Evidence map›Paper›PMID 28132103›Full record

ArticleRheumatology international2017

Polymorphisms in the multidrug-resistance 1 gene related to glucocorticoid response in rheumatoid arthritis treatment.

Bart V J Cuppen, Katerina Pardali, Maarten C Kraan, Anne C A Marijnissen, Linda Yrlid, Marita Olsson, Johannes W J Bijlsma, Floris P J G Lafeber, Ruth D E Fritsch-Stork

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics onInternational journal of molecular sciences · 2019
    Pooled it
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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

9 authors at 3 institutions in 3 countries.

Bart V J CuppenRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands. b.v.j.cuppen@umcutrecht.nl.
Katerina PardaliRespiratory and Inflammation iMed, AstraZeneca, Pepparedsleden 1, 431 83, Mölndal, Sweden. katerina.pardali@astrazeneca.com.
Maarten C KraanRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands.
Anne C A MarijnissenRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands.
Linda YrlidRespiratory and Inflammation iMed, AstraZeneca, Pepparedsleden 1, 431 83, Mölndal, Sweden.
Marita OlssonRespiratory and Inflammation iMed, AstraZeneca, Pepparedsleden 1, 431 83, Mölndal, Sweden.
Johannes W J BijlsmaRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands.
Floris P J G LafeberRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands.
Ruth D E Fritsch-StorkRheumatology and Clinical Immunology, University Medical Center Utrecht, F02.127, 3508 GA, Utrecht, The Netherlands.
University Medical Center Utrecht · NLAstraZeneca (Sweden) · SEHanusch Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A substantial proportion of rheumatoid arthritis (RA)-patients experience an insufficient response to glucocorticoids, an important therapeutic agent in RA. The multidrug-resistance 1 (MDR1) gene product P-glycoprotein (P-gp) is an efflux pump that actively transports substrates, such as glucocorticoids, out of the cell. We investigated if the variation in response might be explained by single-nucleotide polymorphisms (SNPs) in the MDR1 gene. RA-patients treated with intravenous methylprednisolone pulses (n = 18) or oral prednisone/prednisolone (n = 22) were included in a prospective cohort, and clinical response was measured after 5 and 30 days, respectively. The C1236T, G2677A/T, and C3435T SNPs were determined, and the functionality of P-gp was assessed by flow cytometry (Rhodamine efflux assay). Carriage of the G2677A/T SNP was significantly associated with response (OR = 6.18, p = 0.035), the other SNPs showed trends. Stratified for received treatment, the effect was only present in methylprednisolone treated patients. Mutant allele carriage significantly decreased functionality of P-gp in B cells, though had a smaller impact in other PBMC subtypes. Carriage of a MDR1 SNP was related to a response to methylprednisolone in this study, which his suggests that RA-patients carrying wild-type alleles might benefit from P-gp inhibition or administration of glucocorticoid analogues that are non-P-gp substrates.

Indexed as

AdultAgedAllelesArthritis, RheumatoidATP Binding Cassette Transporter, Subfamily B, Member 1FemaleGenotypeGlucocorticoidsHumansMaleMethylprednisoloneMiddle AgedPharmacogeneticsPolymorphism, Single NucleotidePrednisolonePrednisoneATP Binding Cassette Transporter, Subfamily B, Member 1GlucocorticoidsMethylprednisolonePrednisolonePrednisoneGlucocorticoidsMDR1Multidrug resistancePolymorphismsRheumatoid Arthritis

Identifiers

PMID28132103
PMCPMC5357283
OpenAlexW2580366921

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.