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)

The clinical significance of serum aspartate aminotransferase (GOT) isozymes was studied in 18 patients with polymyositis. Abnormally high levels of mitochondrial GOT (mGOT) (6.2 +/- 1.2 IU/L, mean +/- SEM; normal, less than 2.0 IU/L) and cytosol GOT (sGOT) (95 +/- 21.6 IU/L; normal, less than 25 IU/L) were observed in sera. In polymyositic muscles, the sGOT level was significantly decreased but mGOT was not. The levels of serum sGOT and mGOT and the ratio of mGOT/tGOT before corticosteroid therapy correlated well with the severity of muscle weakness. Serial determination of CPK, sGOT, and mGOT during corticosteroid therapy revealed that mGOT most rapidly returned to normal. Exercise did not increase serum mGOT in polymyositis.
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PMID:Serum mitochondrial aspartate aminotransferase in patients with polymyositis. 683 Jan 52

Gentamicin sulfate at dosage levels of 10 and 20 mg/kg of body weight was administered twice daily IV to red-tailed hawks. Clinical signs, water consumption, and changes in blood chemical values were monitored. Tissues were examined grossly and ultrastructurally, using light and electron microscopy. Clinical signs of weakness and apnea were attributed to gentamicin-induced neuromuscular blockade in the 20-mg/kg group. Serum values of aspartate transaminase, alanine transaminase, cholesterol, inorganic phosphorus, total protein, albumin, and uric acid increased in some birds. There was a decrease in periodic acid-Schiff staining of proximal tubular brush borders. Increased numbers of cytoplasmic lysosomes, many of which contained myelin figures, in renal epithelial cells were seen at the ultrastructural level. All birds given 20 mg/kg died. Both dosage levels were considered toxic in red-tailed hawks.
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PMID:Toxicity of gentamicin in red-tailed hawks. 688 67

Megaesophagus was diagnosed in 9 adult ferrets. Clinical history of the ferrets included regurgitation, difficulty in swallowing, partial anorexia, and lethargy. Cachexia, dehydration, weakness, and ptyalism were observed on physical examination. Radiography revealed the esophagus of each ferret to be dilated in the thoracic and cervical regions. Of 4 ferrets that had lymphocytopenia, 2 had concurrent leukopenia. Serum biochemical analysis revealed high activity of alanine transaminase (4 ferrets) and aspartate transaminase (3), and hypoglycemia (4). Treatment included administration of fluid, antibiotics, and agents directed against possible primary causes of megaesophagus. Treatments were ineffective, and all of the ferrets died or were euthanatized. All 6 ferrets that were submitted for necropsy had bronchopneumonia, hepatic lipidosis, mild esophagitis, and gastritis. The etiopathogenesis of megaesophagus in the ferrets was not determined.
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PMID:Megaesophagus in nine ferrets. 796 Oct 71

Clinical, diagnostic and biochemical features of generalised glycogenosis are described in 96 Brahman-type calves. Typically the calves were presented when about 6 months of age, with ill-thrift and muscular weakness as the most common signs. Acidic alpha-glucosidase activity was reduced in peripheral blood lymphocytes and skeletal muscle. Muscle glycogen concentration was consistently higher in affected animals than in clinically normal cattle. Other observations in affected calves included elevation of serum aspartate aminotransferase and creatine kinase activities and excessive amounts of high molecular weight oligosaccharides in urine. Fine cytoplasmic vacuolation of neurones in the brain and spinal cord, skeletal muscle, myocardium and of Purkinje fibres were consistent histological observations. Periodic acid-Schiff staining revealed the presence of glycogen-like material in peripheral blood lymphocytes of all affected calves, indicating that this is a useful aid for the diagnosis of glycogenosis. While 3 of the 96 calves showed somewhat different clinical signs, the similarity of pathology and the biochemical and clinical evidence in the remainder suggested that, in these animals, the disease was expressed as a single syndrome.
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PMID:Clinical, diagnostic and biochemical features of generalised glycogenosis type II in Brahman cattle. 828 22

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.
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PMID:Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats. 888 38

Five male children are reported in whom incidental recognition of elevated serum alanine aminotransferase (ALT) activity initiated investigation to identity the cause of suspected hepatocellular injury. All five were later diagnosed with X chromosome-linked muscular dystrophy. The serum level of ALT, generally considered to be specific for hepatocellular injury, was increased two to 25 times above normal in all the reported cases. Paradoxically, the increase in ALT activity was greater than that of serum aspartate aminotransferase (three to 16 times normal), an enzyme whose elevation is generally recognized as being less specific and indicative of muscle, cardiac, kidney, pancreatic, red blood cell or hepatic injury. At presentation to the gastrointestinal service, one case, age 2.5 months, had no symptoms or signs of neuromuscular dysfunction, while the other four had previously unrecognized hypertrophy of the calves, proximal limb weakness, positive Gower's sign or delayed gross motor skills. All five patients had marked elevation of serum creatine kinase activity and histopathologically confirmed muscular dystrophy. The practical clinical implication of this report is that children with elevated serum ALT, in the absence of other signs and symptoms of hepatic injury, may have occult muscular disease--most frequently muscular dystrophy. Although the clinical signs of muscular dystrophy may be subtle or absent, early determination of creatine kinase will suggest the correct diagnosis and minimize extensive and invasive investigation focusing on hepatic injury.
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PMID:Elevated aminotransferase activity as an indication of muscular dystrophy: case reports and review of the literature. 919 75

In 14 patients with polymyositis (PM), 5 patients (2 males and 3 females) were positive for anti-hepatitis C virus (HCV) antibody measured by a second generation assay. We analysed the clinical characteristics and histopathological findings of the biopsied muscles from those 5 patients. They aged from 42 to 65 years averaging 53.6 years. Two asymptomatic patients visited our hospital due to elevated muscle enzyme levels, who had slight weakness in their orbicularis oculi and neck muscles on physical examination. The other 3 patients had moderate weakness of the proximal muscles. Anti-nuclear antibody was positive in 2 of the 5 patients and anti-Jo 1 antibody was negative in all patients. The serum enzymes elevated were creatine kinase (215-2, 207 (IU/l)) and glutamate oxaloacetate transaminase (40-119 (KU)). HCV-RNA was positive in the sera of 4 patients examined. All muscle biopsy specimens revealed variation in fiber size with inflammatory cellular infiltration and observed degenerating and regenerating fibers. The scant infiltration type was observed in 2 asymptomatic patients in whom the infiltrated cells were CD4 positive. The endomysial infiltration type was observed in 3 symptomatic patients; CD8 positive cells were found focally to diffusely in 2 patients examined. The expression of class 1 molecules from the major histocompatibility complex was detected mainly in infiltrated fibers to variable degrees. All of the patients showed a good response to the initial steroid therapy. The present study suggests that autoimmune reaction related to HCV infection causes myositis, therefore anti-HCV antibody should be checked in cases of PM.
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PMID:[Clinical characteristics and muscle histopathology in polymyositis positive anti-hepatitis with C virus antibody]. 921 18

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

A 13-year-old warmblood mare was presented because of progressive weight loss, general weakness and trembling. On examination the horse stood with its head lowered and the limbs placed under the body. On lifting its head spasms of the neck muscles could be observed. At the same time the horse developed trembling over the lower neck and muscle fasciculations continued over the whole body. Additional signs included frequent recumbency, polyphagia and facial hyperaesthesia. The horse showed no signs of ataxia. Haematology was normal. Blood biochemistry revealed slight increased aspartate aminotransferase (AST: 1060 U/I) and creatine kinase levels (CK: 441 U/I). Based on the clinical findings equine motor neuron disease was diagnosed. The horse was euthanatized due to poor prognosis and the progression of symptoms. The typical neurodegenerative changes found on histological examination of the spinal cord confirmed the diagnosis.
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PMID:[Equine motor neuron disease (EMND). A case report]. 928 83

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.
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PMID:Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks. 956 31


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