Evidence map›Paper›PMID 24394199›Full record

ArticleThe pharmacogenomics journal2014

Pharmacogenomics of NAT2 and ABCG2 influence the toxicity and efficacy of sulphasalazine containing DMARD regimens in early rheumatoid arthritis.

M D Wiese, N Alotaibi, C O'Doherty, M J Sorich, V Suppiah, L G Cleland, S M Proudman

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In one paragraph

Article 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 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 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

7 authors at 2 institutions in 1 country.

M D WieseSansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia.
N AlotaibiSansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia.
C O'DohertySansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia.
M J Sorich1] Sansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia [2] Department of Clinical Pharmacology, School of Medicine, Flinders University, Adelaide, South Australia, Australia.
V SuppiahSansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia.
L G Cleland1] Department of Rheumatology, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, Australia [2] School of Medicine, Adelaide University, North Terrace, Adelaide, South Australia, Australia.
S M Proudman1] Department of Rheumatology, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, Australia [2] School of Medicine, Adelaide University, North Terrace, Adelaide, South Australia, Australia.
University of South Australia · AURoyal Adelaide Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sulphasalazine (SSA) is a disease modifying anti-rheumatic drug (DMARD) that is commonly used to treat rheumatoid arthritis (RA). Plasma levels of SSA and its metabolite sulphapyridine are influenced by common polymorphisms in genes that encode N-acetyl transferase 2 (NAT2) and ATP-binding cassette protein G2 (ABCG2). Study participants had early RA that was treated with a combination DMARD regimen that included SSA. Toxicity was defined by cessation of SSA due to adverse effects and response as remission after 12 months of treatment. The effect of variables on toxicity was assessed by a Cox-proportional Hazard model and response by logistic regression. After correction for conventional variables, toxicity in 229 participants was influenced by NAT2 phenotype (hazard ratio=1.74 (95% confidence interval (CI) 1.01-3.21), P=0.044) and remission in 141 participants was associated with ABCG2 genotype (odds ratio=3.34 (95% CI 1.18-9.50), P=0.024). In our sample of early RA patients who were primarily treated with a combination of DMARDs, common variants in genes that encode NAT2 and ABCG2 were associated respectively with toxicity and response to SSA.

Indexed as

PharmacogeneticsAdultAgedAntirheumatic AgentsArthritis, RheumatoidArylamine N-AcetyltransferaseATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2FemaleGenotypeHumansMaleMiddle AgedNeoplasm ProteinsPolymorphism, GeneticProportional Hazards ModelsABCG2 protein, humanAntirheumatic AgentsArylamine N-AcetyltransferaseATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2NAT2 protein, humanNeoplasm ProteinsSulfasalazine

Identifiers

PMID24394199
OpenAlexW2066186986

What OpenQuestion holds

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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.