Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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 five-year-old-girl with a history of recurrent hypoglycemia presented with acidosis, intractable vomiting, and abdominal tenderness; the diagnosis of acute pancreatitis was made by abdominal ultrasonography and supportive biochemical studies. Urinary organic acid analysis revealed metabolites suggestive of HMG-CoA lyase deficiency, and subsequent enzyme assays of lymphocytes and fibroblasts confirmed this diagnosis. Acute pancreatitis, an uncommon condition in childhood, is seen with increased frequency in patients with Reye syndrome, a metabolic disorder with which HMG-CoA lyase deficiency may be confused. The pathogenesis of pancreatitis in Reye syndrome or in HMG-CoA lyase deficiency has not been determined.
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PMID:A child with acute pancreatitis and recurrent hypoglycemia due to 3-hydroxy-3-methylglutaryl-CoA lyase deficiency. 648 80

Three, previously healthy, patients developed profuse vomiting. In the further course of the disease there was a marked deterioration in their general condition with massive metabolic acidosis, cerebral symptoms and, finally, deep coma which ended in death, without any evidence of poisoning. Post-mortem examination revealed diffuse, droplet fatty infiltration of the liver of the degenerative type as well as cerebral oedema without inflammatory signs, findings of Reye's syndrome, rarely seen beyond childhood. The aetiology of this prognostically unfavourable disease remains uncertain, clinical features and laboratory results are very variable. In adults the disease is rarely diagnosed because the syndrome is not known. Only liver biopsy can confirm the diagnosis. Main aim of the symptomatic treatment is to counteract the cerebral oedema.
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PMID:[Fatty liver, metabolic acidosis and brain edema--Reye's syndrome in adults?]. 669 78

Reye's syndrome is a virus-associated biphasic disease that causes acute encephalopathy in infants and children. Epidemiologic and experimental data support the hypothesis that it is a multifactorial disease of modern civilization. Just as young patients seem to be recovering uneventfully from the first phase of the illness, usually a nonspecific viral-like illness such as a respiratory tract infection or gastroenteritis, the second phase, encephalopathy, starts unexpectedly, with vomiting and sensorial changes. Identifying the syndrome early ;in the second phase and referring the child to a specialized centre with the experience, staff and facilities to manage this phase has improved the numbers and neurologic condition of survivors, though the overall mortality is still about 20%. Therapy is primarily directed at facilitating adequate cerebral perfusion pressure.
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PMID:Reye's syndrome: a clinical review. 678 91

Analyses of 23 fatal instances of hepatic injury in patients taking valproic acid reveals that all but three were less than 20 years old, and all but four had been taking the drugs for more than 1 month. Convulsions, facial edema, lassitude, and vomiting were prominent clinical features. Hypoglycemia was recorded in six patients. Rash and eosinophilia were not seen. Values for transaminases were modestly elevated in most patients. Most levels of SGOT were below 500 IU, and SGPT levels were below 200 IU. Livers showed microvesicular steatosis in most patients, usually accompanies by necrosis. Four patients had cirrhosis. Overt valproic acid-induced hepatic injury appears to be rare and hence, by definition, idiosyncratic. That it may be an idiosyncratic exaggeration of a much more frequent phenomenon is suggested by the higher incidence of seemingly trivial injury. The idiosyncrasy appears to be metabolic rather than immunologic, and the available information leads to the plausible hypothesis that a metabolite is responsible for the microvesicular steatosis seen in most fatal cases. The steatosis resembles that of Reye's syndrome and Jamaican vomiting sickness, and there is reason to believe that the metabolite responsible for the steatosis resembles the agent responsible for Jamaican vomiting sickness. A different metabolite is presumably responsible for the necrosis seen in many of the cases.
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PMID:Valproate-induced hepatic injury: analyses of 23 fatal cases. 681 94

A 22-year-old male presented with a brief history of progressive encephalopathy. One week previously, he had developed an upper respiratory infection that resolved spontaneously and was followed by intractable vomiting. He had taken salicylates for several days during the viral syndrome. The diagnosis of Reye's syndrome was confirmed by hepatic histology. Aggressive conservative management was followed by complete metabolic and neurological recovery. There are fewer than 10 reported cases of Reye's syndrome in adults but this disease may be more common than is generally suspected. The diagnosis should be considered in patients presenting with emesis and obtundation, who have recently had a viral illness and exhibit elevated blood ammonia and transaminases with normal cerebrospinal fluid. Confirmation is achieved by liver biopsy. Therapy is directed toward aggressive reduction of increased intracranial pressure.
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PMID:Reye's syndrome in the adult: case report and review of the literature. 685 15

In a one-year prospective study we assessed the incidence of Reye's syndrome in children presenting with the acute onset of vomiting after a prodromal upper-respiratory-tract infection or varicella, and with serum alanine or aspartate aminotransferase levels at least three times higher than normal, and a paucity of neurologic findings. Of 25 patients meeting the above criteria, 19 had liver biopsies yielding adequate tissue for diagnostic purposes. Biopsy specimens from 14 of these 19 patients (74 per cent) were diagnostic of Reye's syndrome, according to rigorous light-microscopical, histochemical, and ultrastructural criteria. None of the biopsy specimens contained evidence of other acute pathologic processes, including hepatitis. A wide spectrum of mitochondrial alterations existed at the ultrastructural level, ranging from mild to severe lesions that were indistinguishable from those seen in comatose patients with Reye's syndrome. Our findings suggest that the clinical complex of vomiting, hepatic dysfunction, and minimal neurologic impairment after varicella or an upper-respiratory-tract infection usually represents Reye's syndrome. This syndrome occurs more frequently than previously recognized.
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PMID:Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper-respiratory-tract infection. 686 12

Vomiting, lethargy and metabolic acidosis were the main initial symptoms of metabolic disease in a 1 month old girl. Her older sister had died from a similar disease, considered to be Reye's syndrome, at an age of 15 months. The urine of the present case contained 2-methylcitric acid, 3-hydroxypropionic acid, N-propionylglycine, 2-hydroxy-3-methylbutyric acid, N-tiglylglycine, 3-hydroxyvaleric acid and glutaric acid. These metabolites are all known to be associated with propionyl-CoA accumulation. Free propionic acid was not detected in the urine. In addition, the urine contained 3-oxo-2-methylvaleric acid and 3-hydroxy-2-methylvaleric acid, probably formed by condensation of two molecules of propionyl-CoA. The identity of these metabolites was confirmed by synthesis. An elevated urinary concentration of maleic acid and fumaric acid was another constant abnormality. The activity of propionyl-CoA carboxylase in leucocytes was about 20% of the normal activity. The girl was teated with a low-protein diet since the diagnosis was made at an age of 1 month, and her psychomotor development was satisfactory at an age of 2 1/2 years. She had a few episodes of acidosis during infections.
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PMID:Propionyl-CoA carboxylase deficiency: case report, effect of low-protein diet and identification of 3-oxo-2-methylvaleric acid 3-hydroxy-2-methylvaleric acid, and maleic acid in urine. 731 94

A case of Reye's syndrome in a four-year-old child on long-term salicylate medication for rheumatoid arthritis is reported. Severe fatty changes of the liver, lipid vacuolation in the renal proximal tubules, and severe brain oedema were the prominent postmortem findings. Symptoms of a trivial infection and vomiting just before death added to the resemblance of this case to Reye's syndrome.
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PMID:Reye's syndrome in a child on long-term salicylate medication. 735 24


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