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Pharmacogenetic guidance: individualized medicine promotes enhanced pain outcomes

Authors Dragic LL, Wegrzyn EL, Schatman ME, Fudin J

Received 22 June 2017

Accepted for publication 18 October 2017

Published 22 December 2017 Volume 2018:11 Pages 37—40

DOI https://doi.org/10.2147/JPR.S144560

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Katherine Hanlon


Lisa Lynn Dragic,1 Erica L Wegrzyn,2 Michael E Schatman,3–5 Jeffrey Fudin2,6

1Central Arkansas Veterans Healthcare System, Little Rock, AR, USA; 2Department of Pharmacy, Albany Stratton VA Medical Center, Albany, NY, USA; 3Research and Network Development, Boston Pain Care, Waltham, MA, USA; 4Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, USA; 5Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, USA; 6Scientific and Clinical Affairs, Remitigate, LLC, Delmar, NY, USA

Abstract: The use of pharmacogenomics has become more prevalent over the past several years in treating many disease states. Several cytochrome P450 enzymes play a role in the metabolism of many pain medications including opioids and antidepressants. Noncytochrome P450 enzymes such as methylenetetrahydrofolate reductase (MTHFR) and catechol-O-methyl transferase (COMT) also play a role in the explanation of opioid dosage requirements as well as in response to certain antidepressants. We present the case of a patient with reduced COMT and MTHFR expression treated with leucovorin 10 mg daily for the management of chronic pain. The use of leucovorin in this patient decreased pain scores, which were clinically significant and increased functionality. This case demonstrates the importance of pharmacogenetics testing in patients, as this can help direct providers to better therapeutic options for their patients.

Keywords: pharmacogenetic, depression, pain, MTHFR, COMT, methyl tetrahydrofolate reductase, catechol-O-methyltransferase

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