Non-response to consecutive antidepressant therapy caused by CYP2D6 ultrarapid metabolizer phenotype

Breil, Fleur; Verstuyft, Céline; Orostegui, Lupe; Buhl, Catherine; Alvarez, Jean‐Claude; Chouinard, Guy; Becquemont, Laurent

doi:10.1017/s1461145708008742

Cited by 9 publications

(2 citation statements)

References 11 publications

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“…It has been reported that CYP2D6 PMs have greater susceptibility to adverse effects44,45 and lower treatment response15,16 to antidepressants than EMs due to higher plasma drug concentrations. On the other hand, reduced antidepressant efficacy in CYP2D6 UMs was attributed to insufficient plasma drug concentrations to produce the desired therapeutic effects with the usual doses 46,47. The frequency of CYP2 D6 * 10 is relatively high in Asian IMs, and lower catalytic activities toward various psychotropic drugs, including antidepressants, were observed in patients with CYP2D6 * 10/ * 10 or CYP2D6 * 10/ * null genotypes 25.…”

Section: Discussionmentioning

confidence: 99%

CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression

Han

Chang

Choi

et al. 2013

Psychiatry Investig

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ObjectiveCytochrome P450 (CYP) enzymatic activity, which is influenced by CYP genetic polymorphism, is known to affect the inter-individual variation in the efficacy and tolerability of antidepressants in major depressive disorder (MDD). Escitalopram is metabolized by CYP2D6, and recent studies have reported a correlation between clinical outcomes and CYP2D6 genetic polymorphism. The purpose of this study was to determine the relationship between the CYP2D6 P34S polymorphism (C188T, rs1065852) and the efficacy of escitalopram treatment in Korean patients with MDD.MethodsA total of 94 patients diagnosed with MDD were recruited for the study and their symptoms were evaluated using the 21-item Hamilton Depression Rating scale (HAMD-21). The association between the CYP2D6 P34S polymorphism and the clinical outcomes (remission and response) was investigated after 1, 2, 4, 8, and 12 weeks of escitalopram treatment using multiple logistic regression analysis and χ2 test.ResultsThe proportion of P allele carriers (PP, PS) in remission status was greater than that of S allele homozygotes (SS) after 8 and 12 weeks of escitalopram treatment. Similarly, P allele carriers exhibited a greater treatment response after 8 and 12 weeks of escitalopram treatment than S allele homozygotes.ConclusionOur results suggest that the P allele of the CYP2D6 P34S polymorphism is a favorable factor in escitalopram treatment for MDD, and that the CYP2D6 P34S polymorphism may be a good genetic marker for predicting escitalopram treatment outcomes.

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Section: Discussionmentioning

confidence: 99%

CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression

Han

Chang

Choi

et al. 2013

Psychiatry Investig

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“…The clinical consequence of this may include concentration-related drug toxicity and or therapeutic failure [11, 12]. Therefore, adverse drug reactions resulting from poor drug handling due to enzyme polymorphisms should be preventable if appropriate dosing could be achieved.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of CYP2D6 phenotype in the Yoruba Nigerian population

Adedeji

Igbinoba

Fakeye

et al. 2017

Expert Review of Clinical Pharmacology

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Background: There is a lack of information on CYP2D6, a major metabolizing enzyme, in Africa ethnic nationalities. The objective was to determine CYP2D6 phenotype in Yoruba Nigerians using dextromethorphan (DEX). Method: A total of 89 healthy volunteers received 30 mg of DEX orally followed by blood and urine sample collection at 3-hour and over 8 hours post-dose, respectively. DEX and dextrorphan (DOR) concentrations were determined using High Performance Liquid Chromatography (HPLC). The metabolic ratio (MR, DEX/DOR) were plotted for the phenotype determination. Results: The log MR that separated poor (PMs) from normal metabolizers (NMs) was 0.28 and 0.75 for urine and plasma, respectively. Two subjects (2.3%) identified as PMs had a mean MR of 17 and 3.2 in plasma and urine, significantly higher than that of NMs (p<0.0001). A positive correlation between urine and plasma MR was noted. Conclusion: The prevalence of PMs in the Yoruba Nigerians was similar to that reported among blacks.

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Ist die Genotypisierung von CYP-Enzymen sinnvoll?

Hiemke¹,

Frieling²

2015

DNP

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Non-response to consecutive antidepressant therapy caused by CYP2D6 ultrarapid metabolizer phenotype

Cited by 9 publications

References 11 publications

CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression

CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression

Evaluation of CYP2D6 phenotype in the Yoruba Nigerian population

Ist die Genotypisierung von CYP-Enzymen sinnvoll?

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