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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old woman was admitted to the hospital because of swelling of both forearms and muscle weakness in the limbs. Laboratory examination revealed abnormally high levels of serum creatine kinase, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase. Polymyositis was diagnosed, and prednisolone was administered. Her condition had been well controlled on prednisolone until several months before admission, when bilateral blepharoptosis and diplopia developed. An edrophonium test was positive: muscle weakness was transiently alleviated. High titers of anti-acetylcholine receptor antibodies were found. A chest CT scan showed a mass in the anterior part of the mediastinum. We diagnosed myasthenia gravis associated with thymoma. After an extended thymectomy, the patient's condition improved. When muscle weakness recurs after remission of polymyositis, myasthenia gravis should be considered.
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PMID:[Polymyositis followed by myasthenia gravis]. 889 Jun 8

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 toxicity of Rhazya stricta leaves for Najdi sheep is described in 9 sheep assigned as untreated controls, Rhazya-treated at 0.25 g/kg/d and Rhazya-treated at 1 g/kg/d. The oral use of 1 g/kg/d caused body weight depression, ruminal bloat, diarrhea, dyspnea and weakness of the hind limbs. Enterohepatonephropathy, pulmonary congestion, hemorrhage and emphysema, lymphocytes in vital organs, and congestion of the blood vessels of the heart were associated with increases in serum AST and LDH, in elevated bilirubin and urea concentrations, and decreased total protein, albumin and calcium concentrations, and leucopenia and anemia.
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PMID:Toxicity of Rhazya stricta to sheep. 955 56

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

Myotonic dystrophy (DM) is an autosomal dominant multisystem disorder. Little evidence suggests the existence of liver damage in a small number of patients. We have prospectively evaluated liver and gallbladder function in 53 patients with DM in relation to clinical and genetic parameters. None of the patients had an enlarged liver, signs of cirrhosis, or portal hypertension. All were free of medication, and none were pregnant or had a history of alcohol abuse. In 35 (66%) patients, serum activity of at least one of six liver enzymes assayed was abnormal. An elevated level of alkaline phosphatase was found in 50.9%, of gamma-glutamyltransferase in 52.8%, of 5' nucleotidase in 43.4%, of serum aspartate aminotransferase in 35.8%, of serum alanine aminotransferase in 33.9%, and of lactate dehydrogenase in 37.7%. Liver function test results did not correlate with severity of muscle weakness, disease duration, or serum levels of creatine kinase, glucose, or lipids. Motility of gallbladder and abdominal ultrasonography were normal. Cytosine-thymidine-guanine repeat expansion by southern blot did not correlate with liver enzyme abnormalities. We conclude that elevation of liver enzymes is frequent in DM and should be included as an additional laboratory finding of the disease.
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PMID:Abnormal liver test results in myotonic dystrophy. 964 14

The records of 14 cases of bovine hypokalaemia observed between 1983 and 1996 were reviewed. The most common history included a protracted, often infectious, disease. All age groups were represented. Although previously reported as a risk factor, isoflupredone acetate had not been administered to five of the cases. The following clinical signs were recorded in 10 cases: abnormal position of the head and neck, severe weakness, rumen hypomotility or atony, abnormal faeces, anorexia and tachycardia. Cardiac dysrhythmia was observed in six cases. Acid-base imbalance (alkalosis in 10 cases), hyperglycaemia and increased activities of aspartate aminotransferase and creatine kinase were associated with hypokalaemia ranging from 1.35 to 2.49 mmol/litre. Treatments included symptomatic treatment, supportive care and potassium chloride given intravenously and orally at an average total daily dose of 42 g/100 kg bodyweight (26 g by mouth and 16 g intravenously) for an average of five days. Eleven cases recovered after an average of three days.
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PMID:Description of 14 cases of bovine hypokalaemia syndrome. 983 71

The HELLP syndrome is a serious complication of pregnancy, found most frequently in conjunction with severe preeclampsia. The incidence of this disease in preeclampsia is between 2 and 12%. The diagnosis is based on typical laboratory findings, i.e. haemolysis--H, elevated liver enzymes--EL and a low-platelet count--LP. Haemolysis is defined as microscopic finding of an abnormal peripheral blood smear, elevated total bilirubin above 1.2 mg/dl and elevated lactate dehydrogenase above 40 mukat/l. Transaminases (AST above 4.2 mukat/l) are also elevated. For HELLP a low platelet count is typical (number of thrombocytes less than 100,000 mm3). The symptoms include above all pain in the epigastrium, in the right subcostal area, nausea and vomiting. Non-specific symptoms resembling viroses are lassitude, general weakness, headache and fatigue. A correct differential diagnosis and early assessment of the diagnosis are decisive for starting treatment which can prevent the development of serious complications such as disseminated intravascular coagulopathies and hepatorenal failure. Treatment of the HELLP syndrome is symptomatic with the objective to stabilize the general condition of the mother, improved haemodynamic conditions and the impaired haemocoagulation. A very important therapeutic step is early termination of pregnancy which depends on ther mother's condition and the condition of the foetus with regard to gestational age.
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PMID:[The HELLP syndrome]. 992 33


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