Evidence map›Paper›PMID 27091191›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2016

A candidate gene investigation of methylphenidate response in adult attention-deficit/hyperactivity disorder patients: results from a naturalistic study.

Tor-Arne Hegvik, Kaya Kvarme Jacobsen, Mats Fredriksen, Tetyana Zayats, Jan Haavik

Abstract read
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  7. Review and Meta-analysis on the Impact of theBiological psychiatry global open science · 2022
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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

5 authors.

Tor-Arne HegvikDepartment of Biomedicine, University of Bergen, 5009, Bergen, Norway. tahegvik@gmail.com.
Kaya Kvarme JacobsenDepartment of Biomedicine, University of Bergen, 5009, Bergen, Norway.
Mats FredriksenDivision of Mental Health and Addiction, Vestfold Hospital Trust, 3101, Tønsberg, Norway.
Tetyana ZayatsDepartment of Biomedicine, University of Bergen, 5009, Bergen, Norway.
Jan HaavikDepartment of Biomedicine, University of Bergen, 5009, Bergen, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a common childhood onset neuropsychiatric disorder with a complex and heterogeneous symptomatology. Persistence of ADHD symptoms into adulthood is common. Methylphenidate (MPH) is a widely prescribed stimulant compound that may be effective against ADHD symptoms in children and adults. However, MPH does not exert satisfactory effect in all patients. Several genetic variants have been proposed to predict either treatment response or adverse effects of stimulants. We conducted a literature search to identify previously reported variants associated with MPH response and additional variants that were biologically plausible candidates for MPH response. The response to MPH was assessed by the treating clinicians in 564 adult ADHD patients and 20 genetic variants were successfully genotyped. Logistic regression was used to test for association between these polymorphisms and treatment response. Nominal associations (p < 0.05) were meta-analysed with published data from previous comparable studies. In our analyses, rs1800544 in the ADRA2A gene was associated with MPH response at a nominal significance level (OR 0.560, 95 % CI 0.329-0.953, p = 0.033). However, this finding was not affirmed in the meta-analysis. No genetic variants revealed significant associations after correction for multiple testing (p < 0.00125). Our results suggest that none of the studied variants are strong predictors of MPH response in adult ADHD as judged by clinician ratings, potentially except for rs1800544. Consequently, pharmacogenetic testing in routine clinical care is not supported by our analyses. Further studies on the pharmacogenetics of adult ADHD are warranted.

Indexed as

PharmacogeneticsAdultAttention Deficit Disorder with HyperactivityCentral Nervous System StimulantsFemaleGenetic VariationGenotypeHumansMaleMeta-Analysis as TopicMethylphenidateMiddle AgedReceptors, Adrenergic, alpha-2Treatment OutcomeYoung AdultADRA2A protein, humanCentral Nervous System StimulantsMethylphenidateReceptors, Adrenergic, alpha-2ADHDADRA2AMethylphenidatePharmacogeneticsStimulants

Identifiers

PMID27091191
PMCPMC4969350

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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.