Evidence map›Paper›PMID 23588108›Full record

SynthesisThe pharmacogenomics journal2014

Meta-analysis of the association between dopamine transporter genotype and response to methylphenidate treatment in ADHD.

J Kambeitz, M Romanos, U Ettinger

Open access · bronzeAbstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in The pharmacogenomics journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 8 pooled it
5.6field-weighted citation impact, top 3% of its field
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

34 citing papers in PubMed, 8 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Guideline
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Methylphenidate effects on brain activity as a function of SLC6A3 genotype and striatal dopamine transporter availability.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Trial
  10. Trial
  11. Article
  12. Dopamine Transporter andJournal of child and adolescent psychopharmacology · 2024
    Article
  13. Article
  14. Review
  15. Associations betweenFrontiers in pediatrics · 2022
    Article
  16. Article
  17. Observational
  18. Genetics of ADHD: What Should the Clinician Know?Current psychiatry reports · 2020
    Review
  19. Review
  20. Review
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

3 authors at 3 institutions in 1 country.

J KambeitzDepartment of Psychiatry, University of Munich, Munich, Germany.
M RomanosDepartment of Child and Adolescent Psychiatry, University Hospital of Würzburg, Würzburg, Germany.
U EttingerDepartment of Psychology, University of Bonn, Bonn, Germany.
Ludwig-Maximilians-Universität München · DEUniversitätsklinikum Würzburg · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent childhood-onset neuropsychiatric disorder. Treatment with methylphenidate, which blocks dopamine and noradrenaline transporters, is clinically efficacious in reducing the symptoms of ADHD. However, a considerable proportion of patients show no or only insufficient response to methylphenidate. Following a pharmacogenetic approach, a number of studies have suggested that heterogeneity in treatment response across subjects might to some extent be due to genetic factors. In particular, a variable number tandem repeat (VNTR) polymorphism in the 3' untranslated region of the SLC6A3 gene, which codes for the dopamine transporter, has been considered as a predictor of treatment success. However, the literature has so far been inconsistent. Here we present results of a meta-analysis of studies investigating the moderating effect of the SLC6A3 VNTR on response to methylphenidate treatment in subjects with ADHD. Outcome measures from 16 studies including data from 1572 subjects were entered into a random-effects model. There was no significant summary effect for the SLC6A3 VNTR on the response to methylphenidate treatment (P>0.5) and no effect on specific symptom dimensions of hyperactivity/impulsivity and inattention (all P>0.2). However, in a subanalysis of naturalistic trials, we observed a significant effect of d=-0.36 (P=0.03), indicating that 10R homozygotes show less improvement in symptoms following treatment than the non-10/10 carriers. This meta-analysis indicates that SLC6A3 VNTR is not a reliable predictor of methylphenidate treatment success in ADHD. Our study leaves unanswered the question of whether other genetic polymorphisms or nongenetic factors may contribute to the observed heterogeneity in treatment response across ADHD subjects.

Indexed as

Polymorphism, Genetic3' Untranslated RegionsAttention Deficit Disorder with HyperactivityDopamine Plasma Membrane Transport ProteinsDopamine Uptake InhibitorsGenotypeHumansMethylphenidateTandem Repeat SequencesTreatment Outcome3' Untranslated RegionsDopamine Plasma Membrane Transport ProteinsDopamine Uptake InhibitorsMethylphenidateSLC6A3 protein, human

Identifiers

PMID23588108
OpenAlexW2034027897

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.