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Consolato Sergi - One of the best experts on this subject based on the ideXlab platform.
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co ingestion of aspirin and acetaminophen promoting fulminant liver failure a critical review of Reye Syndrome in the current perspective at the dawn of the 21st century
Clinical and Experimental Pharmacology and Physiology, 2018Co-Authors: Deepak Dinakaran, Consolato SergiAbstract:In the pediatric population, there is some evidence of possible interaction, synergism, and co-toxicity of aspirin and acetaminophen. The toxicity of salicylates such as aspirin in this population is well known and documented, specifically in the form of Reye Syndrome. The possible toxic synergism with aspirin and acetaminophen, however, is not previously described; though case reports suggest such co-toxicities with low levels of aspirin and other compounds can exist. In vitro studies into mechanistic processes of salicylate toxicity propose that there are a bi-directional link and potentiation with glutathione (GSH) depletion and salicylate toxicity. Data may suggest a plausible explanation for salicylate and acetaminophen toxic synergism. Further studies investigating this potential toxic synergism are warranted. Given the lack of awareness in the clinical community about potential toxic synergism between these relatively common medications, caution is advised in the co-administration of these drugs, particularly in communities using natural or alternative therapy. This article is protected by copyright. All rights reserved.
Irene T Schulze - One of the best experts on this subject based on the ideXlab platform.
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role of influenza b virus in hepatic steatosis and mitochondrial abnormalities in a mouse model of Reye Syndrome
Hepatology, 1991Co-Authors: Kathleen B Schwarz, Saroj Larroya, Carole Vogler, Jeffrey C Sippel, Sharon Homan, Ronald Cockrell, Irene T SchulzeAbstract:The hepatic steatosis observed in the influenza B virus mouse model of Reye Syndrome has been attributed to infectious virus or, alternately, to decreased food intake in the virus-treated mice or impurities in the virus preparation. To resolve this issue, 4- to 6-wk-old male Balb C mice were given, by intravenous injection, 12,800 hemagglutination units of influenza B Lee/40 virus in phosphate buffered saline/1% bovine serum albumin using virus prepared by ultracentrifugation from infected allantoic fluid, by sucrose density-gradient purification of virus prepared by ultracentrifugation from infected allantoic fluid or by irradiation of virus prepared by ultracentrifugation from infected allantoic fluid to inactivate virus. The infectivity titer of virus prepared by ultracentrifugation from infected allantoic fluid was much higher than that of sucrose density-gradient purified virus prepared from infected allantoic fluid: 50% egg infectious dose for virus prepared by ultracentrifugation from infected allantoic fluid was 3.9 × 104/hemagglutination unit vs. 8.7 50% egg infectious dose/hemagglutination unit for sucrose density-gradient purified virus prepared from infected allantoic fluid. Control mice received phosphate-buffered saline/1% bovine serum albumin or uninfected allantoic fluid diluted in phosphate-buffered saline/1% bovine serum albumin. Mice were fasted to eliminate dietary variation, and livers were obtained 36 hr after virus administration. Of the above treatments, only virus prepared by ultracentrifugation from infected allantoic fluid caused clinical illness and increased hepatic triglycerides (p < 0.02) compared with controls. Hepatic triglycerides in virus prepared by ultracentrifugation from infected allantoic fluid correlated with histopathological vacuolization scores (r = 0.5773; p < 0.03). Hepatic mitochondrial enzymes succinate dehydrogenase and glutamate dehydrogenase were decreased (p < 0.003) in mice given virus prepared by ultracentrifugation from infected allantoic fluid compared with mice given phosphate-buffered saline/1% bovine serum albumin. Two mechanisms that could explain this finding—peroxidation of and changes in the composition of mitochondrial membrane lipids—were investigated. Treatment with virus prepared by ultracentrifugation from infected allantoic fluid did not result in increased mitochondrial lipid peroxidation, as measured by conjugated dienes, but was associated with a 27% increase in hepatic mitochondrial cholesterol compared with treatment with phosphate-buffered saline/1% bovine serum albumin (p < 0.05). We conclude that treatment of young mice with virus prepared by ultracentrifugation from infected allantoic fluid leads to hepatic steatosis and illness resulting from the high titer of infectious virus in the preparation and not from viral proteins or nonviral components of the infected or uninfected allantoic fluid or from dietary factors. Administration of virus to young mice results in depression of hepatic mitochondrial enzymes, similar to findings in children with Reye Syndrome. The possibility that these abnormalities are the consequence of increased hepatic mitochondrial cholesterol deserves further investigation. (HEPATOLOGY 1991;13:96–103).
Nobutake Matsuo - One of the best experts on this subject based on the ideXlab platform.
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symmetrical thalamic lesions on ct in influenza a virus infection presenting with or without Reye Syndrome
Brain & Development, 1993Co-Authors: Toshiro Nagai, Akira Yagishita, Yutaka Tsuchiya, Shinji Asamura, Hiroshi Kurokawa, Nobutake MatsuoAbstract:In Reye encephalopathy, diffuse brain swelling is a well known CT finding, but focal CT lesions have not been documented. We report 2 children with Reye encephalopathy and 2 children with non-Reye encephalopathy both associated with influenza A virus infection in whom symmetrical low density lesions of the thalamus and brainstem were detected on CT. These symmetrical low density lesions were present in the acute phase and decreased in size within a few weeks in all, and are still seen 2 years later as clearly defined small round areas in 3 surviving patients. Paired influenza A virus titers in blood showed 4-fold or more increase in all. Myelin basic protein (MBP) in CSF was increased in 2 of the 3 subjects studied. Liver biopsy showed diffuse lipid droplet infiltration in 2, focal infiltration in 1, and normal morphology in 1. The above data suggest that the symmetrical low density lesions were associated with influenza A virus infection, most likely consisting of edema, demyelination, and necrosis. We suspect that there is a continuum of Reye Syndrome and virus-associated encephalopathy with significant overlap.
Kathleen B Schwarz - One of the best experts on this subject based on the ideXlab platform.
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role of influenza b virus in hepatic steatosis and mitochondrial abnormalities in a mouse model of Reye Syndrome
Hepatology, 1991Co-Authors: Kathleen B Schwarz, Saroj Larroya, Carole Vogler, Jeffrey C Sippel, Sharon Homan, Ronald Cockrell, Irene T SchulzeAbstract:The hepatic steatosis observed in the influenza B virus mouse model of Reye Syndrome has been attributed to infectious virus or, alternately, to decreased food intake in the virus-treated mice or impurities in the virus preparation. To resolve this issue, 4- to 6-wk-old male Balb C mice were given, by intravenous injection, 12,800 hemagglutination units of influenza B Lee/40 virus in phosphate buffered saline/1% bovine serum albumin using virus prepared by ultracentrifugation from infected allantoic fluid, by sucrose density-gradient purification of virus prepared by ultracentrifugation from infected allantoic fluid or by irradiation of virus prepared by ultracentrifugation from infected allantoic fluid to inactivate virus. The infectivity titer of virus prepared by ultracentrifugation from infected allantoic fluid was much higher than that of sucrose density-gradient purified virus prepared from infected allantoic fluid: 50% egg infectious dose for virus prepared by ultracentrifugation from infected allantoic fluid was 3.9 × 104/hemagglutination unit vs. 8.7 50% egg infectious dose/hemagglutination unit for sucrose density-gradient purified virus prepared from infected allantoic fluid. Control mice received phosphate-buffered saline/1% bovine serum albumin or uninfected allantoic fluid diluted in phosphate-buffered saline/1% bovine serum albumin. Mice were fasted to eliminate dietary variation, and livers were obtained 36 hr after virus administration. Of the above treatments, only virus prepared by ultracentrifugation from infected allantoic fluid caused clinical illness and increased hepatic triglycerides (p < 0.02) compared with controls. Hepatic triglycerides in virus prepared by ultracentrifugation from infected allantoic fluid correlated with histopathological vacuolization scores (r = 0.5773; p < 0.03). Hepatic mitochondrial enzymes succinate dehydrogenase and glutamate dehydrogenase were decreased (p < 0.003) in mice given virus prepared by ultracentrifugation from infected allantoic fluid compared with mice given phosphate-buffered saline/1% bovine serum albumin. Two mechanisms that could explain this finding—peroxidation of and changes in the composition of mitochondrial membrane lipids—were investigated. Treatment with virus prepared by ultracentrifugation from infected allantoic fluid did not result in increased mitochondrial lipid peroxidation, as measured by conjugated dienes, but was associated with a 27% increase in hepatic mitochondrial cholesterol compared with treatment with phosphate-buffered saline/1% bovine serum albumin (p < 0.05). We conclude that treatment of young mice with virus prepared by ultracentrifugation from infected allantoic fluid leads to hepatic steatosis and illness resulting from the high titer of infectious virus in the preparation and not from viral proteins or nonviral components of the infected or uninfected allantoic fluid or from dietary factors. Administration of virus to young mice results in depression of hepatic mitochondrial enzymes, similar to findings in children with Reye Syndrome. The possibility that these abnormalities are the consequence of increased hepatic mitochondrial cholesterol deserves further investigation. (HEPATOLOGY 1991;13:96–103).
Michael J Bennett - One of the best experts on this subject based on the ideXlab platform.
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Reye like Syndrome resulting from novel missense mutations in mitochondrial medium and short chain l 3 hydroxy acyl coa dehydrogenase
Molecular Genetics and Metabolism, 2006Co-Authors: Michael J Bennett, Laurie K Russell, Chonan Tokunaga, Srinivas B Narayan, Lu Tan, Adam C Seegmiller, Richard L Boriack, Arnold W StraussAbstract:Abstract Medium- and short-chain l-3-hydroxy-acyl-CoA dehydrogenase (M/SCHAD) deficiency is a recessively inherited disorder of fatty acid oxidation. Currently, only four patients from three families have been reported in the literature. All these patients presented with hypoglycemia associated with hyperinsulinism (HI). This association suggests that there is a role for M/SCHAD in regulating the pancreatic secretion of insulin. We present a fifth patient whose presentation was similar to Reye Syndrome, a feature in common with most of the previously recognized disorders of fatty acid oxidation but with no clinical evidence of HI. Sequencing of the HAD1 gene on chromosome 4 revealed compound heterozygosity for two novel missense mutations, 170A>G, resulting in D45G, and 676T>C, resulting in Y214H. The mutant enzymes were expressed and subjected to kinetic analysis. Y214H has no detectable activity, whilst D45G, which resides in the cofactor-binding pocket, has an altered K m for NADH (96μM versus 24μM for the wild-type). This represents the first kinetic M/SCHAD mutant, which explains the high residual activity in skin fibroblasts. The lack of obvious HI in this patient may be related to the high residual activity and indicates that HI associated with M/SCHAD deficiency may only be present with complete deficiency. The spectrum of M/SCHAD phenotype should be broadened to include acute liver disease.
