Evidence map›Paper›PMID 28045129›Full record

ArticleThe pharmacogenomics journal2018

The glutathione transferase Mu null genotype leads to lower 6-MMPR levels in patients treated with azathioprine but not with mercaptopurine.

M M T J Broekman, D R Wong, G J A Wanten, H M Roelofs, C J van Marrewijk, O H Klungel, A L M Verbeek, P M Hooymans, H-J Guchelaar, H Scheffer and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in The pharmacogenomics journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
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

13 authors at 6 institutions in 1 country.

M M T J BroekmanRadboud University Medical Center, Radboud Institute for Molecular Life Sciences, Department of Gastroenterology, Nijmegen, The Netherlands.
D R WongDepartment of Clinical Pharmacy, Pharmacology and Toxicology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands.
G J A WantenRadboud University Medical Center, Radboud Institute for Molecular Life Sciences, Department of Gastroenterology, Nijmegen, The Netherlands.
H M RoelofsRadboud University Medical Center, Radboud Institute for Molecular Life Sciences, Department of Gastroenterology, Nijmegen, The Netherlands.
C J van MarrewijkRadboud University Medical Center, Radboud Institute for Health Sciences, Department of Human Genetics, Nijmegen, The Netherlands.
O H KlungelDepartment of Pharmacoepidemiology and Pharmacotherapy, Utrecht University, Utrecht, The Netherlands.
A L M VerbeekRadboud University Medical Center, Radboud Institute for Health Sciences, Nijmegen, The Netherlands.
P M HooymansDepartment of Clinical Pharmacy, Pharmacology and Toxicology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands.
H-J GuchelaarDepartment of Clinical Pharmacy and Toxicology, Leiden University Medical Center, Leiden, The Netherlands.
H SchefferRadboud University Medical Center, Radboud Institute for Health Sciences, Department of Human Genetics, Nijmegen, The Netherlands.
L J J DerijksDepartment of Clinical Pharmacy, Máxima Medical Center, Veldhoven, The Netherlands.
M J H CoenenRadboud University Medical Center, Radboud Institute for Health Sciences, Department of Human Genetics, Nijmegen, The Netherlands.
D J de JongRadboud University Medical Center, Radboud Institute for Molecular Life Sciences, Department of Gastroenterology, Nijmegen, The Netherlands.
Radboud University Medical Center · NLRadboud Institute for Molecular Life Sciences · NLRadboud University Nijmegen · NLZuyderland Medisch Centrum · NLLeiden University Medical Center · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2). We designed a case-control study with data from the TOPIC trial to explore the effects of genetic variation on steady state 6-methylmercaptopurine ribonucleotide (6-MMPR) and 6-thioguanine nucleotide (6-TGN) metabolite levels. We included 199 patients with inflammatory bowel disease (126 on AZA and 73 on MP). GSTM1-null genotype carriers on AZA had two-fold lower 6-MMPR levels than AZA users carrying one or two copies of GSTM1 (2239 (1006-4587) versus 4371 (1897-7369) pmol/8 × 10

Indexed as

AdultAnti-Inflammatory Agents, Non-SteroidalAzathioprineCase-Control StudiesFemaleGenotypeGlutathione TransferaseGuanine NucleotidesHumansImmunosuppressive AgentsInflammatory Bowel DiseasesIsoenzymesMaleMercaptopurineMiddle AgedThioinosine6-methylthiopurine ribonucleoside-5'-phosphate6-thioguanylic acidAnti-Inflammatory Agents, Non-SteroidalAzathioprineglutathione S-transferase alphaGlutathione TransferaseGuanine NucleotidesImmunosuppressive AgentsIsoenzymesMercaptopurineThioinosineThionucleotides

Identifiers

PMID28045129
OpenAlexW2561670050

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.