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)

Cytomegalovirus (CMV) infection in inmunocompetent hosts generally is asymptomatic or may present as a mononucleosis syndrome but rarely can lead to severe organ complications. We report a case of simultaneous hepatic and pericardic CMV infection in a 36-year old immunocompetent man. He was admitted to coronary unit with fever, chest pain radiated to shoulders, changes on electrocardiogram with diffuse ST elevation and modest laboratory elevations in the MB fraction of creatine kinase (CK-MB) of 33.77 microg/L (0.1-6.73), serum cardiac troponin T of 0.904 ng/mL (0-0.4), creatine kinase of 454 U/L (20-195) and myoglobin of 480.4 microg/L (28-72). Routine laboratory test detected an elevation of aminotransferase level: alanine aminotransferase 1445 U/L, aspartate aminotransferase 601 U/L. We ruled out other causes of hepatitis with normal results except IgM CMV. The patient was diagnosed with myopericarditis and hepatitis caused by cytomegalovirus and started symptomatic treatment with salicylic acid. In few days the laboratory findings became normal and the patient was discharged.
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PMID:Cytomegalovirus hepatitis and myopericarditis. 1727 38

Using the urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration, effects of participation in a two-day ultramarathon race period on oxidative DNA damage were investigated in Japanese nonprofessional runners. Before the first day (baseline), after the first day (mid-race) of 40-km running, and after the second day (post-race) of 90 km running, biomaterials were successfully sampled from 95 participants (males, 79; females, 16) who completed the full race. We analyzed urine for 8-OHdG and blood for aspartate aminotransferase (AST), creatine phosphokinase (CPK) and myoglobin, and evaluated fluctuation in the values at three sampling time points. Adjusted baseline urinary 8-OHdG levels (microg/g creatinine) (mean +/- standard deviation) showed no significant differences between males and females, at 2.85 +/- 1.17 and 3.04 +/- 1.56, respectively. In males, mid-race urinary 8-OHdG levels rose to 3.29 +/- 1.15 (p < 0.01), but then returned to 2.73 +/- 1.16 at the post-race time point (p < 0.01). In females, a similar increase to 3.32 +/- 1.47 and subsequent decline to 2.80 +/- 1.47 were noted. In contrast, AST, CPK and myoglobin were increased at both mid- and post-time points and particularly the latter, independent of the sex. Extreme prolonged exercise in a two-day ultramarathon race period causes oxidative DNA damage but antioxidant repair systems are apparently induced to protect against oxidative DNA stress with physical exercise.
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PMID:Changes of urinary 8-hydroxydeoxyguanosine levels during a two-day ultramarathon race period in Japanese non-professional runners. 1761 24

Stable coronary artery disease (CAD) can cause repetitive reversible myocardial ischaemia, and it seems to be possible that reversibly injured myocardium releases small amounts of soluble cytoplasmic proteins. Hence, the aim was to evaluate the effect of stable CAD on baseline serum levels of cardiac biomarkers. We studied 68 consecutive outpatients referred for gated myocardial perfusion imaging. Before a treadmill exercise test, blood samples for measurement of creatine kinase (CK), CK-myocardial band (CK-MB) mass, myoglobin, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were collected. Normal perfusion patterns were detected in 29 (43%) patients (group 1) and perfusion defects were detected in 39 (57%) patients (group 2). Baseline serum levels of biomarkers except CK were significantly higher in group 2 (p=0.001). Stable CAD increases baseline levels of CK-MB mass, myoglobin, AST and LDH in the serum and this increase is related to the extent and severity of the perfusion defect and to some extent the ejection fraction of the left ventricle.
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PMID:Baseline serum levels of cardiac biomarkers in patients with stable coronary artery disease. 1770 51

Rhabdomyolysis is a clinical and biochemical syndrome occurring when skeletal muscle cells erupt and result in release of creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and myoglobin into the interstitial space and plasma. Mechanical trauma, compression, excessive muscle activity and ischemia are frequent causes, but non-traumatic rhabdomyolysis is usually caused by a toxic reaction to drugs. In this study, 181 patients suspected of rhabdomyolysis were admitted to the poisoning center of Loghman-Hakim Hospital in Tehran during one year (September 2004 to September 2005) were studied. Patients were included on the basis of physical examination and blood analysis for CPK and LDH. Rhabdomyolysis was confirmed if CPK level has been greater than 975 U/L. Out of 181 patients, 64 were female and 117 were male with an age range between 13-78 years. One-hundred and forty-three (79%) patients had CPK greater than 975 U/L. In 6% of the cases, multiple drug poisoning were observed. Two patients (1.1%) had muscle pain, five patients (2.8%) had rigidity and five patients (2.8%) had muscle inflammation. One-hundred and nineteen patients (65.7%) were febrile. The most common cause of rhabdomyolysis was opium. Blood ALT showed an increase in 109 patients (60.9%), AST in 80 patients (44.7%), and LDH in 144 patients (79.6%). Fifty patients (28.2%) had higher blood direct bilirubin and 64 patients (36.4%) showed higher total bilirubin. Six percent of patients had been diagnosed as ARF by indication of creatinine greater than 1.4 mg/dL. Five percent of patients had hypernatremia and 1.1% of patients had hyperkalemia. It is concluded that rhabdomyolysis is a matter of concern in human poisonings and needs special approach to attend.
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PMID:Rhabdomyolysis among acute human poisoning cases. 1788 58

Cardio-vascular diseases and acute coronary syndrome (ACS) in the first place play the first role in the structure of diseases and mortality of world population. Effective method of diagnostics of ACS consists in detecting early and late biomarkers of myocardium necrosis. The article presents characteristics of such biomarkers indices as myoglobin, cardiotroponins, MB-fractions of creatine phosphokinase, cardio-form of protein, lactate dehydrogenase, aspartate aminotransferase. The authors described in the artcile diseases which are accomponied with increase in the level of cardiotroponins.
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PMID:[Early and late biomarkers of late myocardium necrosis in patients with acute coronary syndrome]. 1871 92

Acute rhabdomyolysis is a syndrome characterized by the lesion of skeletal muscle resulting in subsequent release of intracellular contents into the circulatory system, which can cause potentially lethal complications. These contents include myoglobin, creatine phosphokinase, potassium, aldolase, lactate dehydrogenase and glutamic-oxaloacetic transaminase. There are numerous causes that can lead to acute rhabdomyolysis and many of patients present with multiple causes. The most common potentially lethal complication of rhabdomyoloysis is acute renal failure. In this article we present a case of a patient that developed clinical signs of acute rhabdomyolysis after consumption of heroin and alcohol. After approximately nine hours of alcohol and heroin induced coma he had acute compartment syndrome of the right arm, and clinical and laboratory signs of acute rhabdomyolysis with acute renal failure as a complication of rhabdomyolysis. Acute rhabdomyolysis developed in the patient as the result of acute compartment syndrome, with direct toxic activity of alcohol and diamorphine. During the period of coma, due to lying in particular position over a long period of time, pressure upon the certain part of the body caused muscle compression and capillary occlusion in fascial compartments, which led to ischemia. Upon pressure relief and beginning of tissue recovery, post ischemic compartment syndrome occurred with subsequent rhabdomyolysis. Getting out of coma the patient started to complain of severe pain in the right arm, which clinically worsened on passive stretching of the limb, with the loss of sensation and weakness. Laboratory findings showed high levels of creatine phosphokinase as the most sensitive marker of muscular damage. The peak of creatine phosphokinase level can be predictive for the development of acute renal failure because myoglobin level may return to normal within 6 hours after muscle injury. The peak of creatine phosphokinase (186.080 U/L; normal range 0-177) was recorded at 12 hours of admission. Other pertinent laboratory results such as urea, creatinine, prothrombin time, alanine aminotransferase and aspartate aminotransferase were also changed significantly. The peak of potassium level before dialysis was 6.8 mmol/L. Emergency fasciotomy of the anterior and posterior compartment syndrome was performed by a team of physicians after clinical examination. The second look debridement was performed at 48 and 72 hours. The plastic surgical procedure was performed 4 weeks later. On admission the patient also had oliguria with dark brown pigment in his urine. Arterial blood gases revealed metabolic and respiratory acidosis. The patient was hypovolemic and IV rehydratation with crystalloids, sodium bicarbonate and mannitol started immediately upon admission. Despite therapy his urine output decreased. Hemodialysis was initiated at serum potassium level of 6.8 mm/L and continued until his urine output returned to normal in three weeks. The patient was discharged from the hospital after six weeks, with normal urine output, without functional abnormality in his upper right limb. Acute rhabdomyolysis should be considered as a possibility in any patient with prolonged imobilization while in coma as well as in any intoxicated patient. Of course, creatine phosphokinase is the most sensitive indicator of muscle injury and the degree of creatine phosphokinase elevation correlates with the amount of muscle injury and disease severity. Other laboratory findings can help identify common complications of rhabdomyolysis such as acute renal failure, metabolic derangements and disseminated intravascular coagulopathy.
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PMID:[Acute rhabdomyolysis: a case report and literature review]. 1884 54

A 16-year old girl presented with rapid onset of muscular weakness and a history of severe dysphagia, dysphonia and significant wasting. On examination, she was dystrophic (BMI 15.7) and had signs of myopathy. Laboratory findings confirmed myopathy (CPK 106.4 microkat/L (6384 IU/L), AST 2.86 microkat/L (171.6 IU/L), myoglobin 1582 microg/L). There was profound hypokalaemia (S-K 1.8 mmol/L) suggesting hypokalaemic paralysis. Diagnosis of distal renal tubular acidosis (dRTA) was based on combination of hyperchloremic metabolic acidosis, severe hypokalaemia, high urinary pH and positive value of urinary anion gap. There was evidence of other signs of renal tubular impairment (urinary beta-2-microglobulin 213 mg/L, glomerulotubular proteinuria 1.01g/24h). Autoimmune tests (rheumatoid factor, antinuclear antibodies, autoantibodies to Ro/SSA and La/SSB) together with symptoms of xerostomia with swallowing difficulties and atrophic glossitis suggested primary Sjogren's syndrome (SS) as the underlying cause of dRTA. The renal biopsy confirmed chronic tubulo-interstitial nephritis compatible with this diagnosis. Full recovery of muscle weakness and hypokalaemia and acidosis followed after potassium and alkali replacement therapy. Corticosteroids were administered with subsequent addition of cyclosporine A because of disease activity. In conclusion, primary SS is a rare diagnosis in childhood and adolescence and should be considered in patients presenting with hypokalaemic paralysis, as this might be due to dRTA, even in the absence of apparent sicca syndrome.
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PMID:Hypokalaemic Paralysis Revealing Sjogren's Syndrome in a 16-Year Old Girl. 1927 13

The purpose of this investigation was to determine the utility of fast-twitch skeletal muscle troponin I (fsTnI) and urinary myoglobin (uMB) as biomarkers of skeletal muscle injury in 8-week-old Sprague-Dawley rats. fsTnI and uMB were quantified by enzyme-linked immunosorbent assay and compared with standard clinical assays including creatine kinase, aldolase, aspartate aminotransferase, and histopathological assessments. Detectable levels of uMB were normalized to urinary creatinine to control for differences in renal function. Seven compounds, including those with toxic effects on skeletal muscle, cardiac muscle, or liver, were evaluated. fsTnI was typically nondetectable (< 5.9 ng/ml serum) in vehicle-treated female and male rats but increased in a dose-dependent manner to at least 300 ng/ml in cerivastatin-induced severe fast-twitch specific myotoxicity. Minimal myopathy induced by investigational compounds BMS-600149 and BMS-687453 increased serum fsTnI to about 30-50 ng/ml, suggesting a reasonable dynamic range for detecting mild to severe skeletal muscle toxicity. In direct contrast, fsTnI was only marginally increased relative to population control values in rats treated with triamcinolone acetonide, which produces muscle atrophy or the cardiotoxins isoproterenol and CoCl2. uMB was typically nondetectable (< 1.6 ng/ml urine) in vehicle-treated female and male rats but increased to approximately 140, 300, and 30 ng/mg creatinine in rats treated with cerivastatin, BMS-687453, and triamcinolone acetonide, respectively. Cardiotoxicity also increased uMB in rats treated with isoproterenol and CoCl2 with urine concentrations ranging from 20 to 30 ng/mg creatinine. Severe hepatotoxicity (coumarin) did not significantly affect serum fsTnI or uMB levels. Collectively, these data suggest that fsTnI is specific for skeletal muscle toxicity, whereas uMB is nonspecific, increasing with skeletal muscle and cardiac toxicity. Accordingly, the complement of fsTnI and uMB, in conjunction with standard clinical assays may comprise a useful diagnostic panel for assessing drug-induced myopathy in rats.
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PMID:Biomarkers of drug-induced skeletal muscle injury in the rat: troponin I and myoglobin. 1962 85

Acute coronary syndrome is a set of symptoms interpreted as being the result of cardiac ischemia. The subtypes of acute coronary syndrome, depending on the degree of cardiac ischemia, include unstable angina and two forms of myocardial infarction. Determination of serum cardiac markers plays a key role in the diagnosis of acute myocardial infarction. Serum markers such as aspartate transaminase, lactate dehydrogenase, and creatine kinase are no longer used because they lack cardiac specificity and sensitivity. According to the NACB (National Academy of Clinical Biochemistry) recommendations, two serum cardiac markers need to be determined for routine diagnosis of acute myocardial infarction, i.e. one showing early elevation in serum (up to six hours after chest pain), and the other, late marker that is elevated six to nine hours after chest pain, has high sensitivity and specificity for detection of myocardial injury, and remains elevated for several days of the symptom onset. In current clinical practice, myoglobin, CKMB mass (improved diagnostic sensitivity in relation to CKMB activity) and cardiac troponins are commonly determined. CKMB mass is a cardiospecific marker, but can also be elevated in skeletal muscle damage. Myoglobin is not cardiospecific, but has high early sensitivity (fast and reliable exclusion of acute myocardial infarction) and the possibility of rapid assessment of the success of thrombolytic therapy. Cardiac troponins are late markers for the diagnosis of myocardial injury. They are markers with highest specificity and sensitivity for acute myocardial infarction. New markers such as ischemia modified albumin, heart fatty acid binding protein, glycogen phosphorylase isoenzyme BB, carboanhydrase 3, and new tehnologies are under investigation to advance our knowledge about heart disease.
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PMID:[Biochemical markers in the diagnosis of acute coronary syndrome]. 1968 56

A case of colchicine-induced rhabdomyolysis is reported. A 48 year old African-American male with history of hypertension and chronic gout on colchicine 0.6 mg daily presented with symptoms of a community acquired pneumonia. The patient was started on 500 mg of clarithromycin orally twice daily and represented to the emergency room after 3 days complaining of severe muscle pain. His liver panel showed elevations in the serum aminotransferases; AST 513 mU/ml (nl 15-41) and ALT 182 mU/ml (nl 17-63). His complete blood count showed an elevated white blood cell count of 18,800/ml (nl 4,000-10,000/ml). Urine analysis was positive for myoglobin with no red cells present. Serum creatine kinase (CK) was 22,996 mU/ml (nl 31-221) with a normal troponin I 0.18 (nl <0.4).Investigations confirmed the presence of rhabdomyolysis and discontinuation of colchicine and clarithromycin resulted in resolution of clinical and biochemical features of rhabdomyolysis. By hospital day four, his muscle soreness had improved markedly. His serum CK improved to 3,389 mU/ml (nl 31-221 mU/ml) and serum creatinine improved to 1.5 mg/dl (nl 0.8-1.2). On hospital day five, the patient was discharged on oral anti-hypertensive medication and a ten-day course of doxycycline. Metabolism of colchicine by the cytochrome P450 3A4 system has been previously described, but this is the first published report of colchicine associated rhabdomyolysis secondary to drug metabolism interactions with an antibiotic. A review of medications that are metabolized via the cytochrome 3A4 and A-SLAVED-LIVER (Amiodarone, Simvastatin, Lovastatin, Atorvastatin, Verapamil, Erythromycin, Diltiazem, cLarithromycin, Itraconazole, Voriconazole, colchicinE, Ritonavir) pneumonic was established.
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PMID:Short term treatment with clarithromycin resulting in colchicine-induced rhabdomyolysis. 2541 92


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