Encephalopathy and Fatty Degeneration of the Viscera a Disease Entity in Childhood

Reye, R. D. K.; Morgan, Graeme; Baral, Jim

doi:10.1016/s0140-6736(63)90554-3

Cited by 765 publications

(212 citation statements)

References 2 publications

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“…did not correlate with plasma ammonia. In Reye's syndrome, the hepatic mitochondrial enzymes CPS-I and OCT have been found to be drastically reduced (at least during the first days of the clinical symptoms), the cytoplasmatic enzymes of the urea cycle being normal [ 11,[45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Urinary purines and pyrimidines in patients with hyperammonemia of various origins

Gennip

Bree-Blom

Grift

et al. 1980

Clinica Chimica Acta

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SummaryExcretion patterns of pyrimidines and purines in patients with various types of hyperammonemia have been investigated by a-dimensional thin-layer chromatography and high pressure liquid chromatography (HPLC). For the quantitative analysis of pseudouridine, uracil and uridine a new procedure has been developed, consisting of pre-fractionation with Dowex 1 X 8, followed by dual column HPLC on a strong anion-exchanger and a reverse phase column. Thymine has also been analyzed in the pre-fractionated urine by a new HPLC method using the reverse phase column in combination with a strong cationexchange column. Quantitative data for urinary pyrimidines and uric acid in hyperammonemia are given. In patients with a defect in one of the urea cycle enzymes, the level of pyrimidine excretion was found to depend on plasma ammonia concentrations.In other hyperammonemic patients, an increased excretion of erotic acid, uracil and uridine has only been found in one of the two pati'ents with lysinuric protein intolerance, all other patients showing normal excretion patterns, Elevated uric acid excretions have been found frequently in our patients with hyper~monemia, but they did not always coincide with high plasma ammonia levels. A possible explanation for the difference in the excretion levels of the various pyrimidines is discussed.

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Section: Discussionmentioning

confidence: 99%

Urinary purines and pyrimidines in patients with hyperammonemia of various origins

Gennip

Bree-Blom

Grift

et al. 1980

Clinica Chimica Acta

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show abstract

“…15 In 1963, Reye et al reported clinical and pathology findings for "Reye's Syndrome" cases at one Australian hospital. 3 Encephalopathy occurred in 21 children, including 17 deaths, since 1951. Onset generally began within days of mild illnesses, and was characterized by vomiting, irritability, agitation, stupor, or coma with hyperpnea, decreased cerebrospinal fluid glucose, elevated alanine aminotransferase and aspartate aminotransferase levels, and cerebral edema.…”

Section: Reye's Syndromementioning

confidence: 99%

“…Reye's syndrome (RS), nephrogenic systemic fibrosis (NSF), and pure red cell aplasia (PRCA) are three sADRs that were clinical mysteries when first identified in 1951, 2000, and 1998. [2][3][4] Unexpected associations with pharmaceuticals were published 29,6, and 4 years later, respectively. [4][5][6][7] Overall, 81, 13, and 17 years elapsed between introduction of the implicated drug into practice and identification of the causal relationships with these three unique sADRs.…”

Section: Introductionmentioning

confidence: 99%

Linking Drugs to Obscure Illnesses: Lessons from Pure Red Cell Aplasia, Nephrogenic Systemic Fibrosis, and Reye’s Syndrome. A Report From the Southern Network on Adverse Reactions (SONAR)

et al. 2012

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Identification of serious adverse drug reactions (sADRS) associated with commonly used drugs can elude detection for years. Reye’s syndrome (RS), nephrogenic systemic fibrosis (NSF), and pure red cell aplasia (PRCA) among chronic kidney disease (CKD) patients were recognized in 1951, 2000, and 1998, respectively. Reports associating these syndromes with aspirin, gadodiamide, and epoetin, were published 29, 6, and 4 years later, respectively. We obtained primary information from clinicians who identified causes of these sADRs and reviewed factors contributing to delayed identification of these toxicities. Overall, 3,500 aspirin-associated RS cases in the United States, 1,605 gadolinium-associated NSF cases, and 181 epoetin-associated PRCA cases were reported. Delays in FDA regulation of over-the- counter medications and administration of aspirin to children contributed to development of RS. For NSF, in 1996, the Danish Medicine Agency approved high-dose gadodiamide administration to chronic kidney disease (CKD) patients undergoing MR scans. Overall, 88 % of Danish NSF cases were from two hospitals and 97 % of United States’ NSF cases were from 60 hospitals. These hospitals frequently administered high-doses of gadodiamide to CKD patients. Another factor was the decision to administer linear chelated contrast agents versus lower risk macrocyclic chelated agents. For PRCA, increased use of subcutaneous epoetin formulations to CKD patients, in part due to convenience and cost-savings considerations, and a European regulatory requirement requiring removal of albumin as a stabilizer, led to toxicity. Overall, 81, 13, and 17 years elapsed between drug introduction into practice and identification of a causal relationship for aspirin, erythropoietin, and gadodiamide, respectively. A substantial decline in new cases of these sADRs occurred within two years of identification of the offending drug. Clinicians should be vigilant for sADRs, even for frequently-prescribed pharmaceuticals, particularly in settings where formulation or regulatory changes have occurred, or when over-the-counter, off-label, or pediatric use is common

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“…Após a descrição de Reye e col. 19 Parece-nos razoável que a possibilidade de SR seja lembrada em crianças com encefalopatia de causa desconhecida, posto que a maioria não apresenta sintomatologia de disfunção hepáticas.…”

Section: Comentariosunclassified

“…e grave, com infiltração lipídica de diversas vísceras 3,6,7,8,9,14,18 descrita como entidade clínica e patologicamente distinta por Reye, Morgan e Baral em 1963 19 . Contribuíram para que a síndrome não fosse reconhecida antes, a realização pouco frequenle de biópsia hepática e o raro emprego de técnicas histoquímicas adequadas para gordura 1^ Habitualmente ocorre um ou vários dias após infecção viral e se caracteriza por manifestações de encefalopatia difusa associada a alterações hepáticas funcionais; dessa forma o coma, as convulsões e a hepa¬ tomegalia podem preceder em 48 a 72 horas à parada cárdio-respiratória e à morte.…”

unclassified

Síndrome de reye: relato de caso

Silva¹,

Soares

Moura-Ribeiro

1986

Arq. Neuro-Psiquiatr.

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Encephalopathy and Fatty Degeneration of the Viscera a Disease Entity in Childhood

Cited by 765 publications

References 2 publications

Urinary purines and pyrimidines in patients with hyperammonemia of various origins

Urinary purines and pyrimidines in patients with hyperammonemia of various origins

Linking Drugs to Obscure Illnesses: Lessons from Pure Red Cell Aplasia, Nephrogenic Systemic Fibrosis, and Reye’s Syndrome. A Report From the Southern Network on Adverse Reactions (SONAR)

Síndrome de reye: relato de caso

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