Evidence map›Paper›PMID 28841649›Full record

Trial reportPloS one2017

Glycoprotein YKL-40: A potential biomarker of disease activity in rheumatoid arthritis during intensive treatment with csDMARDs and infliximab. Evidence from the randomised controlled NEO-RACo trial.

Tuija Väänänen, Katriina Vuolteenaho, Hannu Kautiainen, Riina Nieminen, Timo Möttönen, Pekka Hannonen, Markku Korpela, Markku J Kauppi, Kari Laiho, Oili Kaipiainen-Seppänen and 6 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.9field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  12. Neuroinflammation and Autophagy in Parkinson's Disease-Novel Perspectives.International journal of molecular sciences · 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

16 authors at 9 institutions in 1 country.

Tuija VäänänenThe Immunopharmacology Research Group, Faculty of Medicine and Life Sciences, University of Tampere and Tampere University Hospital, Tampere, Finland.
Katriina VuolteenahoThe Immunopharmacology Research Group, Faculty of Medicine and Life Sciences, University of Tampere and Tampere University Hospital, Tampere, Finland.ORCID http://orcid.org/0000-0003-0017-1291
Hannu KautiainenDepartment of General Practice, University of Helsinki, Helsinki, Finland.
Riina NieminenThe Immunopharmacology Research Group, Faculty of Medicine and Life Sciences, University of Tampere and Tampere University Hospital, Tampere, Finland.
Timo MöttönenDepartment of Rheumatology, University of Turku and Turku University Hospital, Turku, Finland.
Pekka HannonenDepartment of Medicine, Jyväskylä Central Hospital, Jyväskylä, Finland.
Markku KorpelaDepartment of Internal Medicine, Centre for Rheumatic Diseases, Tampere University Hospital, Tampere, Finland.
Markku J KauppiDepartment of Medicine, Päijät-Häme Central Hospital, Lahti, Finland.
Kari LaihoDepartment of Medicine, Päijät-Häme Central Hospital, Lahti, Finland.
Oili Kaipiainen-SeppänenDepartment of Medicine, Kuopio University Hospital, Kuopio, Finland.
Riitta LuosujärviRheumatology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Tea UusitaloDepartment of Medicine, Hämeenlinna Central Hospital, Hämeenlinna, Finland.
Toini UutelaDepartment of Medicine, Lapland Central Hospital, Rovaniemi, Finland.
Marjatta Leirisalo-RepoRheumatology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Eeva MoilanenThe Immunopharmacology Research Group, Faculty of Medicine and Life Sciences, University of Tampere and Tampere University Hospital, Tampere, Finland.
NEO-RACo Study Group
Tampere University · FIUniversity of Helsinki · FICentral Finland Health Care District · FIKanta-Hämeen Keskussairaala · FIKuopio University Hospital · FILapland Central Hospital · FIPäijät-Hämeen Keskussairaala · FITampere University Hospital · FIUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveYKL-40, a chitinase-like glycoprotein associated with inflammation and tissue remodeling, is produced by joint tissues and recognized as a candidate auto-antigen in rheumatoid arthritis (RA). In the present study, we investigated YKL-40 as a potential biomarker of disease activity in patients with early RA at baseline and during intensive treatment aiming for early remission.

methodsNinety-nine patients with early DMARD-naïve RA participated in the NEO-RACo study. For the first four weeks, the patients were treated with the combination of sulphasalazine, methotrexate, hydroxychloroquine and low dose prednisolone (FIN-RACo DMARD combination), and subsequently randomized to receive placebo or infliximab added on the treatment for further 22 weeks. Disease activity was evaluated using the 28-joint disease activity score and plasma YKL-40 concentrations were measured by immunoassay.

resultsAt the baseline, plasma YKL-40 concentration was 57 ± 37 (mean ± SD) ng/ml. YKL-40 was significantly associated with the disease activity score, interleukin-6 and erythrocyte sedimentation rate both at the baseline and during the 26 weeks' treatment. The csDMARD combination decreased YKL-40 levels already during the first four weeks of treatment, and there was no further reduction when the tumour necrosis factor-α antagonist infliximab was added on the combination treatment.

conclusionsHigh YKL-40 levels were found to be associated with disease activity in early DMARD-naïve RA and during intensive treat-to-target therapy. The present results suggest YKL-40 as a useful biomarker of disease activity in RA to be used to steer treatment towards remission.

Indexed as

AdultAntirheumatic AgentsArthritis, RheumatoidBiomarkersChitinase-3-Like Protein 1FemaleHumansInfliximabMaleMiddle AgedAntirheumatic AgentsBiomarkersCHI3L1 protein, humanChitinase-3-Like Protein 1Infliximab

Identifiers

PMID28841649
PMCPMC5571914
OpenAlexW2746312628

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Registered trials

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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.