Evidence map›Paper›PMID 33451338›Full record

ArticleArthritis research & therapy2021

The baseline interferon signature predicts disease severity over the subsequent 5 years in systemic lupus erythematosus.

Lloyd Mai, Arundip Asaduzzaman, Babak Noamani, Paul R Fortin, Dafna D Gladman, Zahi Touma, Murray B Urowitz, Joan Wither

Abstract read
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In one paragraph

Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

32 citing papers in PubMed, 1 synthesis or guideline 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

8 authors.

Lloyd MaiDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
Arundip AsaduzzamanDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
Babak NoamaniDivision of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Canada.
Paul R FortinDivision of Rheumatology, Department of Medicine, Centre de recherche du CHU de Québec - Université Laval, Quebec City, QC, Canada.
Dafna D GladmanDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
Zahi ToumaDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
Murray B UrowitzDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
Joan WitherDivision of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada. Joan.Wither@uhnresearch.ca.ORCID 0000-0001-5961-9228

Funding

CIHR QNT 78341
6 · The paper itself

Abstract

objectivesType I interferons (IFNs) play an important role in the pathophysiology of systemic lupus erythematosus (SLE). While cross-sectional data suggest an association between IFN-induced gene expression and SLE disease activity, interest in this as a biomarker of flare has been tempered by a lack of fluctuation with disease activity in the majority of patients. This led us to question whether IFN-induced gene expression might instead be a biomarker of overall disease severity, with patients with high levels spending more time in an active disease state.

methodsLevels of five interferon-responsive genes were measured in the whole peripheral blood at baseline visit for 137 SLE patients subsequently followed for 5 years. Log transformed values were summed to yield a composite IFN5 score, and the correlation with various disease outcomes examined. Receiver operator characteristic analyses were performed for outcomes of interest. Kaplan-Meier curves were generated to compare the proportion of flare-free patients with high and low IFN5 scores over time.

resultsThe baseline IFN5 score was positively correlated with the adjusted mean SLE disease activity index-2000, number of flares, adjusted mean prednisone dose, and number of new immunosuppressive medications over the subsequent 5 years. Optimal cut-offs for the IFN5 score were determined using Youden's index and predicted more severe outcomes with 57-67% accuracy. A high baseline IFN5 level was associated with a significantly increased risk of subsequent flare.

conclusionsMeasurement of the type I IFN signature is a useful tool for predicting the subsequent disease activity course.

Indexed as

Interferon Type ILupus Erythematosus, SystemicCross-Sectional StudiesHumansImmunosuppressive AgentsSeverity of Illness IndexImmunosuppressive AgentsInterferon Type IDisease courseInterferonSLEDAI-2KSystemic lupus erythematosus

Identifiers

PMID33451338
PMCPMC7811214

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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.