Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of ornithine carbamyl transferase (S-OCT), glutamic oxaloacetic transaminase and glutamic pyruvic transaminase were compared for 37 Reye's syndrome patients with regard to variation with clinical stage an serum ammonia levels. In stage I patients, the mean S-OCT activities were greater and the serum ammonia levels lower than found with patients in the more advanced stages. Covariation of these two parameters was found only in the more advanced stages. No significant correlation with stage or serum ammonia levels was found for S-GOT or S-GPT activities. These observations are discussed in terms of their relevance to reports of an early transient decrease of hepatic OCT activity in Reye's syndrome.
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PMID:Serum ornithine carbamyl transferase activities in Reye's syndrome. 706 88

In the course of the A/Brazil (H1N1) outbreak of 1978-1979, two cases of Reye's syndrome occurred in Grayling, Michigan, an area with a county-wide population of 2056 school age children. School absenteeism peaked at levels between 16-28 per cent. Clinical histories and paired blood specimens were collected from 860 school children; the initial blood was obtained shortly after the peak of the outbreak. Serologic results confirmed that type A H1N1 virus was the cause of the outbreak. Serum alanine aminotransferase (SGPT) and creatine phosphokinase (CPK) values were determined on all initial blood specimens and a sample of the second specimens. CPK results did not correlate with infection, illness or SGPT values. SGPT values of 60 IU/l or greater were found in 1.5 per cent of those tested. The elevated values were not associated with illness but were associated with influenza infection. Based on the excess number with elevated results in those with recent infection, it is estimated that at least 2.7 per cent of individuals infected by type A (H1N1) influenza had associated elevated SGPT.
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PMID:Liver function abnormalities in the course of a type A (H1N1) influenza outbreak: relation to Reye's syndrome. 730 2

The activities of nine enzymes in liver specimens obtained from four children who had died from Reye's syndrome were compared to the corresponding activities of a control group of four children who had died from unrelated causes. At the 95% significance level, the alterations could be classified into three groups. Five activities [lactate dehydrogenase, alanine aminotransferase, glucose 6-phosphatase, cytochrome oxidase, and malate dehydrogenase (mitochondrial plus cytosolic)] showed no change. Three enzymes [glutamate dehydrogenase, isocitrate dehydrogenase (NADP), and monoamine oxidase] were decreased. One activity (glucose 6-phosphate dehydrogenase) was increased. The malate dehydrogenase isozymes were resolved by electrophoresis, and the two bands were stained and measured. The ratio of cytosolic:mitochondrial enzyme was significantly greater in Reye's syndrome than in the control group. These results lend further support to the view that in Reye's syndrome the impairment of hepatic function is largely confined to the mitochondria. The lowered activity of monoamine oxidase means that the abnormalities extend to the outer mitochondrial membrane. Imbalances of the cytosolic:mitochondrial enzyme activities were evaluated in needle biopsy specimens from four other children under conditions where neurologic abnormalities were less severe. Two patients had elevated ratios of both glutamate:lactate dehydrogenase and cytosolic:mitochondrial malate dehydrogenase activities, and a third had only an abnormal malate dehydrogenase ratio. In contrast to these Reye's syndrome patients, a fourth case admitted with a provisional diagnosis of Reye's syndrome showed no abnormality in either ratio in stage IV coma.
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PMID:Comparison of cytosolic and mitochondrial hepatic enzyme alterations in Reye's syndrome. 745 35

Fulminant hepatic failure (FHF) is a poorly understood condition in which total liver failure occurs and is thought to be caused by a variety of conditions including Reye's syndrome, hepatitis, drug overdoses, and vascular insufficiency. While this condition is an uncommon one, it carries with it a high fatality rate and must therefore be diagnosed as rapidly as possible. Six patients have been observed over a two-year period with biopsy and/or autopsy-confirmed FHF: one with acute hepatitis B-delta; three with histories of alcoholism, two of them with cirrhosis; one with acute tylenol overdose; and one with hepatic vascular insufficiency. All of these patients, except one, exhibited a rapid, fatal downhill course after onset of symptoms. In all of these patients, a consistent elevation was observed in serum levels of aspartate aminotransferase (AST) or serum glutamate oxaloacetate transaminase (SGOT) and alanine aminotransferase (ALT) or serum glutamate pyruvate transaminase (SGPT) such that the ratio of AST to ALT was significantly greater than 1 and in serum levels of ammonia. Other liver function tests were found to be abnormal but not in so consistent a pattern, although total protein and albumin were found to be significantly decreased in all of these patients. The stereotypical elevation of the transaminases with high AST-to-ALT ratios and the rise in ammonia appear to characterize this life-threatening illness most reliably.
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PMID:Serum analyte pattern characteristic of fulminant hepatic failure. 820 19

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

We reported a 35-year-old male patient with Reye's syndrome, who showed temporarily lesions of claustrum, striatum, hippocampus and amygdala on CT, MRI and PET scan. He was previously healthy and affected upper respiratory infection. After taking 4 tablets of aspirin (335 mg x 4), he developed severe headache and status epileptics. The cerebrospinal fluid showed normal cell count and protein. The serum GOT and GPT elevated to 499 IU/l and 221 IU/l respectively. The parainfluenza virus type I titer was 32 times on admission and increased up to 128 times two weeks later. In spite of the anticonvulsant, status epileptics lasted for about one month and he needed mechanical ventilation. On 13-18 days of illness, abnormal lesions appeared in bilateral claustrum and striatum on CT and MRI. On 49 days of illness, abnormal lesions appeared in bilateral hippocampus and amygdala. All these lesions changed into normal on MRI on 111 days of illness. The 18F-FDG PET study on 80 days of illness revealed high uptake on striatum, hippocampus and amygdala bilaterally and changed into normal on 130 days of illness. He has improved markedly but showed long-standing abnormal signs of limbic dementia. We suggested this patient could be suffered from post infectious encephalitis in limbic system after Reye's syndrome.
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PMID:[An adult patient of Reye's syndrome--the possible background mechanism of lesions in claustrum, striatum and limbic system and limbic dementia]. 1061 54

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

Twelve cases of Reye's syndrome are presented with different degrees of encephalopathy, hyperammonemia and hypoglycemia; associated to acetyl salicylic acid (ASA) ingestion. The aim of the present retrospective study was to describe our experience in selected patients with Reye's syndrome associated to the ASA ingestion and to underline the influence of hyperammonemia on Reye's encephalopathy. All the cases presented moderate hyperbilirubinemia, elevated alanine aminotransferase, aspartate aminotransferase with an average of 302+/-205 UI/L and 285+/-149 UI/L respectively. Arterial blood ammonia averaged 172.4+/-71.3 micromol/L and glycaemia averaged 35.2+/-17.0 mg/dl. A high mortality was found in our series (41.7%). Considering that encephalopathy is the leading syndrome in these cases, the influence of ammonia on brain tissue was described. Glutamate is an excitotoxic neurotransmitter, capable to produce neuron and astrocyte damage and apoptosis. The presence of ASA could cause the onset of the mitochondrial permeability transition and the mitochondrial swelling in the astrocyte, leading to hyperammonemia. In Reye's syndrome, hyperammonemia and perhaps the increase of glutamate are the leading factors in the mechanism of brain damage and encephalopathy. Aspirin must be carefully administrated and controlled by professionals. Furthermore, parents must be informed about the risks in the use of this drug in children.
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PMID:Reyes's syndrome, encephalopathy, hyperammonemia and acetyl salicylic acid ingestion in a city hospital of Buenos Aires, Argentina. 1914 21

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


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