title: Reyes's syndrome, encephalopathy, hyperammonemia and acetyl salicylic acid ingestion in a city hospital of Buenos Aires, Argentina.
abstract: Twelve cases of Reye's syndrome are presented with different degrees of encephalopathy, hyperammonemia and hypoglycemia; associated to acetyl salicylic acid (ASA) ingestion. The aim of the present retrospective study was to describe our experience in selected patients with Reye's syndrome associated to the ASA ingestion and to underline the influence of hyperammonemia on Reye's encephalopathy. All the cases presented moderate hyperbilirubinemia, elevated alanine aminotransferase, aspartate aminotransferase with an average of 302+/-205 UI/L and 285+/-149 UI/L respectively. Arterial blood ammonia averaged 172.4+/-71.3 micromol/L and glycaemia averaged 35.2+/-17.0 mg/dl. A high mortality was found in our series (41.7%). Considering that encephalopathy is the leading syndrome in these cases, the influence of ammonia on brain tissue was described. Glutamate is an excitotoxic neurotransmitter, capable to produce neuron and astrocyte damage and apoptosis. The presence of ASA could cause the onset of the mitochondrial permeability transition and the mitochondrial swelling in the astrocyte, leading to hyperammonemia. In Reye's syndrome, hyperammonemia and perhaps the increase of glutamate are the leading factors in the mechanism of brain damage and encephalopathy. Aspirin must be carefully administrated and controlled by professionals. Furthermore, parents must be informed about the risks in the use of this drug in children.
authors.affiliation: Cátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, U.B.A., Junín 956, 1113, Buenos Aires, Argentina.
authors.forename: Abraham
authors.initials: A
authors.lastname: Lemberg
authors.forename: María A
authors.initials: MA
authors.lastname: Fernández
authors.forename: Carlos
authors.initials: C
authors.lastname: Coll
authors.forename: Diego O
authors.initials: DO
authors.lastname: Rosello
authors.forename: Salvador
authors.initials: S
authors.lastname: Romay
authors.forename: Juan C
authors.initials: JC
authors.lastname: Perazzo
authors.forename: Ester J
authors.initials: EJ
authors.lastname: Filinger
mesh_terms: D000410:Alanine Transaminase / Q000187:drug effects / Q000378:metabolism; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001118:Argentina / Q000453:epidemiology; D001219:Aspartate Aminotransferases / Q000187:drug effects / Q000378:metabolism; D001241:Aspirin / Q000009:adverse effects*; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D005260:Female; D018698:Glutamic Acid / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D022124:Hyperammonemia / Q000139:chemically induced* / Q000503:physiopathology; D006932:Hyperbilirubinemia / Q000139:chemically induced; D008297:Male; D008933:Mitochondrial Swelling / Q000187:drug effects; D012189:Retrospective Studies; D012202:Reye Syndrome / Q000139:chemically induced* / Q000401:mortality / Q000503:physiopathology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018698:Glutamic Acid; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001241:Aspirin