A genome-wide association study of tramadol metabolism from post-mortem samples. View Full Text


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Article Info

DATE

2019-04-11

AUTHORS

Frank R Wendt, Anna-Liina Rahikainen, Jonathan L King, Antti Sajantila, Bruce Budowle

ABSTRACT

Phase I tramadol metabolism requires cytochrome p450 family 2, subfamily D, polypeptide 6 (CYP2D6) to form O-desmethyltramadol (M1). CYP2D6 genetic variants may infer metabolizer phenotype; however, drug ADME (absorption, distribution, metabolism, and excretion) and response depend on protein pathway(s), not CYP2D6 alone. There is a paucity of data regarding the contribution of trans-acting proteins to idiosyncratic phenotypes following drug exposure. A genome-wide association study identified five markers (rs79983226/kgp11274252, rs9384825, rs62435418/kgp10370907, rs72732317/kgp3743668, and rs184199168/exm1592932) associated with the conversion of tramadol to M1 (M1:T). These SNPs reside within five genes previously implicated with adverse reactions. Analysis of accompanying toxicological meta-data revealed a significant positive linear relationship between M1:T and degree of sample polypharmacy. Taken together, these data identify candidate loci for potential clinical inferences of phenotype following exposure to tramadol and highlight sample polypharmacy as a possible diagnostic covariate in post-mortem genetic studies. More... »

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    URI

    http://scigraph.springernature.com/pub.10.1038/s41397-019-0088-y

    DOI

    http://dx.doi.org/10.1038/s41397-019-0088-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113356004

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30971809


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