Evidence map›Paper›PMID 41317376›Full record

SynthesisRheumatology (Oxford, England)2026

Factors associated with interstitial lung disease among patients with idiopathic inflammatory myopathies.

Jesse C Wilkerson, Frederick W Miller, Matthew F Bridge, Gary J Larson, Shepherd H Schurman, Stavros Garantziotis, Payam N Farhadi, Adam Schiffenbauer, Lisa G Rider

Abstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Rheumatology (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jesse C WilkersonDLH, LLC, Bethesda, MD, USA.
Frederick W MillerEnvironmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.
Matthew F BridgeDLH, LLC, Bethesda, MD, USA.
Gary J LarsonDLH, LLC, Bethesda, MD, USA.
Shepherd H SchurmanClinical Research Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Stavros GarantziotisImmunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Payam N FarhadiEnvironmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD, USA.
Adam SchiffenbauerEnvironmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD, USA.
Lisa G RiderEnvironmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-6912-2458

Funding

Environmental/genetic Risk Factors and Pathogenesis of Autoimmune DiseaseZIAES101074 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RIDER, LISA · 2009 to 2025
$34.6M
SCIENTIFIC, OPERATIONS, AND ADMINISTRATIVE RESOURCES (SOAR) TO NIH.75N95021D00012 · NIDA · KELLY SERVICES, INC. · PI SPROSE, SARA · 2021 to 2021
$57k
Intramural NIH HHS ZIA ES101074NIDA NIH HHS 75N95021D00012NIH HHS
6 · The paper itself

Abstract

objectivesIdiopathic inflammatory myopathies (IIM) are heterogeneous disorders that often affect the lungs as IIM-associated interstitial lung disease (IIM-ILD). We used Meta-ANalysis of Transethnic Associations (MANTRA) and machine learning methods to evaluate predictors of IIM-ILD.

methodsSubjects (N = 450) were enrolled in studies at the National Institutes of Health. We studied adult (N = 262) and juvenile (N = 188) DM (N = 276), PM (N = 109) and overlap myositis (N = 61) patients with clinical, autoantibody, HLA, and single nucleotide polymorphism (SNP) data, with (N = 162) or without (N = 288) ILD. Logistic regression and MANTRA analyses were used to evaluate the associations of SNPs (Muc5b rs35705950, TOLLIP rs5743890 and rs3750920, TLR5 rs5744168, and TERT rs2736100) previously identified as risks for idiopathic pulmonary fibrosis (IPF). Classification and regression tree (CART) and gradient boosting machine learning were used to simultaneously evaluate the clinical, autoantibody, HLA and SNP data for their relative predictive power of ILD.

resultsSmoking status, older age, African American heritage and certain HLA genes were associated with IIM-ILD, but anti-synthetase, myositis-associated and anti-MDA5 autoantibodies showed the strongest risk associations, with an increased odds of ILD by up to 20-fold. Conversely, anti-signal recognition particle, anti-TIF1 (P155/140) and anti-NXP2 autoantibodies showed the strongest protective effects, with decreased odds of ILD by up to 40%. The effects of some HLA allele groups and IPF SNPs on ILD were inconsistent and weaker.

conclusionsThis sample of IIM patients showed autoantibodies to be the strongest predictive or protective factors for ILD, yet the full range of associations of IIM-ILD remain undefined.

Indexed as

Lung Diseases, InterstitialMyositisAdultAgedAutoantibodiesFemaleGenetic Predisposition to DiseaseHumansMachine LearningMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsAutoantibodiesdermatomyositisinterstitial lung diseasemyositis-associated autoantibodiesmyositis-specific autoantibodiesoverlap myositispolymyositis

Identifiers

PMID41317376
PMCPMC12711402

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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.