. 218 59

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.
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PMID:Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom? 252 Mar 58

We studied the behaviour of serum myoglobin and of serum enzymes in 25 young men, before and after physical stress. The stress appeared to markedly increase myoglobin, aldolase and CK activity and to a lesser extent GOT. Myoglobin, aldolase return to normal levels within 24 hours but CK appeared to decrease more slowly. The simultaneous determination of some organic-specific enzymes (CK-MB, gamma-GT, GPT) permitted us to state that the myocardium and liver are not involved in the increase of tests following muscular stress.
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PMID:[Variations in serum myoglobin due to physical exertion]. 613 26

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


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