From the National Institute of Allergy and Infectious Diseases: Summary of a workshop on disease mechanisms and prospects for prevention of Reye's syndrome.
Identifieur interne : 000474 ( PubMed/Checkpoint ); précédent : 000473; suivant : 000475From the National Institute of Allergy and Infectious Diseases: Summary of a workshop on disease mechanisms and prospects for prevention of Reye's syndrome.
Auteurs : J R La MontagneSource :
- The Journal of infectious diseases [ 0022-1899 ] ; 1983.
Descripteurs français
- KwdFr :
- Acides gras (métabolisme), Adolescent, Adulte, Animaux, Calcium (métabolisme), Carnitine (métabolisme), Enfant, Enfant d'âge préscolaire, Grippe humaine (), Humains, Mitochondries du foie (métabolisme), Modèles animaux de maladie humaine, Nourrisson, Nouveau-né, Rats, Risque, Syndrome de Reye (), Syndrome de Reye (métabolisme), Syndrome de Reye (épidémiologie), Transport biologique, États-Unis d'Amérique.
- MESH :
- métabolisme : Acides gras, Calcium, Carnitine, Mitochondries du foie, Syndrome de Reye.
- épidémiologie : Syndrome de Reye.
- Adolescent, Adulte, Animaux, Enfant, Enfant d'âge préscolaire, Grippe humaine, Humains, Modèles animaux de maladie humaine, Nourrisson, Nouveau-né, Rats, Risque, Syndrome de Reye, Transport biologique, États-Unis d'Amérique.
- Wicri :
- geographic : États-Unis.
English descriptors
- KwdEn :
- Adolescent, Adult, Animals, Biological Transport, Calcium (metabolism), Carnitine (metabolism), Child, Child, Preschool, Disease Models, Animal, Fatty Acids (metabolism), Humans, Infant, Infant, Newborn, Influenza, Human (complications), Mitochondria, Liver (metabolism), Rats, Reye Syndrome (epidemiology), Reye Syndrome (metabolism), Reye Syndrome (prevention & control), Risk, United States.
- MESH :
- chemical , metabolism : Calcium, Carnitine, Fatty Acids.
- geographic : United States.
- complications : Influenza, Human.
- epidemiology : Reye Syndrome.
- metabolism : Mitochondria, Liver, Reye Syndrome.
- prevention & control : Reye Syndrome.
- Adolescent, Adult, Animals, Biological Transport, Child, Child, Preschool, Disease Models, Animal, Humans, Infant, Infant, Newborn, Rats, Risk.
Abstract
The workshop participants identified several areas that are worthy of investigation. A better understanding of the populations at risk is necessary. First, the geographic distribution of cases is poorly understood, and efforts should be made to determine whether the apparent clustering of cases in the states bordering the Great Lakes is real or reflects better reporting and identification of cases in these states than in other regions. Second, reports of cases among siblings or relatives suggests either an underlying metabolic risk factor or the possibility of a common environmental risk factor. Further studies of carnitine metabolism would be appropriate in this regard. Third, epidemiologic experience with Reye's syndrome suggests that clusters of cases may occur more frequently when new influenza A or B viruses become epidemic. This pattern was observed most clearly in 1978 during the epidemic of A/USSR/77 (H1N1) influenza virus infection. Additional suggestive evidence was obtained during the epidemic of A/Asian/57 (H2N2) influenza in 1957-1958 [20] and that of B/Hong Kong/72 influenza in 1973-1974. This feature suggests that first infections with these viruses are more likely than reinfections to produce the rare sequela of Reye's syndrome. Fourth, the reported association of Reye's syndrome with the use of acetylsalicylate in the treatment of the antecedent illness requires further study. In this situation the potential risk factor has been recognized as a mitochondrial toxin capable of uncoupling oxidative phosphorylation. Finally, the question of a toxic product produced as a consequence of the prodromal infection or present coincident with the infection remains unresolved.(ABSTRACT TRUNCATED AT 250 WORDS)
DOI: 10.1093/infdis/148.5.943
PubMed: 6631079
Affiliations:
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type="abstract" xml:lang="en">The workshop participants identified several areas that are worthy of investigation. A better understanding of the populations at risk is necessary. First, the geographic distribution of cases is poorly understood, and efforts should be made to determine whether the apparent clustering of cases in the states bordering the Great Lakes is real or reflects better reporting and identification of cases in these states than in other regions. Second, reports of cases among siblings or relatives suggests either an underlying metabolic risk factor or the possibility of a common environmental risk factor. Further studies of carnitine metabolism would be appropriate in this regard. Third, epidemiologic experience with Reye's syndrome suggests that clusters of cases may occur more frequently when new influenza A or B viruses become epidemic. This pattern was observed most clearly in 1978 during the epidemic of A/USSR/77 (H1N1) influenza virus infection. Additional suggestive evidence was obtained during the epidemic of A/Asian/57 (H2N2) influenza in 1957-1958 [20] and that of B/Hong Kong/72 influenza in 1973-1974. This feature suggests that first infections with these viruses are more likely than reinfections to produce the rare sequela of Reye's syndrome. Fourth, the reported association of Reye's syndrome with the use of acetylsalicylate in the treatment of the antecedent illness requires further study. In this situation the potential risk factor has been recognized as a mitochondrial toxin capable of uncoupling oxidative phosphorylation. Finally, the question of a toxic product produced as a consequence of the prodromal infection or present coincident with the infection remains unresolved.(ABSTRACT TRUNCATED AT 250 WORDS)</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">6631079</PMID><DateCompleted><Year>1983</Year><Month>12</Month><Day>20</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>11</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1899</ISSN><JournalIssue CitedMedium="Print"><Volume>148</Volume><Issue>5</Issue><PubDate><Year>1983</Year><Month>Nov</Month></PubDate></JournalIssue><Title>The Journal of infectious diseases</Title><ISOAbbreviation>J. Infect. Dis.</ISOAbbreviation></Journal><ArticleTitle>From the National Institute of Allergy and Infectious Diseases: Summary of a workshop on disease mechanisms and prospects for prevention of Reye's syndrome.</ArticleTitle><Pagination><MedlinePgn>943-50</MedlinePgn></Pagination><Abstract><AbstractText>The workshop participants identified several areas that are worthy of investigation. A better understanding of the populations at risk is necessary. First, the geographic distribution of cases is poorly understood, and efforts should be made to determine whether the apparent clustering of cases in the states bordering the Great Lakes is real or reflects better reporting and identification of cases in these states than in other regions. Second, reports of cases among siblings or relatives suggests either an underlying metabolic risk factor or the possibility of a common environmental risk factor. Further studies of carnitine metabolism would be appropriate in this regard. Third, epidemiologic experience with Reye's syndrome suggests that clusters of cases may occur more frequently when new influenza A or B viruses become epidemic. This pattern was observed most clearly in 1978 during the epidemic of A/USSR/77 (H1N1) influenza virus infection. Additional suggestive evidence was obtained during the epidemic of A/Asian/57 (H2N2) influenza in 1957-1958 [20] and that of B/Hong Kong/72 influenza in 1973-1974. This feature suggests that first infections with these viruses are more likely than reinfections to produce the rare sequela of Reye's syndrome. Fourth, the reported association of Reye's syndrome with the use of acetylsalicylate in the treatment of the antecedent illness requires further study. In this situation the potential risk factor has been recognized as a mitochondrial toxin capable of uncoupling oxidative phosphorylation. 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