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)

A total of 42 birds from a flock of 104 farmed ostriches showed signs of toxicity after the accidental inclusion of monensin in their concentrate ration. The initial clinical signs were muscle weakness and ataxia which progressed to recumbency, dyspnoea and death, despite intensive supportive therapy. The serum activity of the enzymes creatine kinase, aspartate aminotransferase and lactate dehydrogenase was high in the affected birds, indicating significant muscle pathology. Few gross lesions were identifiable postmortem, but widespread lesions of degenerative myopathy were present at the histopathological level. However, these degenerative changes were restricted to the skeletal muscle and there was no evidence of cardiomyopathy in any of the birds examined. The birds were fed a ration which contained 215 to 224 ppm monensin for 13 days. New clinical cases ceased to occur shortly after the withdrawal of the source of monensin, but all the individuals which showed clinical signs of toxicity died or were euthanased on humane grounds.
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PMID:Monensin toxicity in a flock of ostriches. 922 93

The selenium status of sheep was evaluated during the reproductive stage in a region of low selenium level. Serum selenium concentration, whole blood glutathione peroxidase activity (GSH-Px), which is a good indicator of protection against oxidative damage, as well as the activities of creatine kinase (CK) and aspartate aminotransferase (AST), the plasma indicators of muscle damage, were evaluated in a group of ewes during gestation and lactation and in their lambs. The selenium requirements of ewes were found to increase during lactation. There were no differences in GSH-Px activity between the experimental and the control groups throughout the reproductive stage. In the second half of pregnancy GSH-Px activity was subnormal. In spite of this, no evidence of existing pathologic conditions associated with selenium deficiency was found, since the muscle markers CK and AST were within the normal range. In the same way, no distinct symptoms of nutritional myopathy were observed in the lambs, suggesting that the low selenium level found in the ewes did not cause alterations in their development.
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PMID:The influence of reproductive stage on the selenium status of sheep in a low-selenium region. 970 15

Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied. A 57-year-old man with AIDS, who had been treated with zidovudine for 3 years, developed fatigue and weight loss. Serum creatine kinase and hepatic enzyme levels were high. Lactic acidosis was present. Liver biopsy showed diffuse macrovacuolar and microvacuolar steatosis. After withdrawal of zidovudine, creatine kinase, aspartate aminotransferase, and alanine aminotransferase levels normalised within 5 days, and lactacidaemia decreased. Acidosis persisted. The patient became confused and febrile and died 8 days after detection of high blood lactic acid. A muscle sample obtained at autopsy showed mitochondrial abnormalities with ragged-red fibres and lipid droplet accumulation. Southern blot analysis showed depletion of mitochondrial DNA, affecting skeletal muscle and liver tissue. No depletion was found in myocardium and kidney. This case emphasises that zidovudine treatment can induce mitochondrial multisystem disease, as revealed in our case by myopathy, liver steatosis and lactic acidosis.
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PMID:Zidovudine-induced mitochondrial disorder with massive liver steatosis, myopathy, lactic acidosis, and mitochondrial DNA depletion. 1070 83

Ten years' experience of treatment with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin in 45 hypercholesterolemic high-risk patients is reported. All patients started with 20 mg simvastatin/day. The simvastatin dose was increased to 40 mg in 22 patients. Fourteen patients needed further addition of cholestyramine. Simvastatin reduced plasma cholesterol by 33% after 1 month and was further reduced after adjustment of the lipid-lowering treatment. The mean reduction in plasma cholesterol varied between 30% and 35% in 2 to 10 years. Low-density lipoprotein cholesterol demonstrated mean reductions of 34% to 42%. Mean plasma triglycerides were reduced by 26% after 1 month and by 1% to 19% the following years. High-density lipoprotein (HDL) cholesterol increased initially by 8% and remained elevated at 7% to 11% during the first 6 years, but then dropped slightly below baseline. HDL2 cholesterol increased by 9% to 25% the first 6 years and then decreased. HDL3 cholesterol showed a persistent elevation during simvastatin treatment. About half of the subjects had minor transient but clinical insignificant increases in creatine kinase. No cases of myopathy were seen. Mean serum aspartate aminotransferase and alanine aminotransferase increased significantly but within the normal ranges during the 10 years. The tolerability and compliance of simvastatin treatment was excellent as judged from patients' reports and from analyses of low-density lipoprotein cholesterol. This 10-year study demonstrates that simvastatin is an effective and safe drug with excellent tolerability with only few minor side effects, and causes a pronounced and persistent cholesterol-lowering effect during long-term treatment of hypercholesterolemic patients at risk.
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PMID:Efficacy and safety of simvastatin for high-risk hypercholesterolemia. 1019 May 17

Lesions consistent with exertional myopathy (EM) were documented postmortem in four North American river otters (Lutra canadensis) during translocation for a population restoration project. Clinical signs in these otters included depression, anorexia and shock. Gross lesions in one otter included locally extensive linear, pale areas within the subscapularis, rectus abdominis, quadriceps, and dorsal laryngeal muscles. Microscopic lesions were characterized by acute to subacute myofiber necrosis of varying severity, and occurred in a variety of skeletal muscles as well as cardiac muscle in one otter. Based on these observations, we conducted a retrospective review of records of otters which experienced similar capture, transfer, and holding protocols between 1995 and 1997, but with a successful outcome (n = 69). Significant elevations in serum aspartate aminotransferase (AST) and creatine kinase (CK) were observed in 19 (28%) of the otters, but may have been higher due to delayed sample collection from some otters. However, none of the otters with elevated enzymes exhibited clinical signs suggestive of EM. These findings indicate that river otters may develop EM when translocated, but many cases may be mild or clinically inapparent.
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PMID:Exertional myopathy in translocated river otters from New York. 1047 89

Skeletal muscle samples from 38 draft horse-related animals 1-23 years of age were evaluated for evidence of aggregates of glycogen and complex polysaccharide characteristic of equine polysaccharide storage myopathy (EPSSM). Cardiac muscle from 12 of these horses was also examined. Antemortem serum levels of creatine kinase (CK) and aspartate aminotransferase (AST) from 9 horses with EPSSM and 5 horses without EPSSM were compared. Skeletal muscle from 17 horses contained inclusions of periodic acid-Schiff (PAS)-positive, amylase-resistant complex polysaccharide. Similar inclusions were also present in the cardiac muscle of 1 horse. A vacuolar myopathy with aggregates of PAS-positive, amylase-sensitive glycogen was seen in 8 other horses, and these findings are also considered diagnostic for EPSSM. Antemortem serum activities of CK and AST were often higher in EPSSM horses than in horses without EPSSM. Using the presence of amylase-resistant complex polysaccharide as the criterion for diagnosis of EPSSM, the incidence in this population was 45%. Inclusion of horses with aggregates of glycogen but no amylase-resistant complex polysaccharide as representative of the range of pathologic findings in horses with EPSSM resulted in a 66% incidence in this population.
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PMID:Incidence of polysaccharide storage myopathy in draft horse-related breeds: a necropsy study of 37 horses and a mule. 1124 65

Three adult brown pelicans (Pelicanus occidentalis) were observed to be weak, anorexic and unresponsive to antibiotics, anti-inflammatory drugs, vitamins including vitamin E, and steroids. Blood chemistry revealed high activities of aspartate aminotransferase, creatinine kinase and lactate dehydrogenase. Radiographs of the birds' leg muscles revealed multiple opacities suggestive of calcification; the gross lesions included white streaks in the leg, wing, and heart muscles, and the microscopical lesions consisted of various degrees of degeneration and necrosis characterised by eosinophilia, variations in fibre size, loss of striations, myolysis, mineralisation, and proliferation of mononuclear cells in the skeletal muscles and the myocardium. The levels of heavy metals, selenium and vitamin E in the birds' livers were not abnormal. The level of peroxide in their diet of capelin fish was high, 69 meq/kg, (normal <20 meq/kg) consistent with rancid feed, and the level of vitamin E was very low, 0.5 iu/kg (normal 20 to 30 iu/kg). It was concluded that the myopathy was probably caused by vitamin E deficiency due to feeding the pelicans a rancid diet.
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PMID:Myopathy in brown pelicans (Pelicanus occidentalis) associated with rancid feed. 1191 85

The clinical correlation between serum muscle enzymes, muscle pathology and muscle weakness was studied in 100 Thai patients (22 males and 78 females) with polymyositis (PM) and dermatomyositis (DM). Their mean +/- SD age and duration of disease were 45.0 +/- 13.9 years and 6.3 + 13.4 months, respectively. There was idiopathic PM in 37 cases, idiopathic DM in 13, PM/DM associated with malignancy in 5 and PM associated with connective tissue disease in 45. Serum muscle enzymes including creatine phosphokinase, lactate dehydrogenase and aspartate aminotransferase were elevated in 87 per cent, 92 per cent, and 82 per cent of cases, respectively. Abnormal electromyographic findings that were compatible with inflammatory myopathy were found in 76 per cent of cases. Seventy-seven per cent had an abnormal muscle biopsy that was consistent with polymyositis. There was a significant correlation between serum muscle enzymes and muscle pathology (p < 0.01). The degree of muscle weakness correlated better with the degree of muscle destruction (p = 0.01) than the degree of muscle inflammation (p = 0.03). The erythrocyte sedimentation rate showed no correlation with serum muscle enzymes, muscle pathology or muscle weakness.
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PMID:Serum muscle enzymes, muscle pathology and clinical muscle weakness: correlation in Thai patients with polymyositis/dermatomyositis. 1207 17

Although colchicine induced myopathy has been described in patients with chronic renal failure, colchicine induced myopathy with myotonia has been reported very rarely. A 49-year-old man with chronic renal failure was hospitalised for investigation of fatigue, malaise and severe pain in all extremities. He was on colchicine therapy for 5 months. Neurological examination showed mildly decreased sensation in a distal symmetric pattern in lower extremities, moderate proximal limb weakness, hyporeflexia and severe myalgia on palpation. No clinical evidence of myotonia was present. Laboratory studies showed elevated creatine phosphokinase (CK), lactic dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Electromyographic (EMG) findings were compatible with myopathy and abundant, widespread myotonic discharges were determined. Muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, CK, LDH, AST and ALT levels were normalised and the symptoms were disappeared gradually. In conclusion, the detection of myopathic motor unit potentials with myotonic discharges on EMG in patients on colchicine therapy is an important finding and it is possible to suggest that this clue may lead to the invasive procedure of muscle biopsy unnecessary.
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PMID:Colchicine-induced myopathy with myotonia in a patient with chronic renal failure. 1295 45

Niacin extended-release/lovastatin is a new combination product approved for treatment of primary hypercholesterolemia and mixed dyslipidemia. This open-labeled, multicenter study evaluated the safety of bedtime niacin extended-release/lovastatin when dosed as initial therapy and patient compliance to treatment in various clinical practice settings. A total of 4,499 patients with dyslipidemia requiring drug intervention was enrolled at 1,081 sites. Patients were treated with 1 tablet (500 mg of niacin extended-release/20 mg of lovastatin) once nightly for 4 weeks and then 2 tablets for 8 weeks. Patients also received dietary counseling, educational materials, and reminders to call a toll-free number that provided further education about dyslipidemia and niacin extended-release/lovastatin. Primary end points were study compliance, increases in liver transaminases to >3 times the upper limit of normal, and clinical myopathy. Final study status was available for 4,217 patients (94%). Compliance to niacin extended-release/lovastatin was 77%, with 3,245 patients completing the study. Patients in the southeast and those enrolled by endocrinologists had the lowest compliance and highest adverse event rates. Flushing was the most common adverse event, reported by 18% of patients and leading to discontinuation by 6%. Incidence of increased aspartate aminotransferase and/or alanine aminotransferase >3 times the upper limit of normal was <0.3%. An increase of creatine phosphokinase to >5 times the upper limit of normal occurred in 0.24% of patients, and no cases of drug-induced myopathy were observed. Niacin extended-release/lovastatin 1,000/40 mg, dosed as initial therapy, was associated with good compliance and safety and had very low incidences of increased liver and muscle enzymes.
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PMID:Safety and compliance with once-daily niacin extended-release/lovastatin as initial therapy in the Impact of Medical Subspecialty on Patient Compliance to Treatment (IMPACT) study. 1527 93


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