Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
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Reye's syndrome, a condition characterized pathologically by cerebral edema and fatty change of the liver, has been described extensively in the medical literature as a disease manifested clinically by encephalopathy and coma. This is a report of five cases of Reye's syndrome occurring as sudden, unexpected deaths outside of the hospital. In each of these cases, there is a vague history of a previous viral illness. A history of aspirin intake is inconstant. Each child either had no significant past illnesses or there was a history of repeated upper respiratory infections. The classic progression of signs and symptoms usually described for Reye's syndrome, where vomiting usually precedes encephalopathy and coma, was not present in any of the cases. Results of autopsies showed the characteristic findings for Reye's syndrome, and additional tests showed no other explanation for the deaths. This manifestation of the disease is seldom described in medical literature, but it may be encountered occasionally by the medical examiner.
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PMID:Reye's syndrome. A diagnosis occasionally first made at medicolegal autopsy. 849 79

A seven-month-old girl was admitted to the Pediatrics Department of Mackay Memorial Hospital with the following symptoms and signs: (1) high fever for more than five days; (2) injection of bilateral conjunctiva; (3) bright red lips with strawberry tongue; (4) edematous change of palms and soles, followed by digit desquamation; (5) an ill-defined, erythematous plaque on the scar of the BCG. Kawasaki disease was diagnosed, and high dose aspirin (100 mg/kg/day) and intravenous gamma-globulin (IVIG) (400 mg/kg/day) were given for four days. The patient was afebrile on the second day after IVIG infusion, and was discharged six days after admission. A small single daily dose of aspirin (10 mg/kg/day) was given after the afebrile days. Unfortunately, vomiting and consciousness disturbance were noted one day after discharge. Laboratory data showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT) and ammonia. Hypoglycemia and prolonged PT and PTT were also noted. Reye syndrome was suspected, and the patient was admitted to the intensive care unit for further management. A liver biopsy gave findings consistent with Reye syndrome. In spite of intensive treatment, the infant expired on the second day after admission. In a review of the literature, no correlation between these two syndromes was found. This rare case is presented to warn that Reye syndrome may follow Kawasaki disease when aspirin has been prescribed at a high dose.
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PMID:Kawasaki disease with Reye syndrome: report of one case. 162 54

An increasing number of reports indicate that patients with some inherited metabolic diseases may have symptoms resembling those of Reye's syndrome. We describe 2 patients who developed Reye-like syndrome at the age of 7 months respectively. Conscious disturbance, hepatomegaly, impaired liver function, hyperammonemia, and nonketotic hypoglycemia were noted during acute episode. Blood lactate level was normal in both cases. Liver and muscle biopsy of both patients showed macrovesicular fatty change. Increased density of matrix in hepatocyte mitochondria was noted in patient 1. Stacking of cristae was shown in patient 2. The first patient had another episode of hyperammonemia at 2 years of age. The second patient was admitted three more times due to recurrent vomiting and conscious change at the age of 7 months, 10 months and 13 months respectively. Fatty acid metabolic defect should be considered in children or infants with recurrent Reye-like syndrome.
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PMID:Recurrent acute encephalopathy due to fatty acid metabolic defect--report of two cases. 164 79

By analysing two patients initially diagnosed as Reye syndrome evidence is given that in some patients considered as having Reye syndrome, the syndrome is an escalation of symptoms due to viral disease and to unrecognized drug-induced encephalopathy, mainly by anti-emetics. A detailed drug history, considering all medication--not exclusively aspirin--taken during the full course of the illness is essential to differentiate between Reye syndrome and drug-induced symptoms. In addition, a critical analysis is presented of the four main case-control surveys that have lead to the proposal that salicylates are primary causative agents of Reye syndrome. In these surveys, medications given during the prodromal illness were adequately recorded, but other drugs given after the onset of vomiting have been overlooked or deliberately excluded. New epidemiological studies are needed, recording all drugs given to the patients throughout the full course of their illness until the moment of admission, in order to elucidate the mystery of Reye syndrome.
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PMID:Reye syndrome or side-effects of anti-emetics? 153 63

Serum NEFA profiles in Reye's syndrome are reportedly unique with a disproportionate percent made up of polyunsaturated fatty acids some of which are not ordinarily found in the serum. This pattern is also reflected in the serum triglyceride composition as well. As the liver is probably the sole source of the serum triglyceride in Rye's syndrome because patients are vomiting or in coma, the fatty acid acid composition of the liver triglyceride was examined for insight regarding the lipid abnormalities in this disease. Palmitic acid (16:0) and the sum of all the saturated fatty acids in the liver triglycerides were significantly decreased whereas the sum of the monoenoic fatty acids and the products of delta 9 desaturase activity were increased in Reye's samples. When these data were compared to the fatty acid composition of the serum triglyceride from a separate cohort of Reye's and control subjects, certain inferences regarding hepatic delta 9, delta 6, delta 5, and delta 4 desaturase activities and the elongases can be drawn from the liver and serum triglyceride fatty acid profiles which are unique. Collectively, these data reflect considerable intrahepatic fatty acid desaturation and elongation activity and/or acyl transfer from lipid to lipid of various polyunsaturated fatty acids in Reye's syndrome.
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PMID:Fatty acid composition of hepatic triglycerides in Reye's syndrome: implications for hepatic desaturase abnormalities. 181 59

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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PMID:Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs. 188 58

Reye syndrome (RS) is an acute illness that occurs almost exclusively in children; it is characterized clinically by profuse vomiting and neurologic dysfunction, sometimes progressing to delirium, coma, and death. Continuous national surveillance for RS was established in December 1976. This report summarizes RS cases for the 1989 surveillance year (December 1, 1988-November 20, 1989).
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PMID:Reye syndrome surveillance--United States, 1989. 189 29

Since 1974 we have seen 320 cases of Reye's syndrome in our department. There were 163 boys and 157 girls of a mean age of 20 months. While the number of Reye's syndrome patients admitted increased from 1979 to 1982, it has declined since 1984. Two different approaches to management were used. Prior to 1976 only simple supportive measures were given: Intravenous 10% dextrose solution and electrolytes (Darrow-glucose solution) in equal amounts at a rate of 50-100 ml/kg/day with or without dexamethasone (0.5 mg/kg/day). From 1976, in addition, measures were taken to lower the intracranial pressure by infusing mannitol 1-2 gm and glycerol 1 g/kg given at a frequency related to the severity of the illness, i.e., for grade II, the above combination was given 8 hourly, for grade III 6 hourly, and for grades IV and V 4 hourly, while for grade I only fluid and electrolytes were given. In all cases, clinical progress was closely followed. Intravenous dexamethasone was also given at a dose of 0.5 mg/kg/day. The fatality rate was 50 to 60% prior to 1976 and has fallen to around 20% at present. In contrast to reports from Western countries, we observed more convulsions, respiratory infections and gastrointestinal disorders but less vomiting and no chicken-pox.
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PMID:Treatment of Reye's syndrome at Sumber Waras Hospital. 212 7

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.
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PMID:Microvesicular steatosis of the liver. 217

Reye's syndrome is an acute disease of childhood characterized by non-inflammatory cerebral pathology associated with hepatic pathology (steatosis). When untreated, its course is very severe, with a 30 p. 100 mortality rate. The diagnosis rests on the occurrence of a suggestive clinical sequence (influenza-like syndrome followed by a latent period, then vomiting and disturbances of consciousness) and on particular laboratory findings: high serum ammonia and transaminase levels, hypoprothrombinaemia and frequent hypoglycaemia in neonates. As soon as the condition is diagnosed, massive intravenous carbohydrate therapy must be initiated. Several factors intervene in the pathogenesis of Reye's syndrome; the responsibility of treatment with salicylates and of hereditary enzymopathies is discussed.
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PMID:[Reye's syndrome]. 232 Sep 7


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