Evidence map›Paper›PMID 20112385›Full record

Trial reportArthritis and rheumatism2010

Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-beta/alpha ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort.

Clio P Mavragani, Dan T La, William Stohl, Mary K Crow

Registry-linked trialAbstract readClinical Trial
In one paragraph

Trial report in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02878161 (Screening Protein Predictive of Response to Tumor Necrosis Factor-α Inhibitors Treatment in Chinese Rheumatoid Arthritis From "Real World" and Investigating Its Mechanism Through Signal Pathway), which is not on this map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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.

NCT02878161 phase4unknown statusnot on this mapstarted 2016, after this paper: background citation

Screening Protein Predictive of Response to Tumor Necrosis Factor-α Inhibitors Treatment in Chinese Rheumatoid Arthritis From "Real World" and Investigating Its Mechanism Through Signal Pathway

TypeinterventionalSponsorFen LiRan2016 to 2019Enrolled240ConditionsRheumatoid ArthritisArmsmethotrexate(necessary), infliximab, etanercept, adalimumab, leflunomide (permitted, not necessary)
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

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  17. Hi-Frontiers in medicine · 2020
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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

4 authors at 3 institutions in 1 country.

Clio P MavraganiHospital for Special Surgery, Weill Cornell Medical College, New York, NY, USA.
Dan T La
William Stohl
Mary K Crow
University of Southern California · USCornell University · USHospital for Special Surgery · US

Funding

RHEUMATOLOGY TRAININGT32AR007517 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 1986 to 2014
$2.2M
Interferon in Systemic Lupus ErythematosusR01AI059893 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 2006 to 2010
$2.1M
NIAID NIH HHS AI-059893NIAID NIH HHS R01 AI059893NIAMS NIH HHS T32 AR007517
6 · The paper itself

Abstract

objectiveDespite the substantial clinical efficacy of tumor necrosis factor alpha (TNFalpha) antagonist therapy in patients with rheumatoid arthritis (RA), some patients respond poorly to such agents. Since an interferon (IFN) signature is variably expressed among RA patients, we investigated whether plasma type I IFN activity might predict the response to TNF antagonist therapy.

methodsRA patients (n = 35), the majority of whom were Hispanic, from a single center were evaluated before and after initiation of TNF antagonist therapy. As controls, 12 RA patients from the same center who were not treated with a TNF antagonist were studied. Plasma type I IFN activity was measured using a reporter cell assay, and disease status was assessed using the Disease Activity Score in 28 joints (DAS28). Levels of interleukin-1 receptor antagonist (IL-1Ra) were determined in baseline plasma samples using a commercial enzyme-linked immunosorbent assay. The clinical response was classified according to the European League Against Rheumatism criteria for improvement in RA.

resultsPlasma type I IFN activity at baseline was significantly associated with clinical response (odds ratio 1.36 [95% confidence interval 1.05-1.76], P = 0.020), with high baseline IFN activity associated with a good response. Changes in DAS28 scores were greater among patients with a baseline plasma IFNbeta/alpha ratio >0.8 (indicating elevated plasma IFNbeta levels). Consistent with the capacity of IFNbeta to induce IL-1Ra, elevated baseline IL-1Ra levels were associated with better therapeutic outcomes (odds ratio 1.82 [95% confidence interval 1.1-3.29], P = 0.027).

conclusionThe plasma type I IFN activity, the IFNbeta/alpha ratio, and the IL-1Ra level were predictive of the therapeutic response in TNF antagonist-treated RA patients, indicating that these parameters might define clinically meaningful subgroups of RA patients with distinct responses to therapeutic agents.

Indexed as

Hispanic or LatinoAdalimumabAdultAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsArthritis, RheumatoidCohort StudiesEtanerceptFemaleHumansImmunoglobulin GInfliximabInterferon-alphaInterferon-betaInterleukin 1 Receptor Antagonist ProteinAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsEtanerceptImmunoglobulin GInfliximabInterferon-alphaInterferon-betaInterleukin 1 Receptor Antagonist ProteinReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID20112385
PMCPMC2821991
OpenAlexW156829367

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

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.