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)

A 40-year-old woman with a history of alcohol abuse, drug-related suicide attempts, and depression presented with a flu-like illness, vomiting, and changes in mentation. On admission, therapeutic blood levels of salicylates, trazadone, and acetaminophen were found. A tentative diagnosis of a psychotic crisis with possible superimposed drug overdose was made. The etiology of the patient's acute encephalopathy remained unclear until a plasma ammonia and liver biopsy established the diagnosis of Reye's syndrome. The patient was given supportive therapy and recovered completely.
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PMID:Adult Reye's syndrome. 327 49

Reye's syndrome, characterized by acute encephalopathy and fatty degeneration of the viscera with hepatic failure, is a life-threatening illness that affects children of all ages. Although Reye's syndrome has been investigated extensively, its etiology and pathogenesis remain obscure. Metabolic pathophysiology appears to include a process affecting liver mitochondria. Recently disturbances in fatty acid oxidation have been described with a similar clinical picture. The cause of these events is presumably related to triggering viral illnesses, in ways that are unclear. Since prompt treatment might provide a better chance for recovery, early diagnosis is important.
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PMID:[Reye's syndrome]. 332 94

Sequential examination of neuron-specific enolase in cerebrospinal fluid and serum was performed in 20 comatose children with acute encephalitis, acute encephalopathy, or Reye's syndrome. Neuron-specific enolase activities corresponded to the degree of brain damage. As neuron-specific enolase levels increased to greater than 80 ng/mL, patients had more severe impairment or died. Neuron-specific enolase may be a useful marker for evaluating the degree of neuronal damage and prognosis.
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PMID:Neuron-specific enolase in comatose children. 334 19

Three senile patients developed fatal acute encephalopathy while receiving calcium hopantenate. The clinical, biochemical, and pathological picture was similar to Reye's syndrome. Calcium hopantenate is a pantothenic acid antagonist. The serum levels of calcium hopantenate were high in coma, and that of pantothenic acid examined in one patient was lowered. Evidence obtained indicated that the Reye-like syndrome might be caused by calcium hopantenate possibly due to the induction of pantothenic acid deficiency.
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PMID:Reye-like syndrome following treatment with the pantothenic acid antagonist, calcium hopantenate. 337 35

Despite greater than 23 years of study, an incomplete understanding of the etiology, epidemiology and pathogenesis of Reye's syndrome persists. Better understanding of the disease has been hampered by the lack of a good animal model on which hypotheses of its pathogenesis could be tested. Human studies indicate that a primary mitochondrial injury may lead to complex metabolic disturbances that produce the observed pathophysiology. Specific directions regarding avenues for future research should pursue two lines: a good animal model still needs to be developed in which the biochemical and morphologic alterations identified in Reye's syndrome are duplicated. This model should include an antecedent viral illness but may not require aspirin exposure as an essential ingredient. With the identification of a satisfactory model, specific questions about the roles of environmental toxins or medications may be answered. Study of noncomatose cases of Reye's syndrome should continue. The specific emphasis should be to delineate what factors (NH3, free fatty acids and dicarboxylic acids) may be implicated in the pathogenesis of the CNS disease with the hopes of devising strategies for more effective treatment of encephalopathy and its attendant morbidity and mortality.
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PMID:Reye's syndrome: current concepts. 354 76

Non-narcotic analgesics can produce a variety of hepatic lesions but clinically significant liver damage is uncommon with normal therapeutic use. The pattern of hepatotoxicity caused by the salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol (acetaminophen) and the pyrazolones differs but many of these drugs can cause generalised reactions which involve the liver. Depending on the drugs in question, the risks of liver injury may be conditioned by factors such as age, sex, dose and duration of treatment. Hepatotoxicity associated with the use of salicylates and most NSAIDs has been reported most often in females with collagen diseases but this may simply reflect the greater use of these drugs in such patients. Paracetamol-induced liver damage occurs almost exclusively as a result of overdosage. Except for the microvesicular fatty changes in hepatocytes in patients with Reye's syndrome attributed to salicylate, the acute centrilobular necrosis caused by paracetamol in overdosage and the marked cholestasis produced by benoxaprofen, the pathological changes in hepatic reactions to non-narcotic analgesics are rather variable and nonspecific. About 50% of patients given salicylate in full anti-inflammatory dosage develop minor abnormalities of liver function. There is usually a mild to moderate increase in plasma aminotransferase activity with patchy necrosis and degeneration of hepatocytes. These changes are related to plasma salicylate concentration and are usually rapidly reversible. In a small minority of patients, particularly the young, liver damage is more severe and may be associated with liver failure, acidosis, hypoglycaemia and encephalopathy. This picture closely resembles Reye's syndrome. In overdosage, paracetamol can cause acute hepatic necrosis. Without specific treatment, some 8% of adults suffer severe liver damage with plasma aminotransferase activity greater than 1000 U/L and about 1% die with hepatic failure and encephalopathy. The administration of sulfhydryl compounds such as N-acetylcysteine within 8 to 10 hours effectively prevents liver damage and death. Liver damage has been attributed to the therapeutic use of paracetamol. However, in most reports the dose was excessive and many patients were chronic alcoholics (who seem to be at increased risk). In these cases the features were typical of acute overdosage. A consistent and characteristic pattern of hepatotoxicity is evident with relatively few non-steroidal anti-inflammatory and pyrazolone analgesics. A rank order of relative risk cannot be established and the incidence in relation to use is not known.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Liver damage with non-narcotic analgesics. 354 1

Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by disseminated intravascular coagulation and encephalopathy with a fatal outcome. There have also been isolated reports of chronic active hepatitis associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled chronic active hepatitis but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of non-narcotic analgesics on the liver. 355 80

The occurrence in a previously healthy infant of sudden febrile encephalopathy with shock and metabolic acidosis associated with liver and renal failure and bloody watery diarrhea has been reported by several authors in recent years. We report the same association in a 3 1/2 month-old infant. We discuss the similarities between this clinical picture and malignant hyperthermia and Reye syndrome.
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PMID:[Hemorrhagic shock syndrome with encephalopathy]. 357 85

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
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PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31

A 20-month-old girl with a family history of two siblings who died of an encephalopathy diagnosed as Reye syndrome presented to an emergency room in hypoglycemic coma and was found to have medium-chain acyl-coenzyme A dehydrogenase deficiency. The salient clinical and biochemical features of this newly described inborn error of fatty acid metabolism are described and contrasted to those of classical Reye syndrome. Important clues that should lead the clinician to suspect this disorder, methods of diagnosis, and appropriate acute and long-term therapy are also discussed.
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PMID:Familial Reye-like syndrome: a presentation of medium-chain acyl-coenzyme A dehydrogenase deficiency. 382 38


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