Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Discriminant analysis was used to discriminate between Reye syndrome (RS) patients and non-RS cases based either on conventional blood chemistry data obtained upon admission, or on the activities of hepatic mitochondrial enzymes in biopsy or necropsy tissue. The control group for blood chemistry measurements contained children with upper respiratory tract infections, varicella, etc. who did not develop RS, as well as healthy children. Subjects with no liver disorder (e.g., accidental death, sudden infant death, etc.) or with non-RS liver disorders were used as controls for hepatic enzyme studies. Hepatic damage indicators (aspartate aminotransferase, AST; alanine aminotransferase, ALT; and bilirubin) correctly classified 86-96% of non-RS cases and 61-71% of RS. By contrast, AST and ALT had little prognostic value (63% overall correct). Ammonia effectively classified favorable outcome cases (95% correct) but not unfavorable (14% correct). However, when ammonia was included with stage of coma information 88% of the favorable and 85% of the unfavorable outcome cases were correctly classified. Discriminant analysis of hepatic enzymes (glutamate dehydrogenase and monoamine oxidase activity) for a RS and a non-RS group correctly classified 80% of non-RS and 95% of RS specimens. The function was suitable for the direct evaluation of RS-like mitochondrial enzyme changes in rat liver.
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PMID:Prognosis and diagnosis of Reye syndrome by discriminant analysis. 404 46

Recent experience suggests that a diagnosis of Reye's syndrome based on clinical and biochemical grounds alone may be unreliable. Two patients are presented here, whose clinical manifestation suggested Reye's syndrome. The biochemistry data were also compatible with Reye's syndrome except that the levels of serum AST and ALT were significantly higher with normal serum ammonia level. Blood amino acid and urinary organic acid assay all showed negative findings. Histological findings of the liver showed marked centrilobular necrosis rather than fatty metamorphosis. The muscle biopsies did not show lipid accumulation in the muscle fibers as well. The findings in our patients suggested that a confirmatory diagnosis of Reye's syndrome requires a characteristic pathological findings of the liver in order to differentiate Reye's syndrome from Reye-like syndrome, especially acute encephalopathy associated with centrilobular necrosis of the liver.
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PMID:[Acute encephalopathy associated with centrilobular necrosis of liver mimicking Reye's syndrome--report of two cases]. 838 58

The findings on magnetic resonance imaging (MRI) or computed tomographic scan in 35 children with acute encephalopathy (AE) induced by infections were categorized into five groups: (1) normal findings (11 cases), (2) normal findings in the acute phase followed by mild brain atrophy (1 case), (3) severe brain edema which developed within 48 hours after the onset of AE (7 cases), (4) diffuse cortical necrosis which appeared around 4 days after the onset of AE (9 cases), and (5) symmetric thalamic lesions (7 cases). Their outcomes were as follows: three cases developed epilepsy in (1) and (2); six died and one had a sequel of severe brain damage (SBD) in (3); all cases survived but had SBD in (4), and four died, one had SBD, and 2 recovered in (5). Serum AST were elevated in 7.7 and 6 cases in (3), (4) and (5), respectively. In all of them, there were more than one case having liver histologies consistent with Reye syndrome.
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PMID:[Clinical studies on 35 patients with infection-related acute encephalopathy]. 961 58

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
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PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91

Aspirin is commonly used as an anti-inflammatory therapy for Kawasaki syndrome. Early initiation with high dose aspirin (80 to > 100 mg/kg per day), followed by low-dose therapy at the afebrile stage, has been often used to reduce morbidity and mortality in coronary complications. We report a 10-month-old infant who was diagnosed with Kawasaki syndrome. Sudden onset of poor activity, poor appetite, lethargy, tachycardia, tachypnea, hepatomegaly, increased AST/ALT, coagulopathy and hyperammonemia developed 3 days after the high-dose aspirin therapy. His histopathological and ultrastructural findings from the liver biopsy were compatible with Reye's syndrome. He recovered completely, and there was no recurrence.
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PMID:Reye's syndrome developing in an infant on treatment of Kawasaki syndrome. 1595 35

Children with acute encephalopathy (AEP) or acute encephalitis(AE) show variable findings in the clinical manifestations and on the neuroimaging. Patients with AE present variable symptoms: disturbance of consciousness, seizure, ataxia, dystonia, abnormal behavior, apnea, and others. This variability depends on the location of lesions including basal ganglia, brain stem, cerebellum, or cerebral gray/white matter. In AEP, MRI findings can be categorized into (1) severe brain edema, (2) acute necrotizing encephalopathy, (3) cortical necrosis that appears 4-5 days after the onset, and (4) others. Serum AST elevates in approximately 50% of AEP patients, and among them around 60% develops DIC. The high AST group includes Reye syndrome(RS), mimic RS and AEP with shock syndrome.
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PMID:[Clinical variability in viral infection related acute encephalitis or encephalopathy]. 2140 Aug 54

Dengue Fever (DF) is only rarely considered as a cause of acute liver failure even globally and only a few case reports of acute hepatic failure and encephalopathy occurring in DF in adults are available. We report a case of Acute Liver Failure due to Dengue during a major outbreak in 2010 in Chitwan. A 20 year old previously healthy female presented to the emergency department of Chitwan Medical College with fever, jaundice and altered sensorium. She was tested positive for Dengue IgM. Her biochemical and clinical parameters were suggestive of acute liver failure with total billirubin of 10.1 mg/dL, direct billirubin of 5.2 mg/dL, ALT 5760 IU, AST 14100 IU, alkaline phosphatase of 1250 IU, PT INR of 1.76 and platelet count of 30,000/mm3. Other causes for acute hepatic failure like acute viral hepatitis, leptospirosis, malaria, Reyes syndrome were ruled out. The patient was admitted and managed in the ICU with supportive care and platelet transfusion. With treatment she made a significant clinical and biochemical improvement with AST of 105 IU, ALT of 120 IU and platelet count of 150,000/mm3. She was discharged after 11 days of hospital stay.
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PMID:Fulminant hepatic failure due to dengue. 2261 Aug 74

This study was designed to investigate whether resveratrol could provide protection against Reye's syndrome induced by 4-pentenoic acid in Wistar albino rats. Compared with rats with untreated Reye's syndrome, 1 h pretreatment by low dose resveratrol (10 mg/kg by oral gavage) resulted in marked amelioration in liver functions in the form of significant decrease in serum transaminases (AST, ALT) and plasma ammonia levels, shortening of prothrombin time, and increase in serum albumin levels. In addition, resveratrol prohibited oxidative stress markers, as indicated by a significant increase in GSH and decrease in MDA, with restoration of complex I activity in liver tissues. The classical histopathological presentation in Reye's syndrome of microvesicular steatosis by light microscope and mitochondria distortion by electron microscope has been improved by resveratrol pretreatment. The efficient protection by resveratrol was determined by normalization in serum levels of AST and albumin, as well as complex I activity, GSH, and MDA. In conclusion, pretreatment by resveratrol in low doses could protect against Reye's syndrome partially via prohibition of oxidative stress and restoration of complex I activity. This may provide the opportunity to reconsider aspirin therapy for infants and young children. However, the verification of such results in clinical practice remains a challenge.
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PMID:Resveratrol protects against experimental induced Reye's syndrome by prohibition of oxidative stress and restoration of complex I activity. 2516 5