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

Although frequently unrecognized, Reye's syndrome is a significant cause of serious illness and death in children. Erroneous diagnoses include gastroenteritis, meningoencephalitis, metabolic encephalopathy, drug overdose and primary psychiatric disease. No specific cure is known but early diagnosis and vigorous empirical treatment may increase chances of survival. Although the EEG may be a useful tool in prognosis, it cannot be relied upon in deciding when to initiate or abandon aggressive therapy.
 ...
PMID:Reye's syndrome. 111 34

Reye's syndrome is an acute encephalopathy and fatty liver which has mainly been recognized in children through the age of about 16 years. Since the patients are not jaundiced and the liver may be relatively small at the moment of admission, the diagnosis must be sought by a high index of suspicion and the routine use of liver function studies, especially the SGOT, in all unexplained cases of encephalopathy. Early treatment and appropriate management of cerebral edema seem to reduce the over-all mortality of Reye's syndrome from more than 50% to less than 20%. Alert gastroenterologists may find some adult cases of Reye's syndrome masquerading as acute neurological disease or supposed acute drug reactions.
 ...
PMID:Reye's syndrome (encephalopathy and fatty liver). Diagnosis and treatment. 115 54

The hepatic lesion in Reye's syndrome (acute encephalopathy with fatty degeneration of viscera) was studied by light microscopy of sequential biopsy specimens obtained in 49 children. The hepatic lesion is a morphologically characteristic, rapidly evolving, and reversible toxic hepatitis. In specimens obtained with 48 hr of onset of neurological deterioration, the severity of the diffuse microvesicular steatosis is best appreciated in frozen sections stained for lipid content. Variation in severity of hepatocyte glycogen depletion in early biopsies correlates with other histological measures of severity, and with the occurrence of hypoglycemia, severity of the encephalopathy at the time of admission, and mortality rate. Histochemical studies suggest that the hepatic lesion is attributable to mitochondrial injury and other evidence that supports this hypothesis is briefly reviewed. The etiology of the syndrome and its relationship to the viral disease which usually precedes it are unknown.
 ...
PMID:The hepatic lesion in Reye's syndrome. 115 86

Cerebral biopsies were obtained for electron microscopy 48 and 72 hours after the onset of encephalopathy from a child with severe Reye's syndrome. Gravely ill at the time of craniectomy to relieve cerebral hypertension, the child survived and recovered good brain function; therefore, the biopsy findings appear to reflect the organelle pathology of the brain at a severe yet reversible stage in the disease process. The cardinal ultrastructural changes in the brain in Reye's syndrome are astrocyte swelling and partial deglycogenation, myelin bleb formation and universal injury of neuron mitochondria. The mitochondrial injury consists of matrix disruption with moderate but not massive swelling. Dilatation of rough endoplasmic reticulum and nuclear changes occurred only in neurons with severely altered mitochondria. The organelle pathology of the brain in this case did not resemble the organelle pathology of the brain in human "hepatic encephalopathy" or in experimental ammonia intoxication in primates. The mitochondrial ultrastructure of the cerebral neurons resembled the unique mitochondrial ultrastructural changes seen in the liver parenchyma in Reye's syndrome.
 ...
PMID:Brain ultrastructure in Reye's syndrome. 117 96

Reye's syndrome (fatty infiltration of the liver with encephalopathy) is an uncommon disease of children and has not previously been noted in adult patients. We present a 25-year-old male who survived this syndrome after presenting a stuporous state. Etiologic and pathophysiologic mechanisms are considered.
 ...
PMID:Reye's syndrome in an adult. 120 12

The jejuno-ileal bypass for weight reduction can hardly be considered a non-specific treatment: 3-4% of the patients develop chronic hepatic damage, 1-2% suffer hepatic failure due to massive fatty liver, rapidly progressing liver cirrhosis or hepatic fibrosis. Fatty liver is an invariable sequel of this operation. Once the above-mentioned symptoms set in or an incipient cirrhosis or fibrosis is diagnosed, immediate restoration of normal passage is required. The intestinal bypass syndrome observed in the patient (fem.) (viz. table 1) does not wholly coincide with the enteral bile acid loss syndrome occurring in extensive ileum resection (56) where usually there is no evidence of fatty liver, icterus, cholestasis or encephalopathy. Animal experiments seem to confirm that the blind loop in the broadest sense of the term is responsible for the sometimes fatal hepatic damage. Possibly we are confronted here with a pattern of hepatic damage due to toxic nutritive effects similar to cirrhosis as a sequel of low-protein and low-calorie intake or to the phenomenon observed in animal experiments. The cholestasis confirmed by biopsy and chemical methods is a manifestation of these hepatic disorders. The clinical aspects resemble the Reye syndrome that we know in pediatrics. Patients have to be carefully selected and informed about possible postoperative damage; a continuous clinical follow-up with biopsy of the hepatic tissue is also indicated.
 ...
PMID:[Liver damage following intestinal by-pass surgery for weight reduction]. 122 12

The authors report two cases of Puttman Reye syndrome: one, classical, involving a young child with a fatal encephalopathy with visceral fatty infiltration, the other, less typical, not showing any signs of visceral fatty degeneration. Both cases were subjected to complete anatomical examination of the brain, revealing marked cerebral oedema, in localised areas or in a laminar distribution, with degenerative changes in the neurones and slight demyelinisation. The authors, on the basis both on the classical appearances of the first case as well as the atypical features of the second, envisage a clinical, anatomical and biological link between the Puttman-Reye syndrome,. Thai encephalopathy and Ekiri, which they consider to represent a single entity.
 ...
PMID:[Puttman-Reye syndrome and ekiri. Neuro-anatomical study and attempt at classification]. 123 72

Reye's syndrome (RS) consists of encephalopathy, fatty degeneration of viscera, and elevation of ammonia, certain amino acids, and liver enzymes in the blood. It is most characteristically a disease of children and has been considered to have a poor prognosis despite the use of various treatment regimens. Exchange transfusion (ET) with fresh blood (less than 24 hours old) for the removal of toxic metabolic byproducts in TS is a relatively recent development which appears to have improved the survival rates. However, because RS may occur in epidemic proportions at any time the demand for fresh blood can place an excessive stress on blood resources. We have, therefore, utilized saline-washed (to remove potentially toxic metabolites) red blood cells (RBC's) less than six days old, and fresh frozen citrate-phosphate-dextrose (CPD) plasma in treating this disorder. Nine patients in the Milwaukee community with severe encephalopathy secondary to RS were treated with ET. These patients collectively required 151 units of washed RBC's for 21 ET. Eight of nine patients survived without sequelae. Age of blood used did not correlate with the number of exchanges required or the eventual outcome. A continual computerized EEG in five patients provided objective evidence of the effectiveness of ET. We conclude that ET with saline-washed RBC's reconstituted with fresh frozen plasma (FFP) is a fast, safe, and effective means of treating patients with RS.
 ...
PMID:Exchange transfusion in Reye's syndrome with saline-washed red blood cells. 125 13

Elevated serum free fatty acids (FFA) have been implicated previously as the agent causing encephalopathy and fatty degeneration of the viscera (Reye's syndrome). This study documents a decrease in medium and long chain FFA from elevated levels (1.35 mEq/liter) to low levels (0.30 mEq/liter) in a patient successfully treated with exchange transfusions.
 ...
PMID:Medium and long chain serum free fatty acids in a case of Reye's syndrome. 127 26

Reye's syndrome is difined as fatty degeneration of the viscera with encephalopathy. The signs are change in consciousness after recovery of a viral illness, vomiting, high fever, and progresseve deterioration of the level of consciousness. Signs of brain stem involvement quickly follow. The clinical findings are: mild elevations of serum transaminases (SGOT and SGPT), normal to slightly elevated bilirubin, abnormal blood-clotting functions, normal to low blood glucose, high blood ammonia, and normal cerebrospinal fluid which may be under increased pressure. Death is due to increased intracranial pressure. Therapy is used to stabilize these signs. It includes: infusion of hypertonic glucose followed by insulin, peritoneal dialysis, and exchange transfusion. Intracranial pressure was monitored continually to determine when therapy should be administered.
 ...
PMID:Intracranial pressure monitoring in Reye's syndrome. 127 55


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>