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Query: UMLS:C0035400 (Reye's syndrome)
 879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following reports of a Reye-like syndrome in children resulting from Margosa oil (MO) ingestion, we administered MO to laboratory rats in an attempt to produce an animal model of Reye's syndrome. Male rats were injected intraperitoneally with either MO or corn oil and observed for clinical signs of a toxic response. After 15 h the animals were administered a second dose and the MO-treated animals developed florid neurological symptoms. The animals were then sacrificed and blood samples were analyzed for glucose, ammonia, aspartate aminotransferase, and alanine aminotransferase. Sections of liver, kidney, and brain were examined by light microscopy after Sudan black B, hematoxylin and eosin, and periodic acid-Schiff staining. Liver was additionally examined by electron microscopy. Liver samples were analyzed for hepatic enzyme levels and brain samples were analyzed for water content. There were greatly increased levels of ammonia, aspartate aminotransferase, and alanine aminotransferase and decreased glucose levels in the blood of MO-treated animals. Light microscopy of MO-treated livers revealed fatty infiltration, granularity of the cytoplasm with normal nuclei, and glycogen depletion; electron microscopy revealed mitochondrial pathology in the livers of MO-treated animals. There were no significant morphological changes in brain or kidney specimens although the kidneys did show some fatty infiltration. Hepatic mitochondrial enzyme levels were unchanged and there was no increase in brain water content in the MO-treated animals. Thus, many of the abnormalities seen in Reye's syndrome were seen in this model; however, there were no hepatic enzyme changes despite altered mitochondrial morphology and no evidence of cerebral edema despite a florid encephalopathy. Nonetheless, this model may have important implications for the understanding of the pathogenetic mechanisms of this Reye-like syndrome and, perhaps, Reye's syndrome.
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PMID:Investigation of an animal model of a Reye-like syndrome caused by Margosa oil. 408 Apr 57

Vomiting, drowsiness, metabolic acidosis, polymorphonuclear leucocytosis, and encephalopathy developed in thirteen infants within hours of ingestion of margosa oil. Liver biopsy of one infant and necropsy examination of ICR strain mice after experimentally induced margosa-oil poisoning demonstrated pronounced fatty infiltration of the liver and proximal renal tubules as well as cerebral oedema. Electron microscopy demonstrated mitochondrial damage. These findings indicate that margosa oil may be involved in the aetiology of Reye's syndrome among Indians in Malaysia.
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PMID:Margosa oil poisoning as a cause of Reye's syndrome. 611 Jan

After a viral infection (Coxsackie-A-9) a twelve-year-old boy developed symptoms of acute encephalopathy and fatty degeneration of the liver. A fatal outcome could not be averted. Clinical course, laboratory data, light and electron microscopic examinations were typical for Reye's syndrome, a rare diagnosis in Central Europe.
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PMID:[Reye's syndrome (author's transl)]. 611 85

Retrospective assessment of hepatic and central nervous system involvement associated with chickenpox cases at a large metropolitan medical center reveals that 28 of 58 patients had biochemical, but not inflammatory, evidence of liver involvement. An additional 18 patients had biochemical liver abnormalities along with non-inflammatory encephalopathy (Reye syndrome) and 12 had clear evidence of central nervous system inflammatory involvement (encephalitis). There were no cases of solitary inflammatory liver involvement. Reviewed evidence suggests that the pathogenesis of hepatopathy and hepatoencephalopathy (Reye syndrome) is not caused by replication of virus in the involved organs, but instead is mediated through a cytotoxic mechanism and that the inflammatory brain disease is also not caused by viral replication in brain tissue, but appears to be tissue damage associated with immune cell responses (post-infectious encephalitis). The concept put forth in this essay is that a virus replicating in one organ (skin) could affect the macromolecular function of cells in another organ (liver, brain) bringing about both hepatopathy and hepatoencephalopathy.
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PMID:Chickenpox encephalitis and encephalopathy: evidence for differing pathogenesis. 629 9

The potential for hepatic injury associated with the therapeutic use of salicylates and acetaminophen has recently attracted considerable attention. About 300 cases have been reported in which elevated transaminase levels or other evidence of hepatic injury developed following treatment with salicylates. Review of the spectrum of abnormalities reveals a group of patients (4 percent) with symptomatic liver damage in whom progressive or chronic liver disease is a possibility with continued use of the drug. In a few patients in this group, jaundice developed; several had abnormal prothrombin times; 11 (70 percent) had transaminase values in excess of 500 units; and five patients (30 percent) had encephalopathy and/or Reye's syndrome. In several reports liver damage has also been associated with the use of acetaminophen in therapeutic or near-therapeutic dosages. Of 18 patients, nine appeared to have ingested acetaminophen in amounts approaching overdose. Of the remaining nine patients, six were alcoholics. In the entire group, only five patients did not have a history of alcohol abuse; in three, glutathione depletion was suggested as a possible explanation for hepatotoxicity. The association with alcoholism or glutathione depletion suggests that host susceptibility may play a critical role. In two patients, long-term use of acetaminophen resulted in liver injury suggestive of chronic active hepatitis, possibly on the basis of an idiosyncratic reaction. In a study of chronic liver disease, acetaminophen half-life was prolonged (168 percent) without accumulation at 4 g a day over five days. In a double-blind, two-week, cross-over study, no clinical or laboratory evidence of adverse effects was found. There is, therefore, no evidence that chronic liver disease increases the risk of hepatotoxicity following the administration of acetaminophen in therapeutic doses. Thus, acetaminophen is the preferred antipyretic analgesic in patients with liver disease. Salicylates should be avoided since many of the adverse effects associated with these drugs are similar to the complications of chronic liver disease.
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PMID:Hepatotoxicity following the therapeutic use of antipyretic analgesics. 635 71

Reye's syndrome, encephalopathy and fatty change in the liver and other viscera, typically occurs suddenly in infants and children recovering from a viral illness, particularly influenza or varicella. Its rapid clinical course may suggest a drug-related insult and the differential diagnosis includes a variety of toxins. There are grounds for suspicion that exogenous substances--including aspirin--may be cofactors with recent viral illness in the syndrome's pathogenesis. For these reasons, medical examiners may be called upon to rule the diagnosis in or out, to assess the possibility of direct toxic injury, or to document presence or absence of possible cofactors. With these tasks in mind, this review summarizes the diagnostic, pathologic, and laboratory findings of Reye's syndrome and considers the roles of viral infection, heritable predispositions, and exogenous toxins in its causation. It singles out salicylate treatment for special considerations as a possible cofactor, and concludes with a suggested approach to the forensic medical investigation of possible cases of Reye's syndrome.
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PMID:Reye's syndrome. A review from the forensic viewpoint. 636 91

Transport of the anionic herbicide 2,4-dichlorophenoxyacetic acid by choroid plexus is inhibited significantly by several short and medium chain acids. For both monocarboxylic and dicarboxylic homologs, inhibition clearly increases with chain length. It appears that organic acid compounds of longer chain length, higher brain uptake index, and highest inhibition of choroid plexus transport would be the ones producing the most significant increases in intracranial pressure in metabolic encephalopathy such as Reye's syndrome.
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PMID:Effect of increasing carbon chain length on organic acid transport by the choroid plexus: a potential factor in Reye's syndrome. 640 69

A 4-year-old girl with juvenile rheumatoid arthritis developed fever, protracted vomiting, disturbance of consciousness and decorticate posture following the administration of salicylate. There were elevated levels of transaminases in serum, hyperammonemia and a fatty liver. However, the fatty droplets were different electronmicroscopically from that of Reye's syndrome. This observation emphasizes the importance of electronmicroscopic observation of the liver in the differential diagnosis between Reye's syndrome and aspirin-induced encephalopathy, because the clinico-pathological findings of intoxication are so similar.
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PMID:Simulated Reye's syndrome and salicylate therapy. 646 45

A 12-week-old female infant died from acute encephalopathy mimicking Reye syndrome. Because of positive serum hepatitis B surface antigen (HBs Ag) and perivascular inflammatory cell infiltration in the liver, she was diagnosed as having acute hepatitis. The most striking finding in the present case was extremely excessive lipid accumulation in the striated muscles including biceps brachii, tongue and cardiac muscles. The levels of serum, liver and muscle carnitine were within normal limits, though liver carnitine palmityl transferase (CPT) was markedly decreased in activity. Although the primary metabolic defect has yet to be elucidated, it is assumed that the fulminant hepatic failure induced lipid accumulation in the skeletal muscle by a certain abnormal lipid metabolism.
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PMID:Fatal lipid storage disorder. 648 84

Reye's syndrome (encephalopathy with fatty infiltration of the viscera) is an acute illness of childhood that produces hepatic dysfunction and metabolic encephalopathy. The disease is fatal in as many as 40% of cases. The cause is unknown. Several environmental agents, particularly salicylates and aflatoxin, have been implicated as possible toxins in this disorder. Treatment is directed at controlling intracranial pressure, reversing metabolic abnormalities and providing intensive supportive care. Normal neurologic function returns in most survivors.
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PMID:Reye's syndrome. 649 27


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