Pharmacogenetic testing in psychiatric inpatients with polypharmacy is associated with decreased medication side effects but not via medication changes.
Cytochrome P450
Drug-drug interaction
Drug-genotype interaction
Pharmacogenetics
Polymorphism
Polypharmacy
Journal
Journal of psychiatric research
ISSN: 1879-1379
Titre abrégé: J Psychiatr Res
Pays: England
ID NLM: 0376331
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
12
03
2020
revised:
24
04
2020
accepted:
04
05
2020
pubmed:
23
5
2020
medline:
15
5
2021
entrez:
23
5
2020
Statut:
ppublish
Résumé
In psychiatric patients, medication adverse effects are regularly attributed to psychosomatic causes. However, many psychotropic medications are metabolized by cytochrome P450 (CYP450) enzymes. In the setting of polypharmacy, the activity of these enzymes may produce unfavorable drug-drug interactions (DDI) and drug-genotype interactions (DGI) that contribute to morbidity and mortality. This study sought to estimate the risk of adverse DDI and DGI in psychiatric inpatients with polypharmacy. We assessed whether medication changes made after pharmacogenetics (PGx) testing correlated with changes in side effects and overall improvement. Adult psychiatry inpatients with polypharmacy, defined as 5 or more scheduled prescription medications, completed the 24-item Antidepressant Side Effect Checklist (ASEC) questionnaire on enrollment and underwent PGx testing. Analysis of PGx results focused on whether the CYP2D6 and CYP2C19 phenotypes were "extreme," defined as poor, poor to intermediate, or ultrarapid. Approximately 30 days after PGx results were sent to outpatient providers, patients were contacted to obtain their current medication list and ASEC and Clinical Global Impression Improvement (CGI-I) scores. A total of 80 patients were enrolled, and 52 (65%) completed follow-up. ASEC scores improved from 11.5 (±8.1) to 7.2 (±6.0) (p = 0.0009). Mean CGI-I score was 2.7 (±1.4), between "minimal" to "much improved." However, linear regression revealed that these improvements were not correlated with whether medications were changed. We concluded that the impact of drug-genotype interactions in this small sample of inpatients with polypharmacy was low, and that patient improvement was related not to PGx-guided medication changes but to other treatments during hospitalization.
Identifiants
pubmed: 32442780
pii: S0022-3956(20)30223-5
doi: 10.1016/j.jpsychires.2020.05.002
pmc: PMC9441021
mid: NIHMS1596196
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
105-111Subventions
Organisme : NCATS NIH HHS
ID : UL1 TR002377
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest Mayo Clinic has a financial relationship with OneOme. However, none of the authors have a direct financial or personal relationship with OneOme.
Références
Clin Pharmacol Ther. 2014 Dec;96(6):655-7
pubmed: 25399714
JAMA. 2016 Nov 22;316(20):2092-2093
pubmed: 27893112
Curr Med Res Opin. 2015;31(9):1633-43
pubmed: 26086890
Drug Saf. 2012 Jan;35 Suppl 1:3-20
pubmed: 23446782
Pharmacogenet Genomics. 2011 Jan;21(1):1-9
pubmed: 21192344
BMC Psychiatry. 2017 Jul 14;17(1):250
pubmed: 28705252
Prev Chronic Dis. 2014 Apr 17;11:E62
pubmed: 24742395
Pharmacogenomics. 2009 May;10(5):769-78
pubmed: 19450128
J Affect Disord. 2019 Mar 1;246:62-68
pubmed: 30578947
Br J Psychiatry. 2009 Sep;195(3):202-10
pubmed: 19721108
Eur J Clin Pharmacol. 2004 Jul;60(5):329-36
pubmed: 15168101
PLoS One. 2008 Apr 02;3(4):e1872
pubmed: 18382661
JAMA. 2016 Nov 22;316(20):2115-2125
pubmed: 27893129
Basic Clin Pharmacol Toxicol. 2005 Nov;97(5):296-301
pubmed: 16236141
Neuropsychopharmacology. 2006 Apr;31(4):825-31
pubmed: 16205777
Am J Psychiatry. 2018 Sep 1;175(9):873-886
pubmed: 29690793
Curr Drug Metab. 2014 Feb;15(2):209-17
pubmed: 24479687
Crit Rev Clin Lab Sci. 2019 Nov 2;:1-20
pubmed: 31680605
NCHS Data Brief. 2010 Sep;(42):1-8
pubmed: 20854747
PLoS One. 2017 Feb 2;12(2):e0170905
pubmed: 28151991
J Psychiatr Res. 2019 Apr;111:59-67
pubmed: 30677646
J Psychopharmacol. 2006 Jul;20(4 Suppl):85-94
pubmed: 16785276
N Engl J Med. 2005 May 26;352(21):2211-21
pubmed: 15917386
Clin Interv Aging. 2008;3(2):383-9
pubmed: 18686760
Pharmacol Ther. 2013 Apr;138(1):103-41
pubmed: 23333322
Sci Data. 2017 Oct 31;4:170167
pubmed: 29087369
J Clin Psychopharmacol. 2006 Apr;26(2):211-2
pubmed: 16633156
Eur Neuropsychopharmacol. 2018 Aug;28(8):945-954
pubmed: 30135031
Am J Health Syst Pharm. 2016 Jan 15;73(2):61-7
pubmed: 26721535
Eur J Clin Pharmacol. 2008 Dec;64(12):1181-8
pubmed: 18677622
JAMA Psychiatry. 2018 Aug 1;75(8):769-770
pubmed: 29799933
Psychiatry (Edgmont). 2007 Jul;4(7):28-37
pubmed: 20526405
Clin Pharmacol Ther. 2015 Aug;98(2):127-34
pubmed: 25974703
Eur J Clin Pharmacol. 2015 Feb;71(2):131-42
pubmed: 25529225
Prim Care Companion CNS Disord. 2015 Apr 16;17(2):
pubmed: 26445691
Science. 1999 Oct 15;286(5439):487-91
pubmed: 10521338
JAMA. 1998 Apr 15;279(15):1200-5
pubmed: 9555760
Pharmacogenomics. 2014 Apr;15(5):655-65
pubmed: 24798722
Ther Drug Monit. 2003 Dec;25(6):738-42
pubmed: 14639062
Psychopharmacology (Berl). 2015 Jul;232(14):2609-17
pubmed: 25761838
Gen Physiol Biophys. 2003 Mar;22(1):103-13
pubmed: 12870705
Ther Drug Monit. 2015 Oct;37(5):589-93
pubmed: 25565674
PLoS One. 2015 Mar 04;10(3):e0118991
pubmed: 25739022
Clin Psychopharmacol Neurosci. 2015 Aug 31;13(2):150-6
pubmed: 26243841