Pharmacogenetics of methylphenidate response and tolerability in attention-deficit/hyperactivity disorder

Methylphenidate (MPH) is the most frequently used pharmacological treatment in children with attention-deficit/hyperactivity disorder. However, a considerable interindividual variability exists in clinical outcome, which may reflect underlying genetic influences. We analyzed 57 single-nucleotide pol...

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Veröffentlicht in:The pharmacogenomics journal 2017-01, Vol.17 (1), p.98-104
Hauptverfasser: Pagerols, M, Richarte, V, Sánchez-Mora, C, Garcia-Martínez, I, Corrales, M, Corominas, M, Cormand, B, Casas, M, Ribasés, M, Ramos-Quiroga, J A
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container_issue 1
container_start_page 98
container_title The pharmacogenomics journal
container_volume 17
creator Pagerols, M
Richarte, V
Sánchez-Mora, C
Garcia-Martínez, I
Corrales, M
Corominas, M
Cormand, B
Casas, M
Ribasés, M
Ramos-Quiroga, J A
description Methylphenidate (MPH) is the most frequently used pharmacological treatment in children with attention-deficit/hyperactivity disorder. However, a considerable interindividual variability exists in clinical outcome, which may reflect underlying genetic influences. We analyzed 57 single-nucleotide polymorphisms in 9 dopamine-related candidate genes ( TH , DBH , COMT , DAT1 and DRD1 - 5 ) as potential predictors of MPH efficacy and tolerability, and we considered prenatal and perinatal risk factors as environmental hazards that may influence treatment effects in a gene-by-environment analysis. Our results provide evidence for the contribution of DRD3 ( P =0.041; odds ratio (OR)=4.00), DBH ( P =0.032; OR=2.85), TH ( P =5.5e-03; OR=4.34) and prenatal smoking ( P =1.7e-03; OR=5.10) to the clinical efficacy of MPH, with a higher risk for treatment failure in genetically susceptible subjects whose mother smoked during pregnancy. Adverse events after MPH treatment were significantly associated with variation in DBH ( P =6.4e-03; OR=0.28) and DRD2 ( P =0.047; OR=3.76). This study suggests that the dopaminergic system together with prenatal smoking exposure may moderate MPH treatment effects.
doi_str_mv 10.1038/tpj.2015.89
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subjects 45/22
45/23
45/77
631/208/205
Adolescent
Attention Deficit Disorder with Hyperactivity - diagnosis
Attention Deficit Disorder with Hyperactivity - drug therapy
Attention deficit hyperactivity disorder
Biomedical and Life Sciences
Biomedicine
Central Nervous System Stimulants - adverse effects
Central Nervous System Stimulants - therapeutic use
Chi-Square Distribution
Child
Child, Preschool
Dopamine beta-Hydroxylase - genetics
Dopamine D1 receptors
Dopamine D2 receptors
Dopamine D3 receptors
Dopamine receptors
Dopamine Uptake Inhibitors - adverse effects
Dopamine Uptake Inhibitors - therapeutic use
Drug therapy
Female
Gene Expression
Gene Frequency
Gene-Environment Interaction
Haplotypes
Human Genetics
Humans
Hyperactivity
Methylphenidate
Methylphenidate - adverse effects
Methylphenidate - therapeutic use
Odds Ratio
Oncology
original-article
Pharmacogenetics
Pharmacogenomic Variants
Pharmacotherapy
Phenotype
Polymorphism, Single Nucleotide
Pregnancy
Prenatal experience
Prenatal Exposure Delayed Effects
Psychopharmacology
Receptors, Dopamine D2 - genetics
Receptors, Dopamine D3 - genetics
Risk Factors
Single-nucleotide polymorphism
Smoking
Smoking - adverse effects
Treatment Outcome
Tyrosine 3-Monooxygenase - genetics
title Pharmacogenetics of methylphenidate response and tolerability in attention-deficit/hyperactivity disorder
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