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- Lauren E. Kelly
- Schulich School of Medicine, and
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- Michael Rieder
- Schulich School of Medicine, and
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- John van den Anker
- Children’s National Medical Center, Center for Clinical and Community Research, Washington, District of Columbia;
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- Becky Malkin
- Department of Clinical Pharmacology, London Health Sciences Centre, London, Canada;
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- Colin Ross
- Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, Canada;
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- Michael N. Neely
- Communication Sciences Institute, University of South California, Los Angeles, California;
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- Bruce Carleton
- Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, Canada;
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- Michael R. Hayden
- Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, Canada;
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- Parvaz Madadi
- Department of Clinical Pharmacology, University of Toronto, Toronto, Canada; and
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- Gideon Koren
- Ivey Chair in Molecular Toxicology, University of Western Ontario, London, Canada;
説明
<jats:p>In 2009 we reported the fatal case of a toddler who had received codeine after adenotonsillectomy for obstructive sleep apnea syndrome. The child was an ultra-rapid metabolizer of cytochrome P4502D6 (CYP2D6). We now report 3 additional fatal or life-threatening cases from North America. In the 2 fatal cases, functional gene duplications encoding for CYP2D6 caused a significantly greater production of potent morphine from its parent drug, codeine. A severe case of respiratory depression in an extensive metabolizer is also noted. These cases demonstrate that analgesia with codeine or other opioids that use the CYP2D6 pathway after adenotonsillectomy may not be safe in young children with obstructive sleep apnea syndrome.</jats:p>
収録刊行物
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- Pediatrics
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Pediatrics 129 (5), e1343-e1347, 2012-05-01
American Academy of Pediatrics (AAP)