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)

Reye's syndrome (encephalopathy and fatty liver) is generally considered a disease of children. Four patients, aged 16, 18, 19, and 23 years, with Reye's syndrome were initially seen by internists. A viral prodrome followed by vomiting and encephalopathy without focal neurological signs or jaundice clinically suggested Reye's syndrome. Normal findings of CSF examination (except for increased opening pressure), abnormal findings of liver function tests, and increased blood ammonia further supported the diagnosis. None was hypoglycemic. Reye's syndrome was related to influenza B virus in three patients and to Varicella in another. Three patients survived. Reye's syndrome may be seen intially by general practitioners, emergency room physicians, internists, or psychiatrists. The importance of considering this syndrome in the differential diagnosis of unexplained encephalopathy in adults is stressed.
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PMID:Reye's syndrome in nonpediatric age groups. 48 May 58

The clinical picture of Reye's syndrome, characterized by an acute severe disease of brain and liver, initially has nonspecific generalized symptoms with cough, myalgia, and fever. The prognosis is poor. The disease starts with an infection, quickly followed by vomiting and loss of consciousness. In this phase the serum bilirubin is moderately raised, the transaminases markedly so. In addition to gastro-intestinal bleeding there may be hypoventilation, hypoglycaemia and seizures. Morbid anatomically there is a small-drop fatty infiltration of the liver and other organs with cerebral oedema. Aetiology and pathogenesis remain uncertain. Numerous therapeutic measures have been proposed.
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PMID:[Reye's syndrome in adults (author's transl)]. 68 69

Hypoglycin A is a toxin which causes Jamaican vomiting sickness. In rats treated with this compound, we observed significant increases in a number of amino acids in the plasma and the urine, and detected several unidentified amino compounds in the urine. These changes suggest that hypoglycin, in addition to its known inhibitory effect on acyl-CoA dehydrogenases interferes with some steps in nitrogen metabolism as well. The amino acid abnormalities seen in hypoglycin-treated rats are compared with those seen in Reye's syndrome.
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PMID:Plasma and urine amino acid changes in rats treated with hypoglycin. 69 43

We identified methylenecyclopropylacetic acid, a known metabolite of hypoglycin A, in the urine of two patients with Jamaican vomiting sickness. Excretion of unusual dicarboxylic acids such as 2-ethylmalonic, 2-methylsuccinic, glutaric, adipic and dicarboxylic acids with eight and 10 carbon chains were also detected in both patients. The amounts of these dicarboxylic acids were 70 to 1000 times higher than normal. These metabolites have also been identified in urine of hypoglycin-treated rats. This evidence links hypoglycin A to Jamaican vomiting sickness as its causative agent. Urinary excretion of short-chain fatty acids was also increased up to 300 times higher than normal. These results indicate that, despite their clinical and histologic similarities, the cause and biochemical mechanisms of Jamaican vomiting sickness differ distinctly from those of Reye's syndrome in which these abnormal urinary metabolites are not appreciably increased.
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PMID:Jamaican vomiting sickness. Biochemical investigation of two cases. 94 May 78

This case substantiates the fact that Reye's syndrome can occur in newborns. The clinical features appear to be slightly different in the neonate, in that respiratory distress was the presenting sign in this case and in the one other reported case in a newborn, with no mild preceding illness or vomiting. Thus, Reye's syndrome must be considered when a newborn presents with respiratory distress and evidence of central nervous system and hepatic involvement.
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PMID:Reye's syndrome in a neonate. 101 56

4-Pentenoic acid, an analog of hypoglycin which is believed to cause Jamaican vomiting sickness, was administered intraperitoneally to rats in an attempt to produce the features of Reye's syndrome in rats. Mean ammonia levels in plasma were found to be elevated approximately four-fold after injection of 200 mg/kg pentenoic acid in fed rats. Pentenoic acid caused hypoglycemia in fasted rats and hyperglycemia in fed rats. In chronic experiments rats were injected intraperitoneally every 4 hr with 50 mg/kg body weight of pentenoic acid for 10 doses, followed by a single dose of 200 mg/kg. The livers of the treated group were enlarged and yellow and showed extensive fatty degeneration. The blood-urea-nitrogen (BUN) was significantly higher and the free fatty acids (FFA's) significantly lower in these rats. This study shows that pentenoic acid administered to rats produces findings similar to those of Reye's syndrome and Jamaican vomiting sickness.
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PMID:Production of the features of Reye's syndrome in rats with 4-pentenoic acid. 112 19

Siblings, aged 9 and 7 years, had simultaneous onset of vomiting, disorientation, ataxia, and coma. Both children had prodromal symptoms of upper respiratory tract infections, and had been treated with large doses of aspirin. Laboratory data showed evidence of hepatocellular dysfunction, with an elevated serum ammonia level in one patient; salicylate levels were 50 and 44 mg/100 ml. The child who died had autopsy evidence of cerebral edema and fatty liver. The difficulty in clinically differentiating Reye syndrome from salicylate intoxication is discussed.
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PMID:Acute encephalopathy in siblings. Reye syndrome vs salicylate intoxication. 125 38

A 2 1/2-year-old child died after an illness of three days duration, characterized by a sudden onset, vomiting, coma and a striking hyperammonemia. At autopsy, the liver was practically normal. This is a further example of Reye's syndrome with only minimal fatty infiltration of the liver. It appears that the classical massive and diffuse fatty degeneration of the liver is not an essential feature of the syndrome. The evidence for this is discussed.
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PMID:Reye's syndrome without fatty liver. 127 Mar 22

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.
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PMID:Intracranial pressure monitoring in Reye's syndrome. 127 55

A case of sudden death associated with fatty liver and encephalopathy is described in a 4-year old white boy with medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency. The death was caused by hypoglycemia triggered by fasting and vomiting associated with a minor viral infection. The differential diagnosis of the hepatoencephalopathy is discussed in relation to other conditions, especially Reye's syndrome. The forensic pathologist should be familiar with MCAD and other deficiencies of beta-oxidation of fatty acids as a cause of sudden unexpected death in children in order to advise parents in genetic counseling to prevent disability or death of other affected, but still asymptomatic siblings.
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PMID:Fatty liver, encephalopathy, and sudden unexpected death in early childhood due to medium-chain acyl-coenzyme A dehydrogenase deficiency. 128 65


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