Disease relevance of Reye Syndrome

• Because of its hepatoneurotoxic effects, camphor toxicity may clinically mimic Reye's syndrome [1].
• In contrast, the absence of salicylate use in children in some Pacific islands could contribute to the milder outcome of falciparum malaria than is observed in Africa. Widespread expression of iNOS has also been seen in the tissues of a patient with fatal clinically defined Reye's syndrome [2].
• Several short chain fatty acids, including octanoate, are increased in the plasma of patients with hepatic encephalopathies and Reye syndrome [3].
• Increased HVA in Reye syndrome may reflect cerebral ischemia and release of vasoactive amines (particularly dopamine) into the brain and cerebrospinal fluid (CSF) [4].
• Octanoic acid has been implicated in the pathogenesis of cytotoxic cerebral edema in Reye's syndrome [5].

High impact information on Reye Syndrome

• We studied 83 biopsy-proved cases of Grade I Reye's syndrome to determine the outcome, possible clinical or laboratory predictors of progression to deeper coma grades, and hepatic ultrastructural findings [6].
• Our findings suggest that the prognosis is excellent for survival without sequelae in Grade I Reye's syndrome (98.8 per cent) when management includes hospital surveillance and intravenous glucose and electrolyte infusion [6].
• Serum carnitine in Reye's syndrome [7].
• Dangers of mannitol in treatment of Reye's syndrome [8].
• Transiently reduced activity of carbamyl phosphate synthetase and ornithine transcarbamylase in liver of children with Reye's syndrome [9].

Chemical compound and disease context of Reye Syndrome

• These observations indicate that Reye's syndrome is associated with acquired and transient dysfunction of hepatic mitochondrial urea-cycle enzymes [9].
• Letter: Ornithine or citrulline therapy in treatment of Reye's syndrome [10].
• Letter: Ornithine or citrulline therapy in treatment of Reye's syndrome [11].
• Salicylate and mitochondrial injury in Reye's syndrome [12].
• The model also explains underlying biochemical differences between patients with Reye syndrome and medium-chain acyl CoA dehydrogenase deficiency, another disorder of fatty acid metabolism [13].

Biological context of Reye Syndrome

• The metabolic effects of endotoxin and TNF are similar to those found in Reye's syndrome [14].
• Continuous intraventricular monitoring of intracranial pressure appears to be a useful aid in the management of patients with Reye syndrome, especially those in stage 3 or 4 coma, in which the mortality rate remains high [15].
• Glycerol kinetics and adverse affects were studied in nine patients with Reye's syndrome [16].
• The results may also help to explain why the ingestion of aspirin but not acetaminophen is associated with Reye's syndrome, a disease characterized by impaired energy metabolism and mitochondrial swelling [17].
• We present a first patient with systemic juvenile rheumatoid arthritis in which acute necrotizing encephalopathy developed as a complication of macrophage activation syndrome but not of Reye's syndrome [18].

Anatomical context of Reye Syndrome

• The cases with microvesicular steatosis can be differentiated morphologically from Reye's syndrome by electron microscopy, showing the absence of the mitochondrial changes characteristic of Reye's. Four of seven cases of acyl CoA dehydrogenase deficiency showed some variations from normal in the appearance of the hepatocyte mitochondria [19].
• Skeletal muscle carnitine palmityltransferase and muscle or liver carnitine content were determined in biopsies from children during and after attacks of Reye syndrome [20].
• Reye syndrome in children receiving salicylate therapy for connective tissue disease [21].
• The structural integrity of epithelial cells of the lateral choroid plexus tissues from the ferret model for Reye's syndrome was examined by transmission electron microscopy after the animals were inoculated intranasally with influenza B, were administered aspirin, and/or were fed an arginine deficient diet singly and in combination [22].
• Salicylate has been implicated as a causal factor in Reye's syndrome, as well as in aspirin poisoning, and salicylate has been reported to increase the proton conductance of inner mitochondrial membranes [23].

Gene context of Reye Syndrome

• CDSP may present with acute metabolic derangement simulating Reye's syndrome within the first 2 years of life [24].
• Masking by enzyme inhibitor of raised serum glutamate dehydrogenase activity in Reye's syndrome [25].
• Hepatic glutamate dehydrogenase (GDH) activity was measured in postmortem specimens obtained from two stage V Reye syndrome patients and in three postmortem specimens of normal human liver [26].
• These findings suggest that the pronounced reduction of CPS and OTC activities reported in Reye's syndrome in man are not a general manifestation of the severity of influenza infection [27].
• These results suggest that IFN-alpha may prove to be effective for the treatment of Reye's syndrome [28].

Analytical, diagnostic and therapeutic context of Reye Syndrome

• Utilizing a specific and sensitive radioimmunoassay, palsma and urine tyramine were measured in 14 consecutive patients with liver biopsy-proven Reye's syndrome [29].
• Analysis of serum pentobarbital concentrations in 28 specimens from Reye's syndrome patients was conducted with modifications of three nonspecific immunoassay procedures originally designed to detect barbiturates in serum or urine [30].
• Evaluation of level of consciousness by the Glasgow coma scale in children with Reye's syndrome [31].
• Confirmation of serum salicylate levels in Reye's syndrome: a comparison between the Natelson colorimetric method and high performance liquid chromatography [32].
• In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate [33].

References