Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035400 (Reye's syndrome)
 879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early single photon emission computed tomography (SPECT) using N-isopropyl-p-[123I]iodoamphetamine (123 I-IMP) was performed in seventy-one patients with epilepsy admitted to Kanagawa Rehabilitation Hospital from July 1987 to February 1989; epilepsy and epileptic syndrome 27, encephalitis/encephalopathy 10, clinical Reye syndrome 3, cerebro-vascular disorders 8, sequelae of head trauma 4, cerebral palsy 5, brain anomaly 4, others 10. We classified these cases according to the 1989 criteria of the International League Against Epilepsy, and compared with the findings of the SPECT studies with the EEG and CT. In idiopathic epilepsy, the SPECT findings were within normal limits. Abnormal foci on EEG were not correlated with low uptake areas on SPECT. In the symptomatic epilepsy, especially in the West and Lennox syndromes, SPECT showed a decrease in diffuse cerebral cortical blood flow during ACTH therapy. This was also seen in some cases with normal CT imaging. The results suggest that the hemodynamic pathophysiology of the brain and the indications of therapeutic effectiveness in epilepsy are shown more accurately by SPECT than CT.
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PMID:[Early 123I-IMP SPECT in patients with epilepsy]. 193 Nov 63

The authors compared the intellectual, cognitive and academic abilities of 22 survivors of Reye syndrome attending normal schools with the sibling nearest in age as control. The British Ability Scales, visual and verbal IQ, short-term memory scales and attainment tests were administered to all children. Reye syndrome children as a group differed significantly from the controls only on the basic number skills test. However, children with severe encephalopathy and those whose illness occurred in infancy had significant deficits on many of the tests. 18 children recovered without requiring 'additional educational provision'; the mean IQ of the 22 Reye syndrome children was 101. Nonetheless, these children's poor performance on the basic number skills test has important implications for teachers, and careful monitoring of future educational performance is essential.
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PMID:A sibling-controlled study of intelligence and academic performance following Reye syndrome. 193 33

The growing number of drugs used to treat various diseases and the growing number of invasive procedures used for diagnosis and therapy have generated many iatrogenic diseases. Elderly patients are more likely than the young to react adversely to drugs since the physiological functions of the organs, especially of the kidneys, decrease and pharmacokinetic characteristics altered. In addition, multiple disease states are common in the elderly, and multiple drugs are consequently prescribed. In the present study, adverse effects of so-called "cerebroactive drugs" and "cerebral vasodilators" are discussed. More than 30 kinds of these drugs are on the market in Japan and are widely prescribed for "chronic cerebrovascular diseases" and "dementia syndromes" in the elderly. In contrast, they are rarely used in Western Europe and not on the market in the United States. Among them, calcium hopantenate was the first of "cerebral activators" and was the most popular. In 1986, however, the first cases of toxic encephalopathy induced by calcium hopantenate were reported. It resembled Reye syndrome, showing coma, hepatic failure, lactic acidosis and hypoglycemia and was frequently fatal. More than 47 victims including 11 fatal cases have been reported since. Flunarizine, a cerebral vasodilator, produced high rates of parkinsonism and depression. Multicenter studies have revealed that these side effects occurred in 10-30% of the elderly patients who had taken it. These symptoms usually appeared several months after flunarizine was started. Some of the adverse effects of the drugs may be unpredictable and inevitable, but most of them can be prevented or reduced if physicians are more careful with their patients, and drugs and their adverse effects.2
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PMID:[Iatrogenic diseases in the elderly]. 194 29

Severe encephalopathy, the usual cause of death in Reye's syndrome (RS), is characterized by cerebral edema with associated increases in intracranial pressure (ICP). In previous studies, we have shown that exposure of neonatal mice to nontoxic doses of an industrial surfactant and subsequent infection with mouse-adapted influenza B (Lee) virus result in a significant increase in mortality rate and that this is associated with several of the characteristic features of human RS. In the present study we have measured ICP in the young mice undergoing their version of the disease, and we now report that the animals treated with surfactant plus virus experience increases in intracranial pressure that are significantly in excess of those in any of the three control groups. These findings support our hypothesis that this and the other abnormal biochemical and morphological responses in RS are related in some manner to a chemically compromised host.
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PMID:Surfactant-potentiated increases in intracranial pressure in a mouse model of Reye's syndrome. 198 38

The influenza B virus mouse model of Reye's syndrome was studied to learn more about the encephalopathy in Reye's syndrome. One to 3 days after intravenous influenza B/Lee virus, Balb/c mice became lethargic, seized and lapsed into a fatal coma. Wide-spread cerebral edema without inflammation developed 1-3 days after virus inoculation. Swollen astrocytic foot processes containing increased glial fibrillary acidic protein were located around capillaries. Viral particles were not seen by electron microscopy and complete viral replication did not occur. Immunohistochemical studies demonstrated influenza B viral antigen within many endothelial cells but not within other brain cells. Qualitative (Evans blue dye) and quantitative (percent brain water and technetium -99 pertechnetate) studies of the blood-brain barrier demonstrated abnormalities. This model reproduced many clinical, virologic and pathologic features of the Reye's syndrome encephalopathy. In addition, a non-permissive viral infection of brain endothelial cells occurred which may be important in the pathogenesis of the mouse encephalopathy and may participate in the encephalopathy of Reye's syndrome.
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PMID:The influenza B virus mouse model of Reye's syndrome: clinical, virologic and morphologic studies of the encephalopathy. 216 26

A total of 740 consecutive children aged between 6 months and 12 years who presented with acute encephalopathic illnesses during a three year period were assessed both clinically and by laboratory investigations. Cerebrospinal fluid was examined for the presence of cells or other abnormal substances, and any organisms were cultured. Blood examination included white cell count and estimations of haemoglobin, urea, glucose, and electrolyte concentrations and serum alanine aminotransferase and aspartate aminotransferase. A firm diagnosis was established in 278 patients (38%). Pyogenic meningitis (n = 134), measles encephalopathy (n = 38), and electrolyte imbalance (n = 23) were important causes in this group, cerebral malaria (n = 4) was uncommon and there were no cases of Reye's syndrome. The diagnoses of the remaining 462 were combined under the heading 'acute unexplained encephalopathy'. Altogether 394 of the 462 patients underwent virological investigations for arboviruses and 92 (23%) had one or more indicators of Japanese encephalitis. No other arboviruses could be isolated. Throat swabs from 187 patients with acute unexplained encephalopathy were studied on monkey kidney tissue cell lines of which 14 were positive (8%). These were identified as adenovirus, parainfluenza, influenza, poliomyelitis, Coxsackie, and echovirus; in two cases the virus was untypable. Japanese encephalitis is an important cause of acute childhood encephalopathy in this region. Clinical features of the illness may be mimicked by several disorders which require specific treatment. Thirty four of the 92 died (37%).
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PMID:Virological investigations of acute encephalopathy in India. 203 25

The ultrastructural brain and liver pathology in an infant, who died of acute encephalopathy due to systemic carnitine deficiency (CD), an important condition mimicking Reye's syndrome (RS), was reported. The major finding in the brain was swelling of astrocyte cytoplasm. Expanded mitochondria in nerve cells and myelin sheath splitting in the white matter, which have been reported to be specific to RS, were not observed. Also in contrast to findings in RS, hepatocytes were filled with macrovesicular fat droplets without expanded mitochondria. These findings suggest significant differences in the pathophysiology of acute encephalopathy in CD and RS, although the clinical and laboratory findings during an episode of acute encephalopathy in the former are usually very similar to those in the latter.
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PMID:Brain and liver pathology in a patient with carnitine deficiency. 224 Apr 66

Bilateral vocal cord paralysis and absent laryngeal sensation are previously unrecognized sequelae for Reye's syndrome, a severe acute encephalopathy in children. Four patients were seen at varying periods ranging from 2 weeks to 5 years after their diagnosis of an episode of severe Reye's syndrome over a 20-year period at the Children's Hospital of Los Angeles (Calif). All of the patients had bilateral true vocal cord paralysis with absent laryngeal sensitivity that was documented at endoscopy. As many as 50% of survivors of severe Reye's syndrome have breathy voices or aphonia. It is suggested that some of these children may have vocal cord dysfunction that is not the result of intubation, and are at risk for aspiration and its dangerous sequelae. A vagal nuclear injury is theorized to explain the sensory motor dysfunction of the larynx in these children.
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PMID:Vocal cord paralysis and superior laryngeal nerve dysfunction in Reye's syndrome. 229 40

There are still many problems with the diagnosis and classification of inherited disorders of mitochondrial beta-oxidation. At present only the acyl-CoA dehydrogenase step of the beta-oxidation spiral has been explored in any detail and a large number of patients have disorders that cannot be properly characterized. beta-Oxidation defects may present in a wide variety of ways, the most dramatic being acute encephalopathy with hepatic involvement (atypical Reye's syndrome) or 'sudden' death. Investigations may include urinary and plasma organic acids, metabolic stress tests and assays of overall metabolic pathways or of specific enzymes in cultured fibroblasts, lymphocytes, or other material. Early postnatal diagnosis presents particular difficulties but in medium-chain acyl-CoA dehydrogenase deficiency the diagnosis may be apparent from careful examination of urine. There is as yet little general experience in prenatal diagnosis of this group of disorders except for glutaric aciduria type II. Single prenatal diagnoses of medium-chain acyl-CoA dehydrogenase deficiency and of an incompletely characterized defect of medium-chain fatty acid oxidation have been performed.
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PMID:Disorders of mitochondrial beta-oxidation: prenatal and early postnatal diagnosis and their relevance to Reye's syndrome and sudden infant death. 250 9

Brain water content was measured by gas-chromatography in rats following intraperitoneal injection of drugs and fatty acids related to the etiology of Reye syndrome. A statistically significant increase in brain water content was observed following injection of 5% glucose solution, valproic acid, acetyl salicylic acid, calcium hopantenate, margosa oil, 4-pentenoic acid, linolenate and arachidonate. Seizures occurred in all animals given valproic acid, margosa oil and 4-pentenoic acid, and in 25% of those given 5% glucose solution + anti-diuretic hormone. The results of these studies may help in the selection of appropriate agents for experimental induction of acute encephalopathy and brain edema in animal models of Reye syndrome.
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PMID:Effects of drugs and fatty acids related to Reye syndrome on brain water content in rats. 251 90


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