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|Scopus||Web of Science®||Altmetric|
|Title:||Pharmacogenetics of opioid response|
|Citation:||Clinical Pharmacology and Therapeutics, 2015; 97(2):125-127|
|AA Somogyi, JK Coller and DT Barratt|
|Abstract:||For opioids requiring CYP2D6 O-demethylation to active metabolites, poor metabolizers have reduced metabolite formation and minimal pain reduction. Clinically, this has only reliably been shown for tramadol. Ultra-rapid metabolizers have an increased risk of toxicity especially for codeine. ABCB1 genetics show no consistent findings. In Asian populations, the high OPRM1 118A>G frequency associates with higher opioid dosage requirements. Clinical translation of opioid genetics is premature because many important pain and addiction phenotype factors contribute.|
|Keywords:||Humans; Pain; Cytochrome P-450 Enzyme System; Glucuronosyltransferase; Analgesics, Opioid|
|Rights:||© 2014 American Society for Clinical Pharmacology and Therapeutics|
|Appears in Collections:||Pharmacology publications|
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