Evidence map›Paper›PMID 26810137›Full record

ArticleThe pharmacogenomics journal2017

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

M Pagerols, V Richarte, C Sánchez-Mora, I Garcia-Martínez, M Corrales, M Corominas, B Cormand, M Casas, M Ribasés, J A Ramos-Quiroga

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In one paragraph

Article in The pharmacogenomics journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Investigating genetic correlation and causality between nicotine dependence and ADHD in a broader psychiatric context.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2021
    Article
  5. Observational
  6. Review
  7. Article
  8. Article
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  10. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

M PagerolsPsychiatric Genetics Unit, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain.
V RicharteDepartment of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
C Sánchez-MoraPsychiatric Genetics Unit, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain.
I Garcia-MartínezPsychiatric Genetics Unit, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain.
M CorralesDepartment of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
M CorominasDepartment of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
B CormandDepartament de Genètica, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
M CasasDepartment of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
M RibasésPsychiatric Genetics Unit, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain.
J A Ramos-QuirogaDepartment of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

PharmacogeneticsPharmacogenomic VariantsPolymorphism, Single NucleotideAdolescentAttention Deficit Disorder with HyperactivityCentral Nervous System StimulantsChildChild, PreschoolChi-Square DistributionDopamine beta-HydroxylaseDopamine Uptake InhibitorsFemaleGene-Environment InteractionGene FrequencyHaplotypesHumansCentral Nervous System StimulantsDopamine beta-HydroxylaseDopamine Uptake InhibitorsDRD2 protein, humanDRD3 protein, humanMethylphenidateReceptors, Dopamine D2Receptors, Dopamine D3Tyrosine 3-Monooxygenase

Identifiers

PMID26810137

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.